Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CVR > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Examples of innate response in lung

A

Sputum
Cilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Examples of adaptive response on lung

A

Pus
Swelling
Granuloma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Type 1 hypersensitivity mediators

A

IgE antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Type 1 hypersensitivity timing

A

Immediate- within 1 hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Type 1 hypersensitivity examples

A

Anaphylaxis
Hay fever
Atopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Type II hypersensitivity mediators

A

Cytotoxic
Autoimmune- Antibodies bound to cell antigen
IgG/M binds self antigens on host cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Type II hypersensitivity timings

A

Hours to days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Type II hypersensitivity examples

A

Transfusion reactions
Goodpastures (anti GBM disease)
HDFN
Mycoplasma pneumonia (RBC antigen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Type III hypersensitivity mediators

A

Deposition of immune complexes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Type III hypersensitivity timing

A

Typically 7-21 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Type III hypersensitivity examples

A

Hypersensitivity pneumonitis / allergic alveolitis eg farmers/ hot tub lung
Lupus
Post streptococcal glomerulonephritis
Rheumatoid arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Type IV hypersensitivity mediators

A

T-cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Type IV hypersensitivity timing

A

Days to weeks or months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Type IV hypersensitivity examples

A

Granulomatous disease: Tuberculosis, sarcoidosis and dermatitis
Stevens-Johnson syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Type I

A

Antigen interacts with IgE bound to mast cells or basophils
Degranulation of mediators lead to local effects
Histamine the predominant mediator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Type I treatment

A

Steriods
Adrenaline (0.5 mg or auto injection in community intramuscularly)
Antihistamine
Tryptase measurements
Observation (second peak may occur circa 12 hours)

17
Q

Anaphylaxis

A

Sudden onset
Systemic degranulation of mast cells and histamine release
Skin, eyes, lips swelling, hypotension
Bronchospasm can result in airway occlusion and death if not quickly and accurately managed.

18
Q

Type II

A

Antibodies reacting with antigenic determinants on the host cell membrane
Usually IgG or IgM
Outcome depends on whether complement is activated and if metabolism of cell is affected

19
Q

Anti glomerular basement membrane disease

A

Rare but deadly type II HS disease
Goodpasture syndrome = alveolar involvement
GBM is made of type IV collagen present in alveoli and kidneys (glomeruli)
Alpha 3 subunit becomes antigenic

20
Q

Diagnosis of GBM

A

requires high degree of clinical suspicion
GBM antibodies in serum or on biopsy (usually of kidney)

21
Q

Treatment of GBM

A

Treatment with plasmapheresis (removal of plasma from patient to extract offending Abs)
Immune suppression (cyclophosphamide, steroids, rituximab)
Supportive treatment of lungs (ventilation) and kidneys (haemodialysis / filtration)

22
Q

Mycoplasma pneumonia

A

“Atypical” pneumonia
Cross reacting epitopes
Antibodies to M.Pneumonia also react to I antigen of red cells
Causes agglutination and haemolysis
Up to 50% of cases

23
Q

Type III

A

Antigen-immunoglobulin complexes are formed on exposure to the allergen
These are deposited in tissues and cause local activation of complement and neutrophil attraction

24
Q

Hypersensitivity pneumonitis

A

Formerly “extrinsic allergic alveolitis” (EAA)
Immune complexes formed with a range of different antigens
Deposited in the acinar airways leading to inflammation acutely and scarring chronically
Treatment by removal of antigen +/- immunosuppression

25
Q

Type IV

A

T-cell mediated, releasing IL2, IFᵧ and other cytokines
Requires primary sensitisation
Secondary reaction takes 2-3 days to develop
May result from normal immune reaction – if macrophages cannot destroy pathogen, they become giant cells and form granuloma

26
Q

Mantoux/ tuberculin skin test

A

Subcutaneous injection of tuberculosis protein
Interpreted at 48-72 hours
Diameter of induration determines positivity
Positive only if exposed to TB of vaccine previously

27
Q

Sarcoidosis

A

Possibly reaction to mycobacteria
Multisystem disease causing granuloma
Eyes, skin, lungs, heart, nervous system…

80% regress spontaneously
Some require systemic treatment – steroids, methotrexate, others

28
Q

Consequences of T-cell hyperactivity

A

Diabetes
Thyroid disease
Hepatitis
Nephritis
Myositis
Any –itis!
Life threatening pneumonitis
-MUST STOP DRUG
-Steroids may be helpful

29
Q

Gell and Coombs classification

A

Recognition of foreign antigen can cause collateral tissue damage
Conceptualised in the early 1960s
Imperfect classification, but still holds as description of pathology
Does not hold well for complex immune reactions

30
Q

How many types of hypersensitivity are there

A

4

31
Q

Type I hypersensitivity mechanism

A

Antigen exposure —> Th2 release IL-4 —>B cell release IgM —> become IgE—-> activates FcER1 on mast cells —> allergen causes IgE cross-linking —> degranulation- histamine release

32
Q

Type III hypersensitivity mechanism

A

Antigen-IgG complexes precipitate- complement activation and neutrophil attraction
Can’t be cleared by macrophages

33
Q

Type IV hypersensitivity mechanism

A

Th release cytokines and macrophages become giant cells—> granulomar around pathogens

34
Q

Anaphylaxis

A

Biphasic response
Cytokines released activate granulocytes —> release of newly synthesised mediators from mast cells

35
Q

Systemic effects of anaphylaxis

A

Bronchoconstriction
Hypotension (due to vasodilation)
Angioedema (swelling)
Urticaria (itchy rash)

36
Q

Mechanism of type 1 hypersensitivity

A

Basophils and mast cells
Sensitising agents elicit IgE antibody response
IgE binds to mast cells and basophils causing degranulation and the release of chemical mediators histamine, prostaglandins and leukotrienes
Results in vasodilation and bronchospasm

37
Q

Cough receptors (pulmonary irritant receptors) are protective of the lungs. Which of the following best describes the purpose of coughing?

A

move material from the vocal cords to the pharynx

CVR (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions