Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

nurs pathophysiology > rrd 4 > Flashcards

rrd 4 Flashcards

mech of defense: inflammation and immune fxn and disorders pt 2

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

two types of anti-inflammatories

A
  • steroids
  • NSAIDS “non-steroidal anti-inflammatory drugs”
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

prostaglandins (PGs)

A

group of mediators that have a large variety of functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

PGs are created in the ___ ____ of most cells in the body, in a series of steps called ____ ____.

A

cell membrane, arachidonic pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

PGs are generally categorized as either being _____ or _____.

A

protective, proinflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

basic/simple map of the arachidonic pathway

A
  1. cell membrane phospholipids
  2. arachidonic acid
    3(1). leukotrienes
    3(2). prostaglandins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

where do steroids work in the arachidonic pathway?

A

with phospholipases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

steroids are ____ ____. what is the most common steroid?

A
  • naturally occurring
  • cortisol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

synthetic examples of steroids are ____ based on the structure of ____. what are some examples?

A
  • drugs, cortisol
  • prednisone and solumedrol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

steroids are ______ in their inhibition of prostaglandins. they suppress both ____ and ____ types of prostaglandins.

A

non-specific, proinflammatory, protective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how do steroids suppress both proinflammatory and protective types of prostaglandins?

A

suppress phospholipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

steroids are used for more ______ conditions such as?

A
  • inflammatory
  • acute back injuries, asthma, allergic rxns, bad rashes, lupus, other autoimmune dx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

potential side effects of steroids

A
  • stomach ulcers
  • easier bleeding
  • diminished kidney fxn
  • diminished capacity to combat infection
  • increased skin fragility
  • HTN
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

steroids nickname

A

a double-edged sword

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

NSAIDs

A

non-steroidal anti-inflammatories

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

NSAIDs ____ inflammation, but do so at a ____ place in the arachidonic pathway compared to steroids.

A

suppress, lower

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

NSAIDs are ____ powerful compared to steroids because?

A
  • not as
  • work lower in the arachidonic pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

T/F: NSAIDs do not have as bad of side effects as steroids.

A
  • TRUE
  • not as bad of side effects because they work lower in the arachidonic pathway
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

NSAIDs are used for problems such as? what are they not used for?

A
  • headaches
  • general aches and pains
  • not used for suppressing more serious inflammatory conditons
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

examples of NSAIDs

A
  • aspirin
  • ibuprofen (Motrin)
  • naproxen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

leukotrienes

A

inflammatory mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

prostaglandins 2 categories of fxn?

A
  • proinflammatory
  • protective
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

proinflammatory category of PGs

A

increase inflammatory response as needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

protective category of PGs

A
  • have normal PLATELET clotting fxn
  • maintain the integrity of the GASTRIC mucosa
  • promote healthy RENAL fxn
  • maintain appropriate VASOMOTOR tone
  • maintain normal IMMUNOCYTE fxn
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

ProstaGlandins R Very Important

A
  • P: platelet
  • G: gastric
  • R: renal
  • V: vasomotor
  • I: immunocyte
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

vasomotor tone

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

third line of defense?

A
  • normal immunocyte response
  • acquired immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

immunocyte response

A

a state of acquired defense

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

immunocyte response characterized by:

A
  • involvement of immunocytes/lymphocytes
  • being delayed and specific
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

types of lymphocytes involved in immunocyte response

A
  • T-lymphocytes (T-cells)
  • B-lymphocytes (B-cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

t-lymphocytes (t-cells)

A

defend the body by direct attack against invading microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

subtypes of t-lymphocytes

A
  • CD4 cells
  • CD8 cells
  • memory t-cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

CD4 cells

A
  • helper-T
  • introductory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

CD8 cells

A
  • cytotoxic T-cells
  • act as direct killers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

memory t-cells

A

memorize microbe properties

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

b-lymphocytes (b-cells)

A

defend by a more complicated method

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

subtypes of b-lymphocytes

A
  • b-cells
  • plasma cells
  • memory B cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

B-cells

A

differentiate into plasma cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

plasma cells

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

immunocyte response being specific means?

