Hypersensitivities and immune deficiencies Flashcards
What makes a reaction a hypersensitivity?
If the immune response is out of proportion to the threat or disease.
Type I allergy
- IgE responds to a soluble antigen
- Mast cell has IgE receptor and is activated
- Ex: anaphylaxis, rhinitis, asthma
Type II allergy
- Cytotoxic, antibody dependent
- IgG mediates cytotoxicity (one of our cells)
- antibodies bind to our cells and cause an immune response
- Antibody binds to antigens on the cell surface and destroys or prevents the cell from functioning by:
- lysis, phagocytosis, neutrophil-mediate
- Ex: some drug allergies (PCN), transfusion reactions, hemolytic anemia
Type III allergy
- IgG mediates a soluble antigen found in the blood
- Immune complex formation and deposition- caused by antigens and antibodies piling up faster than can be phagocytozed.
- they start sticking to blood vessels and cause vascular damage
- Ex: Systemic lupus, serum sickness, glomerulonephritis
Type IV allergy
- T-lymphocyte mediated delayed hypersensitivity
- Mediated by T lymphocytes
- Ex: Dermatitis, chronic transplant rejection, tuberculin skin test, Type I diabetes
What type of hypersensitivity are Graves Disease and myesthenia gravis?
How?
- Type II hypersensitivity
- Graves disease: antibody binds to TSH receptors and activates them, causing too much T4 and T3 to be released
- Myesthenia gravis: Antibody binds to ACH receptor on muscle and destroys the receptor
What is the root cause of autoimmune disease?
- a self reactive B or T cell gets out and is activated (by environmental trigger)
- once activated it undergoes clonal proliferation
- For B cells, somatic hypermutation may cause a self-tolerant b cell to mutate into a self reactive B cell
- *Need a genetic predisposition AND an environmental trigger
What are the rheumatic autoimmune diseases?
- Rheumatoid arthritis
- scleroderma
- sjogren’s syndrome
- systemic lupus erythematosus
What are the GI autoimmune diseases?
- chronic active hepatitis
- crohn’s disease
- primary biliary cirrhosis
- ulcerative colitis
What are the endocrine autoimmune diseases?
- graves disease
- Hashimoto’s thyroiditis
- Type-1 diabetes
What are the Neurologic autoimmune diseases?
- multiple sclerosis
- myasthenia gravis
What are the hematologic autoimmune diseases?
- Autoimmune hemolytic anemia
- idiopathic thrombocytopenic purpura
- pernicious anemia
What are the renal autoimmune disorders?
Goodpasture’s syndrome
What are the multiple organ system autoimmune diseases?
- Ankylosing spondylitis
- polymyositis
- psoriasis
- sarcoidosis
- vasculitis
How does Lupus work?
- a person with lupus has antinuclear antibodies (antibodies that attack DNA)
- When there is some kind of cell necrosis (like from cells damaged by UV, the cell walls break and the guts of the cells are exposed
- the antibody is then able to attach to the DNA, starting an immune response against it
- Form aggregates of antibody and DNA that can then get deposited in the glomeruli and cause kidney damage
What is SCID?
- Severe combined immuno deficiency
- Unable to produce B cells or T cells
- Lymph node is empty and useless
- Only have an innate immune system, no adaptable
- Cannot handle any kind of bacteria or viruses they encounter
What is X-linked Agammaglobulinemia?
- defect that prevents maturation of B cells, which make immunoglobulins, so they have no immunoglobulins
What is DiGeorge Syndrome?
- During development, pharyngeal arches do not develop properly and they have no thymus
- Thymus is where T-cells are matured, so this person would have no T-cells
- Also facial abnormalities because the face develops from the pharyngeal arches
How does SCID, X-linked agammaglobunimeia, and digeorge syndrome affect lymph node?
- SCID- The lymph node is empty, basically useless
- agammaglobulinemia- no germinal centers; the cellular reaction is present, but there is no humoral reaction
- DiGeorge- Humoral reaction present, but no cellular reaction
How does HIV work?
- HIV enters CD4 (T-helper) cell
- the HIV RNA is made into DNA and integrated into the host genome
- The virus is then copied and send to other cells
- The CD4 cells start to die off, either from the virus or Cytotoxic T cells (CD8)
- As the person has fewer and fewer CD4 cells, there is no godfather to tell the rest of the immune system what to do and the person starts getting opportunistic infections
How does the entrance inhibitor work?
prevents the virus genetic material from entering the CD4 cell
How do the reverse transcriptase inhibitors work?
Stops ALL the reverse transcriptase from happening in the body. Since we dont do reverse transcriptase anywhere else, it only effects the HIV
How do the integrase inhibitors work?
prevent integration of the viral DNA into our DNA
How do protease inhibitors work?
HIV brough its own protease that cuts up the virus’ giant protein into small, useful pieces. The protease inhibitor prevents it from being able to do that and the large protein is useless
What do the counts of viral load and CD4 cells look like as the disease progresses? (graph)
