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Clinical Pathology > Allergy > Flashcards

Allergy Flashcards

1
Q

How many types of hypersensitive reactions are there

A 
4 types
Type 1- 3 are antigen mediated.
Type 4 is cell mediated.
Type 1- anaphylaxis
Type 2- cytotoxic
Type 3- immune complex
Type 4- delayed type
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2
Q

What are the stages in developing an allergy

A
  • Exposed to antigen
  • APC and B cells take up antigen and present to T cells.
  • T cells recognise the antigen
  • T cells tell B cells to make the antibody.
  • Re- exposure results in antigen antibody complex forming.
  • B cell- Activate complement and attract phagocytic cells.
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3
Q

Type 2 reaction involve which immunoglobulins

A

IgG/IgM

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4
Q

what is another name for type 2 hypersensitivity

A

cytotoxic

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5
Q

What are the clinical features of type 2 hypersensitivity

A

– Onset minutes to hours

– Cell lysis and necrosis

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6
Q

On what surface must the antigen be to trigger a Type 2 hypersensitivity reaction

A

cell surface.

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7
Q

what is a common allergen for type 2 hypersensitivity

A

penicillin

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8
Q

what 2 conations are associated with type 2 hypersensitivity

A

– Erythroblastosis fetalis,

– Goodpasture’s nephritis

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9
Q

What is another name for typer 3 hypersensitivity

A

immune complex

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10
Q

Type 2 reaction involve which immunoglobulins

A

IgG/IgM

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11
Q

What type of antigen is needed for a type 3 hypersensitivity reaction

A

Soluble.

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12
Q

What are the clinical features of at type 3 hypersensitivity reaction

A

– Onset 3-8h

– Vasculitis- when immunocomplexes are filtered through blood vessels it leads to.

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13
Q

what is the tradition cause of typer 3 hypersensitivity

A

serum sickness- due to serum form other animal used to treat a condition e.g. horse serum in tetanus.

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14
Q

What conditions is type 3 hypersensitivity associated with

A

SLE

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15
Q

What other name is given to type 4 hypersensitivity reactions

A

delayed

no antigen- antibody complex.

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16
Q

What type of cell mediated response is type 4 hypersensitivity

A

– Antigen specific T-cell mediated cytotoxicity

– Antigen is taken up and presented to immune cells which can cause tissue damage.

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17
Q

what are the clinical features of type 4 hypersensitivity

A

– Delayed onset 48-72h
– Erythema induration
➢ Put allergen on skin and then leave for 48-72 hrs to see if the reaction occurs.

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18
Q

What are the common antigens for type 4 hypersensitivity

A

metals e.g. nickel

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19
Q

What condition is associated with type 4 hypersensitivity

A

contact dermatitits.

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20
Q

What is the hygiene hypothesis.

A
  • Those components of the immune system involved in responses to parasitic infection are also involved in allergic responses
  • The system has developed to produce a rapid tissue-based response to re-infection.
  • The lack of infectious drive is a contributory factor in allergic disease
  • Change in environment- you get less infection and hence more allergens.
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21
Q

What are Th1 and Th2 used for

A

Th1 -infections

Th2- allergy

22
Q

How are suceptibilty genes involved in sensing the environment.

A

group of genes that encode molecules that directly modulate the effect of environmental risk factors for allergic disease.
e.g – Polymorphisms of glutathione-S-transferase genes have been shown to modulate the effect of exposures involving oxidant stress, such as tobacco smoke and air pollution on asthma susceptibility

23
Q

How are suceptibilty genes involved in barrier function

A

– genes which are responsible for epithelium regulation e.g. ORMDL3/GSDML,34 PCDH1,24 and C11orf30.

24
Q

How are suceptibilty genes involved in the regulation of (atopic) inflammation

A

– This group includes genes that regulate TH1/TH2 differentiation and effector function.
– includes the genes shown to regulate the level of blood eosinophilia

25
Q

How are suceptibilty genes involved in tissues response genes

A

– includes genes that modulate the consequences of chronic inflammation.
– Expressed in fibroblasts and smooth muscel
– Some genes affect more than one disease component.

26
Q

Do you get an allergic response on first encounter with a allergen

A

No

first time you sensitise yourself and then the second time you actually develop a response.

27
Q

How does a allergen cause an allergy

A

– Defect in the barrier and allergen enters.
– Allergen causes damage to the barrier and enter
– Allergen taken up and peptides displayed by the dendritic cells
– These expose the allergen to T cells (TH2 allergy)
– Primary response in up regulation of the allergen.