A

immunocytes only respond fully to microbes that they recognize (have developed memory of)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

immunocyte response being delayed means?

A
  • takes time to develop the ability to recognize and destroy microbes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

antigens

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

antibodies

A
  • IgG, IgE, IgA
  • a group of blood proteins that are made by the immune system in response to and counteract a specific antigen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

due to immunocyte involvement, the person develops?

A

ability to resist certain diseases and conditions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

B and T lymphocytes, and various lymphatic tissues, are?

A

major players in the immune response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

if the T cell is “in charge” of developing immunity, the person developed?

A

cell-mediated immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

if the B cell is “in charge” of developing immunity, the person developed?

A

humoral immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

no matter which type of immunity developed, it involves?

A

a primary and secondary response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

the third line of defense is stimulated by?

A

the second line of defense, as needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

a meningitis bacterial microbe is inhaled and makes it way to the meninges. what line of defense did it breach?

A

1st line of defense - the mucous membranes of nose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

when a meningitis bacterial microbe makes it way to the meninges, what happens next?

A

inflammation takes place as part of the body’s normal healing process attempt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

what happens when local inflammation cannot handle the meningitis bacterial microbe stimulating inflammation in the meninges?

A

systemic inflammatory mediators are released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

_____ identifies that a microbe is present after systemic inflammatory mediators are released.

A

macrophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

once the macrophage identifies the microbe, the macrophage secretes chemotactic substances and calls in?

A

the 3rd line of defense: CD4 cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

after calling the CD4 cell, the macrophage displays the _____ remnant of the antigen on its membrane.

A

phagocytized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

the CD4 ____ the remnant of the antigen that has been phagocytized by the macrophage and _____ the remnant on the _____ _____.

A

accepts, displays, T-cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

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?

A

B-cell system because the microbe is a bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

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?

A

the b-cell differentiates into plasma cells and begins making antibodies against that specific meningitis microbe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

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?

A
  • primary response
  • full
  • S&S of meningitis (probably will be pretty sick!)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

even though the b-lymphocytes can’t help much during the primary response, they begun to create and establish?

A
  • memory/recognition of the meningitis microbe
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

the plasma cells are making ____ so that in the future, the person will be protected and won’t have ____ again.

A

antibodies, S&S

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

the person who developed memory (antibodies) to the specific meningitis microbe has?

A

acquired immunity to that organism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

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.

A

specific, antibodies, secondary response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

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.

A

memory, quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

the 3rd line of defense (acquired immunity) can be categorized as?

A
  • active vs passive FURTHER INTO:
  • natural vs artificial
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

active acquired immunity

A

a persons own immunocyte system developed the antibodies that established immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

natural active acquired immunity

A

person’s plasma cells build up antibodies in response to a microbially-induced illness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

artificial active acquired immunity

A

person’s plasma cells build up antibodies in response to receiving inoculations/vaccinations of a much-weakened or inactive microbe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

other names for vaccinations

A
  • immunizations
  • inoculations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

example of artificial active acquired immunity

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

once immunized, a person has the _______ forever, but they may get ____ in strength & numbers. often, a _____ is given.

A

antibodies, weaker, booster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

MMT given at age ___ to ____ months & booster at age ____ years.

A

12, 15, 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

tetanus boosters must be given every?

A

5 to 10 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

an ______ ____ test may be used to detect the presence of antibodies within the blood.

A

antibody titer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

passive acquired immunity

A
  • they had been given someone else’s antibodies
  • they did not develop the antibodies on their own
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

natural passive acquired immunity

A

transfer of antibodies from mom to baby via placenta or breast milk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

natural passive acquired immunity via placenta

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

natural passive acquired immunity via breast milk

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

artificial passive acquired immunity

A

antibodies are injected during treatment, usually in emergencies or as a stop-gap measure until active immunity can develop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

artificial passive acquired immunity is usually given as a ____ ____ of antibodies to disease that you have a high risk of contracting.

