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Immunology 2 Flashcards

1
Q

Primary vs Secondary Disorder

A

Primary - defect involving T or B cells or lymphoid tissues (inherited in the genesis of the immune system), genetic deficiencies of innate immune (complement proteins and phagocytes)

Secondary - disease or infection that depresses or block immune response (infection, age, malnutrion, chemo, autoimmune disorders, immunosuppression)

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2
Q

AIDS

A

Acquired Immunodeficiency Syndrome

caused by HIV (RNA) a retrovirus

mainly attacks CD4, depleting T cells but also infects macrophages, B cells, dendritic cells and microglial cells

HIV-1 causes global epidemic bc its more readily transmitted

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3
Q

Transmission of AIDs

A
  • contaminated blood
  • sex
  • maternal to child

not transmitted by fomites, household or social contact

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4
Q

General Clinical manifestation of AIDS

A

Stages of infection vary from acute to asymptomatic to symptomatic and correlate with the level of CD4 (lymphocyte) counts

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5
Q

Acute infection of AIDS

A

happens first

1-6 weeks, flu-like symptoms and lymphadenopathy (swelling of lymph nodes)

antibody tests remain NEGATIVE

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6
Q

Asymptomatic phase of AIDS

A

1-20 years

CD4 count of 500 cells/mm or more (going down)

POSITIVE antibody test but no symptoms

seroconversion - emergence of HIV antibodies in blood

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7
Q

Symptomatic phase of AIDS

A

CD4 count is 200-500 cells/mm (LESS)

  • adenopathy (enlarged lymph nodes)
  • non specific symptoms like diarrhea, weight loss, fatigue, night sweats and fever
  • neurologic symptoms from HIV encephalopathy
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8
Q

Table 7.4? page 1014

A
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9
Q

Other clinical manifestations of AIDS

A
  • Neurologic manifestations (pain syndromes, peripheral neuropathies
  • neuromusculoskeletal
  • rheumatologic diseases
  • cardiopulmonary diseases
  • lipodystrophic syndrome
  • AIDs-related lymphoma

-kaposi sarcoma

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10
Q

Pain syndromes with HIV

A
  1. pain associated with HIV infection, immunosuppression, opportunistic infections or comorbidities
  2. pain caused by HIV diagnostic procedures and treatment
  3. pain unrelated to HIV or its treatment (diabetic neuropathy, discogenic pain, -kaposi sarcoma
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11
Q

Prevention of AIDs (when should you obtain testing?)

A
  • received blood or blood products before 1985
  • had sex with multiple partners
  • inject drugs and share needles
  • had sex with someone who injects drugs or shares needles
  • sex without condom with someone with HIV
  • share needles for tattooing or body piercing
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12
Q

3 Facts of HIV treatment

A
  1. HIV meds cannot cure it, they can promote healthier lives and prolong lives of people with HIV
  2. combinations of medicines are taken to prevent HIV from advancing to AIDS
  3. meds can reduce the risk of transmission to others (such as mom to fetus)
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13
Q

Recommended treatment of AIDS

A

HAART - Highly active antiretroviral therapy

Using at least 3 drugs from different classes to suppress virus

NRTIs, NNRTIs, PIs, fusion inhibitors, etc

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14
Q

HIV Precautions for Health Care Workers

A
  • use protective barriers
  • wash hands and Musco membranes after body fluid contamination
  • prevent needle or scalpel sticks
  • ventilation devices for resuscitation
  • if you have open wound or lesion don’t treat or use equipment
  • pregnant workers take extra precautions
  • occupational exposure to HIV should be followed immediately by eval of the exposure source and PEP
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15
Q

Postexposure prophylaxis (PEP)

A

urgent medical concern

preventing infection after high risk exposure

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16
Q

What is Chronic Fatigue and Immune Dysfunction Syndrome

A

CFS used interchangeably with ME (myalgic encephalitis)

illness is not a single disease but combination of factors

subset of chronic fatigue - unexplained fatigue of greater than or equal to 6 months

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17
Q

CFS risk factors

A

higher prevalence in women, minority groups and people with lower educational attainment and occupational status

mean age of onset is 29-35 years

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18
Q

Pathogenesis of CFS

A

Explanations were sought out in viral infections, immune dysfunction, neuroendocrine responses, dysfunction of the CNS, muscle structure, exercise capacity, sleep patterns, genetic constitution, personality and neuropsychologic processes

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19
Q

Fig 7.27 Infection control in immune deficiencies

A

altered defensive mechanisms

infectious agents

revisors

modes of transmission
infection control strategies

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20
Q

Hypersensitivity Disorders

A

tissue damage from inaccurate/overexpression to a substance

4 types:

21
Q

Type 1:

A

IgE-mediated reaction

immediate rate of development

IgE antibody involved binds with mast cell or basophil to activate it

mast cells and basophils release histamine, cause bronchoconstriction (coughing)

cause vasodilation, smooth muscle contraction and edema

seasonal allergic rhinitis

22
Q

What are antihistamines

A

allergy meds like Benadryl

compete with histamine (H1-H4) for histamine receptors on cell membranes (block affects of histamine)

Second generation are non-sedating (non drowsy), more selective to H1 receptor sub-type

23
Q

Type 2:

A

tissue specific - symptoms depend on what organ/tissue expresses the antigen

immediate development

IgG and IgM

Macrophages

autoimmune, thrombocytopenic purpura, GRAVES disease, autoimmune hemolytic anemia