28
Q

How is Ig E produced

A
  • Th2 cells make cytokines- IL4

* IL4 drives B cells to make Ig E.

29
Q

what cells do IgE attach to

A

mast cells.

30
Q

What is the function of mast cells once allege binds to it.

A

Release histamines protease, and chemotactic factors e.g. ECF, NCF.
Secondary de novo molecules such as leukotriene and prostaglandins are made via arachdonic acid.

31
Q

what are the clinical features of Type 1 hypersensitivity

A

Fast onset (15-30 min)

32
Q

what is the role of Th2

A
  • Multiple cytokine release: IL4
  • Innate inflammatory Response by macrophages
  • Drive for immunoglobulin production by B cells.
33
Q

How is B and T cell memory developed

A
  • Differentiation and clonal expansion of allergen-specific T helper 2 (TH2) cells.
  • production of cytokines (interleukin-4 (IL-4) and IL-13), which induce immunoglobulin class switching to IgE and clonal expansion of naive and IgE+ memory B-cell populations.
34
Q

what 3 conditions are in the atopic triad

A

asthma (type 1), rhinitis(type 1 ) and eczema (type 4)

35
Q

where are most cells in asthma and rhinitis

A

nasal mucosa or airways.

this is were the allergen is exposed.

36
Q

symptoms of rhinitis

A

• Blocked nose, runny nose - often with eye symptoms

37
Q

most common cause of rhinitis

A

house dust mite, animal dancers and pollen.

38
Q

what is the treatment for rhinitis

A

Antihistamines (immediate) & Nasal steroids (chronic)

39
Q

most common cause of asthma

A

house dust mite.

40
Q

what causes the damage to at the airways

A

IgE mediated

• DAMAGE TO AIRWAYS due to LATE PHASE RESPONSE- WHICH IS ARACHDONIC ACID MEDIATED.

41
Q

what is the most common cause of atopic dermatitis

A

house dust mite.

42
Q

symptoms of dermatitis

A

Intense itching, blistering/weeping, cracking of skin

43
Q

what tests are used to diagnose allergies

A

• Specific IgE (>0.35 KuA/L)
• Skin prick test (>3mm wheal).
– Test saline, histamine and potential allergen and then prick the skin were each of these are applied so they can enter the skin.
– Should react to histamine and allergen but not saline solution
– Can have unusual results due to skin sensiity in people e.g negative test for antigen even though they are allergic because the skin is not sensitive or on antihistamines.
– Could have chronic epturia- have allergic reaction to something one time but not another.
• Intra-dermal test- similar to SPT but you get more of the substance in the skin
• Oral challenge test – Gold standard
– Give peanut- see if reaction occurs, if not give more and more over time.
• Basophil activation test- test makers which are higher in basophil activation.
• Component resolved diagnostics

44
Q

Treatment for allergic reactions

A

if symptomatic
• Antihistamines- early response treatment
• Steroids- late/ delayed response tretament
• Adrenaline- treat anaphylaxis.
Only used is other 3 don’t work
Immunotherapy (Subcutaneous or Sublingual)- trick immune system into thinking that what they are doing (reacting to the allergen) is wrong.

45
Q

when can immunotherapy be used

A
  • Life threatening reactions to Wasp & Bee sting
  • Severe Hay fever
  • Animal dander allergy
46
Q

when is immunotherapy not useful

A
  • Multiple allergies
  • Food allergy
  • Allergic rashes – Eczema, Urticaria
47
Q

2 main methods of immunotherapy

A
  1. Direct pathway from Th2 to Th1

2. Modify T cells so they produce other antibodies except Ig E.

48
Q

What are the major food allergies

A
  • Water soluble glycoproteins 10 - 60 kd
  • COW’S MILK
  • EGG
  • LEGUMES - PEANUT; SOYBEAN; TREE NUTS
  • FISH
  • CRUSTACEANS / MOLLUSCS
  • CEREAL GRAINS
49
Q

Clinical symptoms caused by food allergies

A 
–	Gastrointestinal
•	vomiting, diarrhoea, oral symptoms
–	Respiratory (upper & lower)
•	rhinitis, bronchospasm
–	Cutaneous
•	urticaria (hives=rash), angioedema (swelling in deep layers of skin)
•	role of food in atopic dermatitis unclear
–	Anaphylaxis
50
Q

most common drug allergy

A

IgE mediated penicillin allergy

51
Q

clinical signs of penicillin allergy

A

angioedema, bronchospasm, anaphylaxis.

Clinical Pathology (45 decks)

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