Chapter 12 Disorders of the Immune System

hypersensitivity

an abnormal and excessive response of the activated immune system that causes injury and damage to the host tissues (4 types)

type 1 hypersensitivity

IgE mediated

type II hypersensitivity

antibody-mediated

type III hypersensitivity

complement-mediated

type IV hypersensitivity

T-cell mediated

type I

rapid response to exposure to antigen

• antigen= allergen

type I hypersensitivity causes what major allergic reaction?

anaphylaxis

major cells involved in type I

type 2 helper T cells, mast cells, basophils, eosinophils

type I mediators released

histamine and arachidonic acid

histamine (primary phase)

increases nitric oxide (relaxes vascular smooth muscles, increases permeability, smooth muscle contraction, bronchial constriction)

arachidonic acid (late phase)

utilized in synthesis of leukotrienes and prostaglandins- longer acting

anaphylaxis

life-threatening, systemic, IgE mediated reaction

• widespread release of histamine

  • vasodilation, hypotension, arterial hypoxia, airway edema

grade 1 anaphylaxis

cutaneous and mucosal reactions (erythema, urticaria)

grade II anaphylaxis

hypotension, tachycardia, dyspnea, GI disturbances

grade III anaphylaxis

bronchospasm, cardiac dysrhythmias, cardiac collapse

grade IV anaphylaxis

cardiac arrest

atopic reactions

local hypersensitivity (allergic rhinitis, bronchial asthma, atopic dermatitis)

type II

IgG or IgM antibodies directed against target antigens on specific host cell or tissue

• 4 types

myasthenia gravis

antibody to acetylcholine receptor inhibits receptor binding of the neurotransmitter

type III

immune complex-mediated disorder

• caused by formation of antigen-antibody immune complexes formed first in plasma then complexes deposited in tissues

• manifestations have to do with the site of immune complex deposition

glomerulonephritis

inflammation of kidney glomuleri (type III)

type IV

cell-mediated and delayed

• T-cell mediated

• principle mechanism of defense against a variety of microorganisms

• causes cell death and tissue injury

contact dermatitis

skin inflammation caused by direct contact with allergens (type IV)

autoimmune disease

failure of body to differentiate between self and non-self

• immunologic response against host tissues (can affect almost any cell type, tissue or organ

systemic autoimmune disease examples

rheumatoid arthritis, systemic lupus erythematosus

blood autoimmune diseases

idiopathic thrombocytopenic purpura

mechanisms of autoimmune disease

loss of self-tolerance but exact mechanism unknown

factors to consider in autoimmune disorders

hereditary, environmental, genetic, etc.

HIV (human immunodeficiency virus)

retrovirus that selectively attacks the CD4+ T lymphocytes (responsible for orchestrating and coordinating the immune response to infection)

transmission of HIV

sexual contact, blood-to-blood contact, perinatally, occupationally

window period

infectious even when no symptoms are present

seroconversion

the point where infected person converts from being negative for presence of HIV antibodies to positive

HIV: steps for replication

• Step 1 Attachment: Binding of virus to CD4 cell

• Step 2 Fusion: Allows for internalization of the virus

• Step 3 DNA synthesis: Must change RNA into DNA using reverse transcriptase

• Step 4 Integration: New DNA enters nucleus of CD4 cell and is inserted into cells original DNA

• Step 5 Transcription: Double-stranded DNA forms a single-stranded mRNA

• Step 6 Translation: Polyprotein created (needed for construction of new virus

• Step 7 Cleavage: Protease cuts polyprotein chain, making new viruses

• Step 8 Maturation: Viral RNA assembled into new HIV viruses and released (budding)

acute infection stage

• increase in viral replication (leads to high viral load and decrease in CD4+ T cell count

• acute mononucleosis-like syndrome (fever, fatigue, myalgias, sore throat, GI problems, etc.)

  • lasts 2-4 weeks

chronic HIV infection (asymptomatic or latent stage)

no s/s of illness

• 10 years

• CD4+ T cell count falls gradually from normal (800-1000) to 200 or lower

• persistent generalized lymphadenopathy

typical progressors

develop AIDS 10-11 years after infection

rapid progressors

develop AIDS in less than 5 years

slow progressors

do no progress to AIDS for more than 15 years

opportunistic infection

involves common organisms that do not produce infection unless there is impaired immune function

prevention

• no cure for HIV or AIDS

• monogamous sexual relationships

• latex condoms

diagnosis

ELISA test- HIV antibody test; followed by a confirmatory test (western blot assay)