A

intramuscular injection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

why is an IM injection of antibodies given in times of emergencies?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

TIG - tetanus immunoglobulin - is made from what?

A

prior-formed antibodies against tetanus antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

when is TIG given?

A

when a patient gets a dirty wound and has either never had tetanus vaccine or has not had a booster in a long time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

advantage to artificial passive acquired immunity

A

can be a powerful, immediate way to fight disease bc disease-specific antibodies will immediately begin attacking microbes (if they have invaded your body)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

disadvantage to artificial passive acquired immunity

A

passive immunity only lasts as long as the antibody lasts - after about 2 wks, the antibody degrades

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

TIG is given as a just in case because?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

humoral immunity is acquired by?

A

actions of B-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

B-cells action’s that gives humoral immunity is triggered to do so by?

A

invasion of particular kinds of microbes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

B-cells, once triggered, differentiate into ______ , which create ____ that are specific for those microbes.

A

plasma cells, antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

antibodies defeat microbes by?

A
  • neutralization (inactivation)
  • opsonization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

neutralization

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

opsonization

A
  • coats bacteria, which promotes phagocytosis
  • optimizes recognition and digestibility of antigen for phagocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

hypersensitivities

A
  • too much immunocyte response
  • response that is supposed to help us goes too fat and harms us
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

subcategories of hypersensitivity responses based on the?

A

target antigen (the antigen that is attacked by antibodies or T-cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

subcategories of hypersensitivity responses based on target antigen

A
  • allergic response (allergic rxn)
  • autoimmune response
  • alloimmune response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

basic definition of allergic response/rxn

A

hypersensitivity to a target antigen (environmental, medical, or pharmaceutical) called allergen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

basic definition of autoimmune response

A

hypersensitivity to self-antigens (the target antigen)
- rxn of our body to our own antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

basic definition of alloimmune response

A

hypersensitivity to another person’s antigens (the target antigen), such as when an organ is transplanted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

allergic hypersensitivity is also called?

A

IgE-mediated reaction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

IgE (immunoglobin E) helps protect and defend against ______ but higher numbers of IgE indicate some of kind _______ response.

A

parasitic infections, allergic hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

examples of allergen

A
  • pollen
  • animal dander
  • meds like penicillin
  • chems like household cleaners, soaps
111
Q

how can a person be exposed to a substance in an allergic hypersensitivity rxn?

A
  • inhalation
  • ingestion
  • injection
  • skin contact
112
Q

when the substance enters the body for the first time, what happens normally?

A
  • primary response (sensitization) triggered, leads to creation of an antibody
  • antibody stands down/hides out in lymph system for the second exposure
113
Q

if an individual who is genetically programmed/predisposed to an allergic rxn, there is a _______ response to that substances that involves?

A

pathologic, IgE antibody

114
Q

after the initial exposure to an allergen, ___ pathologically binds to _____ cells instead of “standing down.” this does what to the cell?

A

IgE, mast, sensitizes the mast cell

115
Q

on ___ exposure to that allergen, the allergen’s receptors bind to the IgE on the _____ mast cell and quickly initiates ______ of mast cell.

A

repeated, sensitized, degranulation

116
Q

upon degranulation of mast cell, what happens after?

A

1). histamine release
2). histamine binds to H1 receptors of surrounding tissue and causes systemic and/or local rxns

117
Q

once a person is sensitized, the S&S appear immediately upon?

