immune 2 Flashcards
(89 cards)
1
Q
immunodeficiency diseases
A
immune response is absent or depressed as a result of a primary/secondary disorder
2
Q
primary immunodeficiency
A
- reflects a defect involving T cells, B cells, or lymphoid tissues
- inherited defects in the genesis of the immune system
3
Q
secondary immunodeficiency
A
- results from an underlying disease/factor that depresses or blocks the immune response
- infection, aging, malnutrition, chemo, autoimmune disorders, or immunosuppression
4
Q
three main avenues of transmission of AIDS
A
- contaminated blood
- sexual activity (anal, vaginal, very rarely oral)
- maternal to child (either through pregnancy, during delivery, or breastfeeding)
5
Q
high-risk behaviors for transmission of AIDS
A
- unprotected anal, vaginal, and oral sex, including having six or more sexual partners in the past year
- sexual activity w/ someone known to carry HIV, or IV drug use
6
Q
HIV is not transmitted by _____
A
fomites, casual household or social contact
7
Q
HIV life cycle
A
binding (also called attachment) → fusion → reverse transcription → integration → replication → assembly → budding
8
Q
HIV is a __________ virus, also known as _________
A
ribonucleic acid (RNA) virus; retrovirus
9
Q
the core of HIV is surrounded by a ___________ envelope containing the __________
A
lipid bilayer; glycoprotein spikes
10
Q
HIV predominantly infects human ____________ cells and destroy them; also infect _____________ cells
A
T4 (helper) lymphocytes (CD4); macrophages, B cells, dendritic cells, and microglial cells
11
Q
what is more readily transmitted HIV-1 or HIV-2?
A
HIV-1 causes the global epidemic
12
Q
acute infection in AIDS
A
- 1-6 weeks
- flu-like sx and lymphadenopathy
- antibody tests remain negative
13
Q
asymptomatic AIDS
A
- CD4 Count of 500 cells/mm³ or More
- 1-20 years
- positive antibody test but remains asymptomatic
- seroconversion: refers to the emergence of HIV antibodies in the bloodstream
14
Q
symptomatic AIDS
A
- CD4 count of 200-500 cells/mm³
- persistent generalized adenopathy
- nonspecific sx (such as diarrhea, weight loss, fatigue, night sweats, and fever)
- neurologic sx resulting from HIV encephalopathy
15
Q
advanced AIDS
A
CD4 count of 200 cells/mm³ or less
16
Q
clinical manifestations of AIDS
A
- neurologic manifestations
- neuromusculoskeletal diseases
- rheumatologist diseases
- cardiopulmonary diseases
- lipodystrophic syndrome
- AIDS-Related Lymphoma
17
Q
Neruologic Manifestations of AIDS
A
- Pain syndromes in individuals w/ HIV disease
- HIV encephalitis
- HIV-associated dementia
- Peripheral neuropathy
18
Q
3 facts to HIV treatment
A
- HIV meds can’t cure the etiologic agent; they can promote healthier lives and prolong the lives of people w/ HIV
- combo of meds are taken to prevent HIV from advancing to AIDS
- the meds can reduce the risk of transmissibility to other people
19
Q
highly active antiretroviral therapy (HAART)
A
a strategy for treating HIV-infected people with a combination of antiretroviral drugs
20
Q
AIDS - Implications for PT
A
- postexposure prophylaxis (PEP) – urgent medical concern
- focus on the management of specific impairments and functional limitations related to chronic HIV infection, its comorbidities, and/or opportunistic infections when they arise
- consider physical fitness, quality-of-life issues, work, activities of daily living, and community management skills
21
Q
HIV precautions for health care workers
A
- use protective barriers (gloves, eye shields, gowns) when handling blood, body fluids, and infectious fluids
- wash hands, skin, and mucous membranes immediately and thoroughly if contaminated by blood or other body fluids
- prevent needle/scalpel sticks
- ventilation devices are available for resuscitation
- any health care worker w/ open wounds/skin lesions shouldn’t treat clients/handle equipment until the lesion(s) heals
- pregnant health care workers should take extra precautions
- occupational exposure to HIV should be followed immediately by evaluation of exposure source and post exposure prophylaxis
22
Q
chronic fatigue and immune dysfunction syndrome
A
- CFS used interchangeably with myalgic encephalitis (ME).
