Chapter 17. Immunology and Immunizations part II Flashcards
Recognize peptide epitopes (fragment of antigens), combined with chemical and MHC proteins to produce two major classes of MHC proteins:
MAJOR HISTOCOMPATIBILITY COMPLEX (MHC) proteins:
Class 1 proteins: Present on all surfaces of body cells.
Class II proteins: Present on specific antigen presenting cell (APC’s)
What type of hypersensitive rxn and symptoms? Causes are:
Resp. allg: grass, animal fur, carpet mites
GI allg: Dairy products, shellfish, and peanut.
Skin allg: topical drugs (procaine).
IV allg: insect venoms.
IgE mediated type I: Anaphylactic reactions. It is treated by epinephrine. (Penicillin’s, bee stings, latex, pea nut).
mediated type I hypersensitivity rxn.
Inflamm of upper and lower resp. tract (asthma), GI and skin.
Atopic dermatitis, pruritis, rhinitis, asthma, and food allergies. Urticaria, eczema.
Approx 50% of pt with asthma secrete IgE.
What type of hypersensitive rxn and causes? Symptoms are:
Hemolytic anemia and thrombocytopenia are more common.
Hyper acute graft rejection
Type II. Cytotoxic/anti-body mediated hypersensitivity:
Transfusion mismatches, hemolytic anemia, Rh disease, specific autoimmune diseases Hashimoto thyroiditis, and myasthenia gravis
What type of hypersensitive rxn and symptoms? Causes are:
Non specific autoimmune disorders such as systemic lupus erythematous, rheumatoid arthritis. Hepatitis infections, local respiratory form of fungal reactions. Penicillin and sulfonamides.
Type III. Antigen-antibody (IgG/IgM) complex
Lymphadenopathy, fever, and rash- first symptoms. More serious: Glomerulonephritis, vasculitis and lupus, arthralgia and arthritis.
Type IV. Delayed type reactions mediated by cell (T cells) causes and symptoms
Causes: Prolong action of protozoa. Mycobacterium Tuberculin test and poison ivy.
Symptoms: Contact dermatitis, microvesicle formation, and spongiosis.
Tuberculin (Monteux test) reaction gives erythema.
Hypersensitive reaction is “ACID”
Hypersensitive reaction is “ACID”
Type 1 - Allergic (<30 min)
Type 2 - Cytotoxic (5-12 hrs)
Type 3 - Immune complex deposition (3-8 hrs) Type 4 - Delayed (24-48 hrs)
- Either hereditary or congenital and at least one basic element to the immune system does not function properly or is absent.
- Invoke decreased immunologic responsiveness
Primary immunodeficiency
-Secondary
Define X-linked gammaglobinemia (hypogammaglobulinemia) and symptoms
-Inherited deficiency in antibody production in which T cell function is relatively normal but B-cells do not fully mature
Symptoms. Pneumonia, sinusitis, meningitis and septicemia
Def. of T cells, B cells and serum Ig. Infx with oppor. orgs occur in the 1st few postnatal and survival for longer than 1yr is rare wo successful bone marrow transplant.
Severe combined immunodeficiency SCIDs
This syndrome is a serious and most fatal condition in which the immune system breaks down and does not respond normally to infection.
Base line assessment including CD4 and viral load.
CD4 <500 cell/microL consider initiating antiretroviral therapy. Give diag. tests.
AIDS: Acquired immune deficiency syndrome
Diagnosis of HIV infection (Positive HIV ELISA antibody test confirmed by western blot).
HIV is retrovirus: stores its genetic info in RNA rather than DNA. When virus enter target cells. The RNA produce cDNA and this incorporate with host DNA and this reverse pattern of human cell which does DNA to RNA.
Tests that are used to diagnose HIV infection.
- ELISA (Enzyme linked immunosorbent assay).
- Western blot
- Polymerase chain reaction (PCR assays)
Stages of HIV reproduction
Stage 1. HIV enters a CD cell (helper T cell)
Stage 2. HIV is a retrovirus that its genetic information is stored on single stranded RNA instead of double stranded DNA found in most organisms. To replicate, HIV uses an enzyme known as reverse transcriptase to convert its RNA into DNA.
Stage 3. HIV DNA enters the nucleus of the CD4 cell and inserts itself into the cell’s DNA then instructs the cell to make many copies of the original virus.
Stage 4. With the help of the protease enzyme, new virus particles are assembled. These newly formed viruses have the cell ready to infect other CD4 cells.
Step 5. Shortly after HIV infection, the CD4 cell count falls sharply in the early stages of HIV infection because the virus targets and destroys CD4 cells. When the body starts to cope with the infection, the CD4 cell count rises again.
In the advance stage, the rate at which the virus reproduces or rate at which the virus reproduces or “replicates” surpasses the rate of CD4 cell turnover, making the body more susceptible to a variety of AIDS-defining illnesses such as (PCP), as the viral load rapidly increases unchecked and the CD4 cell counts decline these illnesses that signal late stage infection eventually lead to death.
Common opportunistic infections.
1. Tuberculosis, bothextra and pulmonary. Atypical mycobacteria such as Mycobacterium avium complex (MAC) may cause infx
2. Oral candidiasis
3. Esophageal candidiasis
4. Herpes zoster
5. Diarrhea
• Protozoal – amoeba, Giardia, isospora belli, cryptosporidium
• Helmints – strongyloids
• Viral – cytomegalovirus
6. Bacterial pneumonia and Pneumocystis carinii pneumonia
7. Toxoplasma encephalitis
8. Cytomegalovirus renitis
Cancers such as Kaposi’s sarcoma and non-Hodgkin’s lymphoma
Type of opportunistic infxs and their CD4 cells/microL
M. tuberculosis— 350
Kaposis sarcoma— 275
Non-Hodgkins lymphoma— 200
P. carinii jerovici (pneumonia)— 100
Cytomegalovirus and M. avium intracellular— 50
ORGAN specific autoimmune disorders Non organ specific autoimmune disorder. • Rheumatic fever • Antithyroid autoimmunities • Myxedema (hypo) • Hashimoto thyroiditis (hypothyroidism) • Graves disease (hyperthyroidism) —Give other examples
• Myasthenia gravis (weakening of muscles)
• Autoimmune pernicious anemia
• Goodpasture’s syndrome
• Autoimmune hemolytic anemia,
thrombocytopenia, neutropenia, lymphopenia
• Insulin dependent diabetes mellitus (IDDM)-type1
• Multiple sclerosis
NON ORGAN: Sjogren syndrome,
Systemic lupus erythromatus.
