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Infections > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What causes an allergic reaction to occur?

A

Often genetic and environmental factors combine and then when exposed to a triggering effect this causes the overall allergic reaction.

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2
Q

What are four examples of triggering events?

A

Hormonal fluctuations (menstruation)
Emotional stress
Nutritional deficit
Chronic flare ups of illness

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3
Q

What do Types 1,2 and 3 hypersensitivity reactions have in common?

A

Their immune system mediator is antibodies.
Type 1: IgE
Type 2: IgG and IgM
Type 3: IgG and IgM

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4
Q

How do the different types compare from exposure to allergens to onset of symptoms?

A

Type 1: 1-30 minutes
Type 2: 5-8 hours
Type 3: 4-6 hours
Type 4: 24-72 hours

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5
Q

What are some examples of Type 1 hypersensitivity?

A

Anything that is immediate and often anaphylactic reaction. Normally the cause of atopic disease such as asthma and allergies such as those to drug and food allergies which can result in anaphylaxis.

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6
Q

What are some of the functions of mast cells?

A

Prevent worms or Gram Negative infections
They release cytokines and histamines which attract effector cells to the site of infection
Enhance the flow of lymph fluid to the lymph nodes.

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7
Q

Explain the mechanism of Type 1 hypersensitivity.

A

Antigen-presenting cells phagocytose the allergen expressing it on the cell surface with a MHC-2 complex.If allergic they also present co-stimulatory molecule. They transport the allergen to the lymph node where they are presented to a naive T cell. Exposure to IL-4, IL-5 and IL-10 causes T cell differentiation into a primed T-helper cell (Th2). Once activated it then release IL-4 which causes B-cell antibody class switching causing a change in production from IgM to IgE. IgE binds to FcE receptors on mast cells, continued exposure causes them to degranulate and release pro-inflammatory mediators. IL-5 is released causing eosinophil activation.

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8
Q

What are the effects of pro-inflammatory mediators released in a IgE mediated Type 1 reaction in early phase?

A

Histamine released by eosinophils and mast cell degranulation binds to H1 receptors on the brochi smooth muscle inducing smooth muscle contraction, restricting the airways and causing difficulty breathing and increased fluid secretions. Also causes vasodilation increases the permeability of the blood vessels causing oedmea and hives, increased fluid in tissue and increased effector reponse there.

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9
Q

When does late phase reactions occur?

A

8-12 hours after second exposure

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10
Q

What happens in late phase Type 2 hypersensitivity?

A

Attraction of basophils and eosinophils recruited to site of allergen due to IL-4, 5 and 10 and leukotrienes.
LTB4 and LTC4 cause smooth muscle contraction and they attract even more immune cells such as neutrophils, mast cells and eosinophils.

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11
Q

What happens if the mast cells are activated in the GI tract?

A

Increased fluid secretion and peristalsis leading to diarrhea and/ or vomiting

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12
Q

What are some examples of anaphylaxis?

A

Normally due to insect bites, horse serum, drug allergies and food allergies

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13
Q

What happens during anaphylaxis?

A

Whole body release of histamine throughout the body, vasodilation, increased permeability of blood vessels causing blood to leak into the tissues. Rapid decrease in blood pressure and blood volume causes shock and fluid can leak into the air sacs causing pulmonary oedema.

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14
Q

Treatment for anaphylaxis?

A

Shock of adrenaline
IV fluids
Antihistamines and corticosteroids

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15
Q

Example of Type 2?

A

Wrong blood transfusion

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16
Q

What is the mechanism of Type 2 hypersensitivity?

A

Self reactive B cells produce IgM and IgG antibodies which bind to antigens on host cells. Antigens are either intrinsic (produced by the body) or extrinsic (from other substances such as drugs Penicillin). IgG binds to penicillin forming an antigen-antibody complex on host tissue. This causes activation of the complement system (C1 binds to Fc portion of the antibody). C3a, C4a and C5a are chemotactic factors which attract neutrophils which degransulate releasing enzymes which form oxygen radicals whch are cytotoxic inducing tissue damage. Formation of the membrane attack complex induces cell lysis

17
Q

What is the mechanism of a Type 3 hypersensitivity reaction?

A

Plasma cells secretes IgM, when an antigen is presented by cross linking two IgM it engulf and presents it with an MHC-2 which then attracts a T-helper cell which binding including CD40. This causes activation of the TH-2 releasing cytokines and inducing class switching to IgG antibodies. IgG binds to immune complexes with soluble antigens.

18
Q

What is the mechanism of a Type 4 hypersensitivity reaction?

A

Antigen is phagocytosed by either dendritic cells or macrophages which allows them to be presented on the cell surface. Th1 helper cells recognise the specific antigen and release chemokines which recruit macrophages to the site of inflammation and cause the release of cytokines. IFN-Y activates macrophages and TNF alpha and beta activate endothelial cells enhancing vascular permeability.

19
Q

What are some of the effects of histamine concentration in the bloodstream?

A

1-2 ng/ml: Gastric acid secretions
3-5 ng/ml: Tachycardia, skin reactions
6-8 ng/ml: decreased arterial pressure
7-12 ng/ml: bronchospasms

20
Q

What concentration of plasma histamine causes a cardiac arrest?

A

100 ng/ml

21
Q

What are the effects of histamine binding to H1 receptors?

A

When bound to H1 receptors on the smooth muscle it causes bronchoconstriction and contraction of gastro-intestinal tract.
Bound to receptors on the endothelium it causes vasodilation which results in leaky vessels resulting in oedema.
When bound to those on sensory nerve endings it causes pain and itching.

22
Q

What are the effects of histamine binding to H2 receptors?

A

It also causes vasodilation as it binds to H2 receptors on smooth muscle in high doses.

23
Q

What are the effects of histamine binding to H4 receptors?

A

Binds to receptors on the immune active cells causing chemotaxis

24
Q

What drugs are used to combat histamine release?

A

Epinephrine- has opposite physiological actions by binding to different receptors.
Histamine release inhibitors such as mast cell stabilisers or Beta 2 agonists.
Antihistamines

25
Q

Describe the metabolism of first generation anti-histamines.

A

Extensively metabolised by cytochrome P450, metabolites are active and excreted by the kidney.

26
Q

What is the duration of action of first generation antihistamines?

A

4-6 hours

27
Q

How do side effects from first generation anti-histamines occur?

A

First generation H1 anti-histamines act on muscarinic receptors causing antichloringeric effect such as dry mouth, urinary retention and blurred vision.

28
Q

What are the effects of histamine overdose?

A

Convulsions- particularly in children

29
Q

What is an additional indication of first generation anti-histamine?

A

Treatment of motion sickness

30
Q

List some first generation anti-histamines.

A

Cyclizine
Chloramphenamine
Promethazine

31
Q

List some second generation anti-histamines.

A

Fexofenadine
Loratadine
Cetrizine

32
Q

What are some of the interactions of first generation antihistamines?

A

With CYP450 inducers, activity decreased
With macrolides, antifungals, calcium antagonists as they competitively inhibit P450, activity increased

Additive CNS depression with:
Opioids
Sedatives
Narcotic analgesics
Alcohol

Additive anticholinergic effect with antichloringeric drugs

33
Q

What are two examples of mast cell stabilisers?

A

Cromolyn and Nedocromyl

34
Q

How are mast cell stabilisers given?

A

Powder by inhalation

35
Q

How do mast cell stabilisers work?

A

They inhibit histamine release by inhibiting chloride channels on mast cells.

36
Q

What are some of the side effects of mast cell stabilisers?

A

Dry mouth, throat irritation, cough, wheezing

Infections (16 decks)

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