- this illness is not a single disease but the result of a combination of factors
- it is a subset of chronic fatigue, a broader category defined as unexplained fatigue of greater than or equal to 6 months’ duration
23
Q
chronic fatigue and immune dysfunction syndrome risk factors
A
- people of every age, gender, ethnicity, and socioeconomic group can have CFS
- women are more susceptible
- mean onset is 29-35 yrs old
- mean illness duration 3-9 years
24
Q
chronic fatigue and immune dysfunction syndrome etiologic factors and pathogenesis
A
viral infections, immune dysfunction, neuroendocrine responses, dysfunction of the CNS, muscle structure, exercise capacity, sleep patterns, genetic constitution, personality, and (neuron)psychologic process
25
infection control in immune deficiencies
factors affecting the immunocompromised person, leading to the selection of the correct infection control strategies to prevent infectious complications
26
altered defense mechanisms in the immunocompromised person
- immune system
- endogenous normal flora
- GI system
- Genitourinary system
- respiratory system
- mucous membrane fxn
- skin breakdown
27
infectious agents in the immunocompromised person
- exogenous and bacteria, fungi, viruses
- opportunistic agents:
→ Tuberculosis
→ Pneumocystis carinii pneumonia
→ cytomegalovirus
→ Candida albicans
28
reservoirs in the immunocompromised person
- the client
- invasive devices: tubing, catheters, needles
- reusable equipment
29
modes of transmission in the immunocompromised person
- direct: hands, broken skin
- indirect: Tubes, needles, dressings, catheters, equipment
- droplet: cough, sneeze
- vehicle: blood
30
infection control strategies for the immunocompromised person
- hand washing
- standard precautions
- clean/sterile techniques
- masks for respiratory diseases
- sterilize/disinfect equipment
- maintain skin integrity
31
Type I Hypersensitivity
- IgE-mediated rxn
- IgE-mediated antibody (on B cells) that's formed from a CD4+ Th2 (T helper 2) cell-dependent mechanism that binds w/ receptors on mast cells and basophils
- in order to activate the mast cell (or basophil), the antigen crosslinks to more than one IgE antibody molecule
- mast cell (or basophil) releases histamine (via degranulation) that induces constriction of vascular and nonvascular smooth muscles, causing vasodilation and increasing venue permeability --> bronchoconstriction; wheal and flare in the skin
32
rate of development of Type I Hypersensitivity
immediate
33
class of antibody involved in Type I Hypersensitivity
IgE
34
principal effect/cells involved in Type I Hypersensitivity
mast cells
35
complement participation in Type I Hypersensitivity
no
36
examples of disorders of Type I Hypersensitivity
seasonal allergic rhinitis
37
Antihistamines MOA
- Block action of histamine at H1 receptor sites
- Compete with histamine for (H1-H4) histamine receptors on cell membranes
- Cannot push histamine off the receptor if already bound
- 2nd generation (non-sedating)
→ more selective to H1 receptor subtype
→ does not cross BBB easily
38
Type II Hypersensitivity
tissue-specific rxn
39
rate of development in Type II Hypersensitivity
immediate
40
class of antibody involved in Type II Hypersensitivity
IgG and IgM
41
principal effect/cells involved in Type II Hypersensitivity
macrophages in tissues
42
complement participation in Type II Hypersensitivity
frequently
43
examples of disorders in Type II Hypersensitivity
- autoimmune thrombocytopenia purpura
- Graves disease
- autoimmune hemolytic anemia
44
Type II Hypersensitivity - clinical manifestation of myasthenia gravis
muscle weakness, paralysis
45
Type II Hypersensitivity - clinical manifestations of graves disease
hyperthyroidism
46
Type II Hypersensitivity - clinical manifestations of insulin-resistant diabetes
