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Internal Med > Immunology 2 > Flashcards

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
Q

Graves disease clinical manifestation

A

type 2

hyperthyroidism

26
Q

Insulin resistant diabetes clinical manifest.

A

type 2

hyperglycemia, ketoacidosis

27
Q

Type 2 Hypersensitivity Mechanisms 1 and 2

A

!; 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
Q

Type 2 Hypersensitivity Mechanism 3 and 4

A

3 - Neutrophil-mediated tissue damage

4 - ADCC antibody-dependent cell-mediated toxicity, NK cells

29
Q

Type 2 Hypersensitivity Mechanism 5

A

unique - does not destroy target cell but causes malfunction

Myasthenia gravis

30
Q

Type 3

A

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
Q

Type 4

A

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
Q

T-cell mediated diseases (know their clinical manifestations)

A

(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
Q

Autoimmune diseases

A

immune mechanisms directed against self

34
Q

types of autoimmune diseases

A

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
Q

Organ specific autoimmune diseases

A

DM type 1
Graves Disease
Hashimoto

36
Q

Systemic Autoimmune disease

A

Myasthenia gravis
Rheumatoid arthritis
Lupus

37
Q

Etiologic and risk factors of autoimmune diseases

A

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
Q

Immunologic tolerance and self-tolerance

A

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
Q

Central tolerance

A

immature lymphocytes that recognize self-antigens during their maturation in central (generative) lymphoid organs

immature lymphocytes are killed by apoptosis

40
Q

Peripheral tolerance

A

mature lymphocytes that recognize self-antigens become either anergic (functionally inactive) or suppressed by regulatory T cells or undergo apoptosis

41
Q

How does autoimmunity occur?

A

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
Q

Types of Lupus

A

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
Q

SLE (may not need to know this specific)

A

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
Q

Lupus incidence

A

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
Q

Lupus Etiology and Risk factors

A

evidence points to interrelated immunologic, environmental, hormonal and genetic factors

Epstein-Barr virus may be risk factor

46
Q

Lupus pathogenesis

A

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
Q

Clinical manifestations Lupus

A

*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
Q

Fibromyalgia clinical manifestations

A

tender points

table 7.13

49
Q

Graft rejection

A

incompatibility of cell surface antigens

HLA matching of donor and recipient can enhance the probability of graft acceptance

Internal Med (25 decks)

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