A

2nd or more exposures

118
Q

S&S of localized rxn of allergic hypersensitivity

A
  • dermatitis (skin rash that can cause itching/swelling)
  • nasal allergic rhinitis
  • conjunctivitis from histamine
  • leukotriene
  • prostaglandin release from mast cells
119
Q

S&S of systemic reaction to allergic hypersensitivity

A

anaphylaxis - occurs when someone is more severely allergic to the antigen

120
Q

____, ____, ____, and _____ such as complement system are overacted throughout body. all S&S for localized rxns become systemic.

A
  • histamine
  • leukotrienes
  • PGs
  • acute phase reactants
121
Q

components of anaphylaxis

A
  • urticaria
  • angioedema
  • N, V, D, cramps
  • wheezing, dyspnea, possibly laryngeal edema
  • hypotension + shock if bad enough
122
Q

urticaria

A

itching all over; hives

123
Q

angioedema

A
  • abnormal vasodilation and edema of small blood vessels
  • usually occurs in lips, tongue, hands
124
Q

where does wheezing during anaphylaxis come from?

A
  • from bronchial edema
  • from leukotriene-induced bronchoconstriction
125
Q

____ can be considered an allergic hypersensitivity. ____ are one of the inflammatory mediators that causes bronchoconstriction, causing dyspnea (___), wheezing, etc.

A

asthma, leukotrienes, SOB

126
Q

what causes hypotension during anaphylaxis?

A

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
Q

treatment for allergic hypersensitivity

A
  • histamine: antihistamine
  • inflammatory properties of PGs: steroids
  • against bronchoconstrictive properties of leukotrienes: leukotriene blockers
128
Q

antigens

A

proteins that can stimulate immunocyte rxn against them

129
Q

a reaction against antigens that are foreign to our own bodies is?

A

normal

130
Q

a reaction against out own, self antigens is?

A

abnormal

131
Q

autoantibody

A

a pathologic antibody because it attacks self antigens (the antigens that are our cell membranes saying self)

132
Q

rheumatic, rheumatism, rheumatologist are words that relate to?

A

inflammation, disturbance, or degeneration of connective tissue structures

133
Q

many connective tissue disorders (ie, rheumatic disorders) are ______ in origin

A

autoimmune

134
Q

reasons why our bodies’ antibodies (or T-cells) sometimes react to own antigens

A
  • sometimes after we fight off an infection, our system stays primed
  • genetic factors are important in autoimmune dzs
  • gender effect is a consideration
135
Q

what does it mean when our system stays primed?

A

instead of standing down (sending post-attack immunocytes back to lymph tissue)
- immunocyte system begins attacking antigens on our own cells

136
Q

example of system staying primed (autoimmune hypersensitivity)

A

rheumatic heart disease (an autoimmune, hyperinflammatory rxn)

137
Q

the etiology of rheumatic heart disease

A

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
Q

possible sequela of strep throat is?

A

bad heart valves due to autoimmune attack, but usually doesn’t occur if strep treated thoroughly by antibiotics

139
Q

w/ genetic factors, presence of certain _______ in people with certain autoimmune dzs is statistically significant

A

HLA antigens

140
Q

gender effect for autoimmune hypersensitivity

A

10:1 ratio females to males

141
Q

autoimmune diseases often categorized according to 2 possible _____, which are?

A
  • drivers
  • autoantibody attack (humoral) VS
  • auto T-cell response (cell-mediated
142
Q

humoral autoimmune response

A

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
Q

cell-mediated autoimmune response

A
  • instead of autoantibody, the attacker is our own T-cells
  • attack our tissue and trigger damaging inflammation and S&S
144
Q

examples of tissue-specific autoimmune diseases

A
  • multiple sclerosis
  • graves disease
  • Goodpasture’s syndrome
  • myasthenia gravis
  • type-1 diabetes
  • celiac disease (sprue)
  • autoimmune hemolytic anemia
145
Q

multiple sclerosis

A
  • 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
Q

Graves disease

A
  • disease that causes most cases of hyperthyroidism
  • autoantibody stimulates thyroid gland cells to oversecrete thyroid hormone (TH) -> causes S&Ss of hyperthyroidism
147
Q