hyperglycemia, ketoacidosis
47
Type III Hypersensitivity
- immune complex-mediated rxn
- involves interaction of antibody and complement, which may attract the polymorphonuclear cells or neutrophils
- kidneys (glomerulonephritis), joints (arthritides or degenerative joint diseases), skin, and blood vessels (vasculitis) are the most common tissues affected
48
rate of development in Type III Hypersensitivity
immediate
49
class of antibody involved in Type III Hypersensitivity
IgG and IgM
50
principal effect/cells involved in Type III Hypersensitivity
neutrophils
51
complement participation in Type III Hypersensitivity
yes
52
examples of disorders of Type III Hypersensitivity
systemic lupus erythematosus
53
Type III hypersensitivity - clinical manifestations of systemic lupus erythematosus
- nephritis
- skin lesions
- arthritis
54
Type IV Hypersensitivity
- cell-mediated rxn
- delayed type hypersensitivity rxn → occurs in contact dermatitis after sensitization to an allergen in the form of cosmetics, topical meds, adhesives, poison ivy, latest sensitivity, or the response to a tuberculin skin test present 48 to 72 hrs after the test
- graft rejection or allergic rxns after receiving transplantation
55
rate of development of Type IV Hypersensitivity
delayed
56
class of antibody involved in Type IV Hypersensitivity
none
57
principal effect/cells involved in Type IV Hypersensitivity
lymphocytes, macrophages
58
complement participation in Type IV Hypersensitivity
no
59
examples of disorders in Type IV Hypersensitivity
contact sensitivity to poison Ivy and metals (jewelry)
60
Type IV hypersensitivity - clinical manifestations of RA
- chronic arthritis w/ inflammation
- destruction of articular cartilage and bone
61
Type IV hypersensitivity - clinical manifestations of MS
demyelination in CNS w/ perivascular inflammation; paralysis, ocular lesions
62
Type IV hypersensitivity - clinical manifestations of Type II diabetes mellitus
insulitis (chronic inflammation in islets), destruction of beta cells; diabetes
63
Type IV hypersensitivity - clinical manifestations of Hashimoto thyroiditis
hypothyroidism
64
Type IV hypersensitivity - clinical manifestations of inflammatory bowel disease
chronic intestinal inflammation, ulceration, obstruction
65
Type IV hypersensitivity - clinical manifestations of autoimmune myocarditis
cardiomyopathy
66
Type IV hypersensitivity - clinical manifestations of contact sensitivity
- epidermal necrosis
- dermal inflammation w/ skin rash and blisters
67
immune mechanisms directed against self-antigens
- the body fails to distinguish self from non-self, causing the immune system to direct immune responses against normal (self) tissue and become self-destructive
- more than 56 autoimmune diseases have been identified
68
Etiologic and Risk Factors of Autoimmune Diseases
- causes often can't be determined
- a combo of factors
→ genetic
→ hormonal
→ environmental influences - exposure to chemicals, other toxins, or sunlight and drugs that may destroy regulatory (suppressor) T cells
→ other factors - viruses, stress, cross-reactive antibodies
- no single gene responsible for autoimmune disease but clusters of genes seem to increase susceptibility
69
immunologic tolerance
the unresponsiveness of certain antigens induced by their exposure to lymphocytes
70
self-tolerance
- lack of recognition and responsiveness to one's own tissue antigens
- autoimmunity indicates loss of self-tolerance
71
central tolerance
- immature lymphocytes that recognize self-antigens during their maturation in central (generative) lymphoid organs
- immature lymphocytes are killed by apoptosis
72
peripheral tolerance
mature lymphocytes that recognize self-antigens become either anergic (i.e., functionally inactive) or suppressed by regulatory T cells or undergo apoptosis
73
how does autoimmunity occur?