FIVE MECHANISMS

24
Q

Myasthenia gravis clinical manifestations

A

type 2

muscle weakness and paralysis

25
Graves disease clinical manifestation
type 2 hyperthyroidism
26
Insulin resistant diabetes clinical manifest.
type 2 hyperglycemia, ketoacidosis
27
Type 2 Hypersensitivity Mechanisms 1 and 2
!; IgG or IgM activates complement cascade which creates the MAC - membrane attack complex MAC punches holes in the cells outer membrane = cell bursting (lysis) Occurs in autoimmune hemolytic anemia where RBC destroyed, or in ABO blood transfusion rxn where incompatible blood types are mixed 2:antobody may cause destruction of the cell via phagocytosis by macrophage
28
Type 2 Hypersensitivity Mechanism 3 and 4
3 - Neutrophil-mediated tissue damage 4 - ADCC antibody-dependent cell-mediated toxicity, NK cells
29
Type 2 Hypersensitivity Mechanism 5
unique - does not destroy target cell but causes malfunction Myasthenia gravis
30
Type 3
Immune complex mediated reaction interaction of antibody and complement proteins ("complex" - work together) Immediate development IgG and IgM Neutrophils Systemic LUPUS, erythematosus Most common tissues affected are kidneys, joints, skin and blood vessels
31
Type 4
Cell-mediated reaction delayed reaction - occurs on skin after allergen exposure via cosmetics, topical meds, adhesives, psoion ivy, latex, TB skin test 48-72 hrs after test No antibodies, T lymphocyte-mediated Lymphocytes and macrophages contact sensitivity to poison ivy and metals (jewelry) graft rejection or allergic reaction after transplant
32
T-cell mediated diseases (know their clinical manifestations)
(type 4) Rheumatoid arthritis - chronic arthritis, destruction of articular cartilage and bone multiple sclerosis - demyelination in CNS, perivascular inflammation, paralysis, ocular lesions Type 1 DM ? 1 or 2 Hashimoto thyroiditis - hypothyroidism IBS - intestinal inflammation, ulceration, obstruction
33
Autoimmune diseases
immune mechanisms directed against self
34
types of autoimmune diseases
more than 56 exist on a continuum localized tissue damage occurs from the presence of specific autoantibodies (Hashimoto's disease) middle - lesion localized in one organ butt antibodies not non-organ-specific diseases in which lesions and antibodies are widespread throughout the body and not limited to one organ ORANG SPECIFIC AND SYSTEMIC
35
Organ specific autoimmune diseases
DM type 1 Graves Disease Hashimoto
36
Systemic Autoimmune disease
Myasthenia gravis Rheumatoid arthritis Lupus
37
Etiologic and risk factors of autoimmune diseases
Often cant be determined, combo of factors - genetic, hormonal, environmental (chemical and toxin exposure, sunlight and drugs may destroy T cells), viruses, stress, cross-reactive antibodies no single gene identified as cause but cluster of genes seem to increase susceptibility
38
Immunologic tolerance and self-tolerance
Immunologic tolerance - unresponsiveness of certain antigens induced by their exposure to lymphocytes self-tolerance - lack of recognition and responsiveness to ones own tissue antigens AUTOIMUNNUITY INDICATES LOSS OF SPECIFIC TOLERANCE
39
Central tolerance
immature lymphocytes that recognize self-antigens during their maturation in central (generative) lymphoid organs immature lymphocytes are killed by apoptosis
40
Peripheral tolerance
mature lymphocytes that recognize self-antigens become either anergic (functionally inactive) or suppressed by regulatory T cells or undergo apoptosis
41
How does autoimmunity occur?
candidate locations on human genome for susceptibility to MS, DM 1, SLE and Chrons disease has been identified epigenetics determine whether the gene is expressed certain bacteria, mycoplasmas and viruses can trigger autoimmunity viruses and microbes share cross-reacting epitopes with self-antigens where microbial antigens tend to attack self-tissue
42
Types of Lupus
Type 3 Lupus erythematosus (lupus) is a chronic inflammatory autoimmune disorder that appears in several forms DLE - discoid lupus erythematosus, affects only skin SLE - Systemic Lupus, can affect any organ in body SLE more severe, no two people will have same symptoms
43
SLE (may not need to know this specific)
latent lupus - features suggestive of SLE but not classic SLE drug-induced lupus - manifests while taking a drugs and ceases after you stop antiphospholipid antibody syndrome - arterial and venous thrombosis, recurrent fetal loss, antibodies directed against phospholipids late-stage lupus - chronic disease greater than 5 years
44
Lupus incidence
found in young women during childbearing years more common in African American women first degree relatives both genetic and environmental factors play a role
45
Lupus Etiology and Risk factors
evidence points to interrelated immunologic, environmental, hormonal and genetic factors Epstein-Barr virus may be risk factor
46
Lupus pathogenesis
three main mechanisms - autoantibodies, vascular abnormalities, inflammatory mediators body produces antibodies against its own cells and antigens, suppressed bodys normal immune fxn and damages tissues organ depedndent
47
Clinical manifestations Lupus
*butterfly skin rash *approx 50% of those with SLE have renal disease arthritis vasculitis - inflammation of cutaneous blood vessels) hair loss (alopecia) pleuritis, pneumonitis, tachycardia, dyspnea neuropsychiatric manifestations, emotional instability/depression
48
Fibromyalgia clinical manifestations
tender points table 7.13
49
Graft rejection
incompatibility of cell surface antigens HLA matching of donor and recipient can enhance the probability of graft acceptance

Internal Med (26 decks)

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