Goodpasture’s syndrome

A
  • autoantibody attacks connective tissue in pulmonary and glomerular basement membrane
  • results in pulmonary hemorrhage and glomerulonephritis
148
Q

myasthenia gravis

A
  • autoantibody attacks acetylcholine receptors on cells of muscles
  • ACh would not have enuf effective post-syn gap receptor
  • S&S of muscle weakness
149
Q

type-1 diabetes

A
  • t-cells destroy insulin-producing cells
  • w/o insulin, glucose accumulates in blood and no energy source for cells
150
Q

celiac disease (sprue)

A
  • 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
Q

autoimmune hemolytic anemia

A
  • 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
Q

autoimmune hemolytic anemia is borderline a systemic disease, but it is not because?

A

blood is considered one tissue

153
Q

there are autoimmune rxns in which antibody & self-antigen pair up into a molecule called?

A

immune complex

154
Q

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.

A
  • immune complex
  • tissue-specific type
  • immune-complex
  • walls of various blood vessels
155
Q

the immune complex ____ the blood vessels and causes inflammation of them (_____), which in turn, causes the ________ to become inflamed.

A

irritates, vasculitis, surrounding tissue

156
Q

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 _____.

A

wide-spread, blood vessels of a variety of tissues

157
Q

examples of systemic autoimmune diseases

A

lupus and rheumatoid arthritis

158
Q

systemic lupus erythematosus (SLE)

A

genetic predisposition and mostly seen in women

159
Q

in everyone, there are normally always bits of ___ in the blood on their way to being disposed of in the ____

A
  • degraded cells and nucleic acids like DNA
  • spleen, liver
160
Q

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 _____.

A
  • antibodies
  • autoantibodies
  • nucleic acids
161
Q

when antibodies attach themselves to DNA, what are they called?

A

immune complexes

162
Q

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?

A
  • connective tissues
  • kidneys, lungs, joints, skin
  • vasculitis
163
Q

in whichever tissues are involved with immune complexes, process is the same - ______ begins, causing S&Ss related to those tissues

A

inflammation

164
Q

specific S&S with SLE (list)

A
  • skin rashes in specific patterns
  • nonerosive arthritis of at least 2 peripheral joints
  • serositis
  • proteinuria
  • seizures
  • fatigue
165
Q

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

A
  • variety
  • flare-ups (exacerbations)
  • remissions
  • great imitators
166
Q

what skin rash patterns does SLE cause?

A
  • classic butterfly malar rash (across cheeks)
  • wolf-like facial appearance, hence lupus
167
Q

serositis

A

inflammation of serous compartments (sacs in body such as pleura and pericardial sac) causes pleurisy, pericarditis

168
Q

SLE diagnosis

A
  • 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
Q

serous fluid

A
  • 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
Q

rheumatoid arthritis (RA) etiology

A

RA immune complex consists of an autoantibody attached to collagen

171
Q

RA inflammation develops anywhere there is ____, but most commonly in ______ of ____ joints such as?

A
  • collagen
  • synovial membranes
  • small
  • hands
172
Q

synovial refers to?

A

lining of joints

173
Q

S&S of RA

A
  • fatigue
  • joint pain, swelling, deformation
  • inflammatory S&S of eyes, heart, lungs, almost any tissue
174
Q

RA diagnosis

A
  • clinical findings of S&S
  • elevated CRP
  • rheumatoid factor (RF): presence of immune complexes (antibody + collagen)
175
Q

RA differs from?

A

osteoarthritis

176
Q

osteoarthritis

A
  • 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
Q

rheumatoid arthritis

A
  • 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
Q

alloimmune hypersensitivity target antigen is>

A

someone else’s cells

179
Q

with alloimmune hypersensitivity, it is not true hypersens. in some respect because?

A
  • 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
Q

alloimmune concerns in nursing are thought of as?