- linkage analysis of human genome has revealed candidate locations for susceptibility to MS, type I diabetes, SLE, and Crohn disease
- a multitude of epigenetic (internal and external) environmental factors that contribute to whether (and when) the gene is expressed
- certain bacteria, mycoplasma, and viruses can trigger autoimmunity
- in the concept of molecular mimicry, virus and microbes share cross-reacting epitopes w/ self-antigens where microbial antigens tend to attack self-tissues
74
systemic lupus erythematosus
chronic inflammatory autoimmune disorder that appears in several forms = discoid lupus erythematosus (DLE) and systemic lupus erythematosus (SLE)
75
discoid lupus erythematosus (DLE) affects...
only the skin (usually the face, neck, and scalp)
76
systemic lupus erythematosus (SLE) affects...
any organ or system of the body
77
generally, SLE or DLE is more severe?
SLE - no two people w/ SLE will have identical sx
78
systemic lupus erythematosus (SLE) - Incidence
primarily a disease of young women
79
systemic lupus erythematosus (SLE) - etiologic and risk factors
- the cause of SLE remains unknown, but evidence points to interrelated immunologic, environmental, hormonal, and genetic factors
- SLE shows a strong familial link, with a much higher frequency among first-degree relatives
- Other factors predisposing to SLE may include physical or mental stress, which can provoke neuroendocrine changes affecting immune cell function; streptococcal or viral infections; exposure to sunlight or ultraviolet light, which can cause inflammation and tissue damage; immunization; pregnancy; and abnormal estrogen metabolism
80
systemic lupus erythematosus (SLE) - pathogenesis
Three main mechanisms are implicated in the development of lupus: autoantibodies, vascular abnormalities, and inflammatory mediators
81
systemic lupus erythematosus (SLE) - clinical manifestations
- for some people, only the skin and joints will be involved
- for others, joints, lungs, kidneys, blood, or other organs and/or tissues may be affected.
82
isoimmune disease
organ and tissue transplantation
- transplantation of almost any tissue is feasible, but the clinical use of transplantation to remedy disease is still limited for many organ systems bc of the rejection rxn
- in all cases of graft rejection, the cause is incompatibility of cell surface antigens
83
fibromyalgia
- chronic widespread pain with allodynia or hyperalgesia to pressure pain and is classified as one of the largest groups of soft tissue pain syndromes (not a disease)
- simply stated, it is a disorder of pain processing (i.e., abnormal pain modulation with hypersensitivity to painful stimuli and reduced pain inhibition)
84
fibromyalgia - incidence
- women experience sx more than men
- sx usually appear btwn 20-55 yrs old
85
fibromyalgia - risk factors
prolonged anxiety and emotional stress, trauma (e.g., motor vehicle accident, work injury, surgery), rapid steroid withdrawal, hypothyroidism, and viral and nonviral infections
86
fibromyalgia - etiologic factors
Possible etiologic theories include diet; viral origin; sleep disorder; occupational, seasonal, or environmental influences; and adverse childhood experiences, including sexual abuse
87
fibromyalgia - pathogenesis
- Its pathogenesis is not entirely understood, although it is currently thought to be the result of a CNS malfunction that increases pain transmission and perception accompanied by ineffective pain inhibition
- the classic condition of central sensitization
- Many researchers have shown that people with fibromyalgia have an autonomic nervous system with a hyperactive sympathetic branch and an underactive parasympathetic branch
- Immune cells, activated in response to infection, inflammation, or trauma, release proinflammatory cytokines that signal the CNS to release glia within the brain and spinal cord
88
Fibromyalgia - clinical manifestations
- The major symptom of fibromyalgia is muscle pain, often described as aching or burning, a "migraine headache of the muscles."
- sleep disturbances result in fatigue and exhaustion
89
Fibromyalgia - medical management
- Effective treatment of the widespread pain of FMS, aributed mainly to an increase in the processing and handling of pain by the CNS, must be directed toward function of the CNS
- Cognitive behavioral therapy, especially combined with exercise, is strongly recommended.
- Other treatment such as acupuncture, herbal or vitamin supplements, chiropractic, hypnotherapy, and meditative movement therapy (e.g., qi gong, tai chi, yoga) often provides palliative relief from symptoms and depression severity for varying periods of time
