MIIM - Immunopathology I - Week 5 Flashcards
What is a possible disadvantage of immune activation in response to an infectious agent?
Damage to the body’s cells
Define immunodeficiency, and name three outcomes.
Failure of all or part of the immune system.
- recurrent infections
- overwhelming infections
- opportunistic infections
Name three abnormal or unwanted responses. Name two mechanisims by which it can occur.
Allergies
Autoimmune diseases
Graft rejection
-hypersensitivity and inflammation can cause them
Define primary immunodeficiency. Describe two possible causes, and ita rarity.
Inherent congenital defect in the immune system
- either genetic or caused by the intrauterine environment
- rare
Define secondary immunodeficiency.
External agents or alterations in other body systems that compromise the immune system.
Name 6 predisposing factors to secondary immunodeficiency.
Age Malnutrition Tumours Cytotoxic drugs / irradiation Other diseases (diabetes) Infections (malaria, HIV)
In the eye, what are diseases found often due to?
Re-activation of latent infections
How many types of hypersensitivities are there?
4
Describe type I hypersensitivity, including what its first phase is, and what it is followed by (2), including its rarity, and possible symptoms (4). Name the later 2 phases.
Sensitisation, followed by Response.
Response include:
Local - rhinitis, bronchoconstriction, conjunctivitis
Systemic - anaphylaxis
Responses both have an immediate and a delayed phase
What are two other names for type I hypersensitivity.
Allergy and atopy
Name one general and three common causes of type I hypersensitivity.
Inocuous environmental antigens like pollen, house dust, and many foods
Consider type I hypersensitivity. What antibodies are produced and in response to what? What happens to these antibodies? What is this called? What happens with subsequent induction of type I hypersensitivity?
IgE antibodies are produced in response to an inocuous antigen (the allergen).
They bind to local mast cells.
After subsequent exposure to the allergen, they can bind to the mast cell-bound IgE antibodies, and result in the symptoms of allergy.
Which adaptive immune system signal is responsible for the sensitisation phase of type I hypersensitivity? What does it result in, and the production of what, by which cell? What is the mediator cytokine? Describe the process briefly.
Signal 3
It results in the differentiation of cells to TH2 cells. This will stimulate B cells to produce IgE antibodies to the allergen. The mediator cytokine is IL-4.
The CD4 TH2 cell is stimulated by a phagocytic cell, and in turn, stimulates B cells, which eventually produce the antibodies.
Define elicitation.
Subsequent allergen exposure leads to mast cell degranulation.
Consider elicitation. What kind of compounds are released, and how quickly? Order them (~5) into three time categories. Describe why the slowest response is so.
30 - 45 secs:
Histamine
Tryptase
10 - 30 mins:
Prostaglandins
Slow:
Cytokines
IL-4*
*Late respons edue to eosinophil and T cell activation
There are many types of allergic responses. What is it dependent on? What are the four main responses?
It is tissue dependent. Main responses are: -vasodilation -vasopermeability -smooth muscle contraction -fluid secretion
Name two allergic responses in the GI tract and two symptoms it can cause.
Responses: -increased fluid secretion -increased peristalsis Symptoms: -diarrhoea -vomiting
Name two allergic responses in the skin and three symptoms it can cause.
Responses: -increased fluid secretion -vasodilation Symptoms: -swelling -itching -urticaria (hives)
Name two allergic responses in the airway and four symptoms it can cause.
Responses: -decreased bronchial diameter -increased mucus Symptoms: -nasal blockage -coughing -phlegm -athsma
Name two allergic responses in the blood vessels and three symptoms it can cause.
Responses: -increased blood flow -increased permeability Symptoms: -increased tissue fluid (oedema) -increased cell infiltrate -anaphylactic shock