A

compatibility issues

181
Q

what does compatibility refer to?

A

“what treatment might cause an untoward immune rxn” due to introducing foreign antigen and having body attack it

182
Q

types of compatibility issues

A
  • histocompatibility
  • ABO/Rh compatibility
183
Q

to be able to distinguish “self” from foreign, almost all body’s cell membranes have “_____” composed of protein called?

A
  • self-antigens
  • histocompatibility antigens or HLAs (human leukocyte antigens)
184
Q

HLAs are found on the ______ of most _____ cells except _____ and are important in certain patient situations such as _____.

A
  • cell membrane
  • body
  • RBCs
  • transplants
185
Q

_____ testing is done on tissue cells (examples?) of both donors and recipients of transplants to see if?

A
  • histocompatibility
  • liver, kidney
  • the HLAs on their cells match
186
Q

the _____ the HLAs match, the _____ likely the transplanted tissue will be attacked by ____ that see it as foreign.

A
  • closer
  • less
  • immunocytes
187
Q

in immunocytes do attack w/ transplants, it is called? what S&S the patient may have in these cases?

A
  • rejection
  • pain over the area, fever, etc.
188
Q

to minimize the possibility of rejection during a transplant, patients are usually on what drug? what is the general purpose?

A
  • immunosuppressant drug
  • makes immune system lethargic so it won’t attack the transplanted tissue
189
Q

RBCs have the ___ blood grp antigens and ____ blood grp antigens on their plasma cell membranes

A

ABO, Rh

190
Q

the ABO portion of your blood type can be? the Rh portion can be?

A
  • A, B, AB, O
  • +/-
191
Q

people w/ certain blood types have ____ antigens and antibodies - nurses need to know which type is ok to give to another type to avoid?

A

specific, transfusion rxn

192
Q

if you have type B blood…

A
  • 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
Q

if person w/ type B blood gets blood from type A person, what happens?

A

anti-A immunoglobulin attack donor type-A RBCs and hemolyze them

194
Q

what does hemolysis from a transfusion rxn cause?

A
  • problems related to clumping effect
  • can block vessels in kidneys (cause kidney failure) and other areas (ischemia to distal tissues)
195
Q

besides hemolytic clumping, a transfusion rxn can also include?

A
  • rash
  • fever
  • low BP
  • body aches
196
Q

a person is either born ___ or ____ the Rh factor on their RBC cell membrane as part of inheritance.

A

with, without

197
Q

a person is/is not? genetically programmed to immediately develop anti-Rh antibodies.

A

is NOT

198
Q

a person w/o the Rh factor who is given Rh+ blood will react how?

A

will be ok the first time they get that blood bc hasn’t developed antibodies yet

199
Q

if the person w/o Rh factor gets Rh+ blood the SECOND time, what happens?

A

may have transfusion rxn

200
Q

normally, mom and fetus blood do/do not? mix during pregnancy. however….

A
  • do NOT
  • but during childbirth, some fetal blood may enter mom’s system
201
Q

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.

A

foreign, antibodies

202
Q

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?

A
  • MAY
  • Rh factor
  • hemolysis
  • erythroblastosis fetalis
203
Q

to prevent hemolytic problems in future pregnancies, mom will get what?

A

Rhogam shot (med to destroy Rh antibodies) just after birth of Rh(+) child and after every Rh(+) child thereafter

204
Q

A+ blood type characteristics

A
  • A antigens & Rh
  • anti-B antibodies
205
Q

A+ can receive

A
  • O +/-
  • A +/-
206
Q

A+ can donate to

A
  • A+
  • AB+
207
Q

A- blood type characteristics

A
  • A antigens
  • Anti-B antibodies
208
Q

A- can receive

A
  • O-
  • A-
209
Q

A- can donate to

A
  • A +/-
  • AB +/-
210
Q

B+ blood type characteristics

A
  • B antigens & Rh
  • anti-A antibodies
211
Q

B+ can receive

A
  • O +/-
  • B +/-
212
Q

B+ can donate to

A
  • B+
  • AB+
213
Q

B- blood type characteristics

A
  • B antigens
  • Anti-A antibodies
214
Q

B- can receive

A
  • O-
  • B-
215
Q

B- can donate to

A
  • B +/-
  • AB +/-
216
Q

AB+ blood type characteristics

A
  • A/B antigens & Rh
  • NO antibodies
217
Q

AB+ can receive

A
  • A +/-
  • B +/-
  • AB +/-
  • O +/-
218
Q

AB+ can donate to

A

AB+

219
Q

AB- blood type characteristics

A
  • A/B antigens
  • NO antibodies
220
Q

AB- can receive

A
  • A-
  • B-
  • AB-
  • O-
221
Q

AB- can donate to

A
  • AB +/-
222
Q

O+ blood type characteristics

A
  • NO antigens & Rh
  • Anti-A/B antibodies
223
Q

O+ can receive

A
  • O +/-
224
Q

O+ can donate to

A
  • A+
  • B+
  • AB+
  • O+
225
Q

O- blood type characteristics

A
  • NO antigens or Rh
  • Anti-A/B antibodies
226
Q

O- can receive

A

O-

227
Q

O- can donate to

A

everyone - universal donor

228
Q

immunodeficiencies generally means?

A

not enough

229
Q

immunodeficiency

A

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
Q

no matter the etiology/type, all immunodeficient diseases have what common characteristic?

A

cause much higher susceptibility to diseases that immunocompetent people get

231
Q

example of high susceptibility with immunodeficient diseases

A
  • everyone gets colds, flus, bacterial infections, etc
  • w/ immunocompromised people, get them MORE easily and virulently
232
Q

higher susceptibility greatly increase the chance of immunocompromised person getting?

A

opportunistic diseases

233
Q

opportunistic diseases

A

disease caused by an increased susceptibility to diseases that immunocompetent people don’t get (ie. microbes that are normally harmless)

234
Q

T/F: immunocompetent people can live with natural flora like yeast, fungi, and certain protozoa

A

TRUE: immunocompetent people have certain resistance to becoming infected with them

235
Q

in immunocompromised people, the normally harmonious flora….

A

the normal flora’s opportunistic nature takes over and they will invade - opportunistic invader/pathogens

236
Q

immunodeficient disorders categories

A
  • mechanism of action
    AND to whether it is
  • congenital or acquired
237
Q

subcategories of mechanism of action for immunodeficiency disorders

A
  • humoral/B-cell immunodeficiency
  • cell-mediated/T-cell immunodeficiency
  • combines B/T cell immunodeficiency
238
Q

congenital/acquired immunodeficiency subcategory of immunodeficiency disorders

A
  • congenital: present at birth
  • acquired: develops after birth
239
Q

combined B-cell and T-cell immunodeficiency

A

diminishment or absence of both humoral and cell-mediated immunity

240
Q

example of congenital B/T cell immunodeficiency

A

SCIDS: severe combined immunodeficiency syndrome caused by diverse genetic mutations that lead to complete absence of all immune fxn (BUBBLE BOY)

241
Q

examples of acquired combined B/T cell immunodeficiency

A
  • irradiation + cytotoxic drugs for cancer wipe out bone marrow - not enuf T/B lymphocytes
  • immunosuppressant drugs post-transplant
  • aging
242
Q

humoral/B cell immunodeficiency

A

most commonly a congenital problem

243
Q

example of humoral/B cell immunodeficiency

A

X-linked hypogammaglobulinemia

244
Q

X-linked hypogammaglobulinemia

A
  • IgG missing or lessened in amt
  • sequela of making fewer/any antibodies, can’t fight dz
245
Q

example of congenital cell-mediated/ T cell immunodeficiency

A

DiGeorge’s syndrome
- genetic defect on chromosome 22 that causes failure of thymus development

246
Q

DiGeorge’s syndrome - failure to develop thymus causes?

A
  • t-cells will not have full maturation bc they normally mature in thymus
  • person will have decreased ability to fight certain infections
247
Q

example of acquired cell-mediated/T cell immunodeficiency

A

AIDS: acquired immunodeficiency syndrome caused by HIV (human immunodeficiency virus)

248
Q

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.

A
  • CD4
  • mount
  • CD4
  • introductory
249
Q

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.

A
  • acquired cell-mediated
  • simian immunodeficiency virus
250
Q

the virus associated with HIV passes from person to person via (portal of entry)?

A
  • 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
Q

groups of highest risk for HIV infection

A
  • 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
Q

HIV is what type of virus?

A

RNA retrovirus

253
Q

a regular RNA virus inserts its ___ into _____ of host cell and takes over _______ protein-building for its own propagation.

A

RNA, cytoplasm, ribosomal

254
Q

a retrovirus inserts its ___ into a host cell’s _____, converts its own _____ to _____ and then back to ____.

A
  • RNA
  • cytoplasm
  • RNA, DNA, RNA
255
Q

steps in RNA retrovirus (HIV) invasion process

A

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
Q

T/F: a person has to be HIV+ and have AIDS at the same time

A

FALSE: minimal destruction of CD4 cells when only HIV+, so AIDS hasn’t appeared yet

257
Q

steps to HIV destruction after invasion

A

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
Q

once the HIV wakes up, the CD4 cells get _____ and more likely the patient will have?

A

destroyed, dx of AIDS

259
Q

diagnosis of HIV

A
  • ELISA lab test (enzyme-linked immunosorbent assay) used FIRST
  • if ELISA (+), second/confirmatory test done called Western Blot
260
Q

ELISA test

A
  • test for presence of antibodies to HIV (as soon as virus enters body, immune response triggered and antibodies detectable by 1-2 wks)
261
Q

with the ELISA, ___ of all infected individuals test (+) w/in ___ of initial infection

A

96%, 2 to 12 weeks

262
Q

if ELISA (-), recommendations for further testing depends on?

A

factors like patient risk status and timing of testing

263
Q

someone can be HIV+ and live for many years _____ getting AIDS.

A

without

264
Q

if ELISA (+), what second/confirmatory test is done? what kind of test is it?

A

Western Blot: more $$$, but more specific and very few false positive

265
Q

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 ____________.

A

<200, opportunistic invasion

266
Q

usual criteria for diagnosis for AIDS

A
  • CD4 level < 200
    AND
  • presence of opportunistic infection
267
Q

examples of most typical opportunistic infection (OI)

A
  • thrush
  • pneumocystis jiroveci (formally carinii) pneumonia (PCP)
  • cytomegalovirus (CMV) retinitis
  • Kaposi’s sarcoma
268
Q

thrush and their drug

A
  • yeast infection of mouth and throat
  • antifungals
269
Q

pneumocystis jiroveci (formally carinii) pneumonia (PCP) and their drug

A
  • a type of fungus that invades the lungs
  • oral and nebulized sulfonamides
270
Q

cytomegalovirus (CMV) retinitis

A

a virus normally harmless invades eyes

271
Q

Kaposi’s sarcoma

A

a type of malignant skin tumor that invades immunocompromised people

272
Q

S&S of AIDS are due to ____ and _____ of tissue. what are they?

A
  • OIs, atrophy
  • weight loss
  • anorexia
  • general cachexia (weakness + body wasting)
  • dementia
273
Q

treatment and prevention of HIV/AIDS

A

education
- latex condoms for prevention
- understand HIV can effect anyone
- drugs targeted at diff phases of viral invasion/replication + treating OIs

274
Q

all immunodeficient diseases (B, T, or combo B/T)….

A
  • 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.)

nurs pathophysiology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions