Brainscape's Knowledge GenomeTM

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


See full index

Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is hypersensitivity?

A

Exaggerated adaptive immune response to harmless environmental antigens. This may lead to inflammation and tissue damage.

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

What is hypersensitivity?

A

Exaggerated adaptive immune response to harmless environmental antigens. This may lead to inflammation and tissue ddamage.

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

What are the four types of hypersensitivity?

A

Types 1-3 are antibody mediated

Type 4 is T cell and macrophage mediated.

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

What are the four types of hypersensitivity?

A

Types 1-3 are antibody mediated where

1) IgE
2) IgG
3) IgG

Type 4 is T cell and macrophage mediated where Th1, Th2 and CTL are involved.

All types occur on different timescales.

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

List some substance with the potential to cause hypersensitivity

A

1) Inhaled: pollen, mold spores, faces
2) Injected: insect venom, drugs
3) Ingested materials: food, oral drugs
4) Contact: plant leaves, industrial, synthetic chemicals, metals

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

Describe Type 1

A

It is an IgE response to pollen, mite faeces and animal proteins.

IgE is in tissues where it binds to high affinity FceR1 receptor on mast cells, basophils, eosinophils

It can make inflammatory reactions in minutes with running nose, breathing difficulties and fatal asph

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

Describe IgE structure characteristics

A

N-linked oligosaccarides attached to constant regions.

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

What are mast cells? What are their functions?

A

They are granule cells resident in mucosal and epithelial tissues lining surfaces. They are also in vascular tissues.
They work to:
i) maintain tissue integrity
ii) alert system of trauma and infection
iii) help repair damage caused by infection or wounds.

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

What are mast cells? What are their functions?

A

They are granule cells (containing histamine inflammatory mediators) resident in mucosal and epithelial tissues lining surfaces. They are also in vascular tissues.
They work to:
i) maintain tissue integrity
ii) alert system of trauma and infection
iii) help repair damage caused by infection or wounds.

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

What are mast cells? What are their functions?

A

They are granule cells (containing prfeormed histamine inflammatory mediators in vesicles) resident in mucosal and epithelial tissues lining surfaces. They are also in vascular tissues.
They work to:
i) maintain tissue integrity
ii) alert system of trauma and infection
iii) help repair damage caused by infection or wounds.

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

What is the result of high affinity binding of Fc receptor and IgE.

A

This means the binding is very long lived.

This is why type 1 hypersenitivity is immediate.

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

What is in mast cell granules?

A

Premade in granule:
-enzymes: trypase, chymase that remodel connective tissue
-toxic: histamines which increase vascular permeability
Made upon activation:
-cytokines: TNF-alpha which promotes inflammation
-chemokine
-lipid mediators
-lipid mediator

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

How does histamine release cause hypersensitivity symptoms

A

Histamine constricts airways and increases mucus causing sneezing and coughing

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

What are mast cells? What are their functions?

A

They are granule cells (they are packed with preformed histamine inflammatory mediators in vesicles) resident in mucosal and epithelial tissues lining surfaces. They are also in vascular tissues.
They work to:
i) maintain tissue integrity
ii) alert system of trauma and infection
iii) help repair damage caused by infection or wounds.

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

What is in mast cell granules?

A

Premade in granule:
-enzymes: trypase, chymase that remodel connective tissue
-toxic: histamines which increase vascular permeability
Made upon activation:
-cytokines: TNF-alpha which promotes inflammation to site of infection.
-chemokine
-lipid mediators
-lipid mediator

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

What are eosinophils? What is their function?

A

They are resident in connective tissue under mucosal epithelial layer.

They produce FceR1 receptor in the presence of cytokines and chemokines at the site of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are eosinophils? What is their function?

A

They are granule cells (containing toxic mediators) resident in connective tissue under mucosal epithelial layer.

They express FceR1 receptor in the presence of cytokines and chemokines at the site of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is in eosinophil granules?

A

Different range from mast cells.

  • enzyme: toxic peroxidase which catalyzing halogenation and collagenase which remodels connective tissue
  • toxic proteins: targets neurotoxins and triggering mast cell histamine release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is in eosinophil granules?

A

Different range from mast cells.

  • enzyme: toxic peroxidase which catalyzing halogenation and collagenase which remodels connective tissue
  • toxic proteins: targets neurotoxins and triggering mast cell histamine release
  • cytokines
  • chemokines
  • lipid mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is a basophil?

A

Similar to mast cells, they are granule cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Type 1: Systemic anaphlaxis

A

Direct/ absorption of allergen like drugs, venoms. This can constrict the airways or circulatory collapse and death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Type 1: wheel and flare

A

Where the allergins like insect bites enter subcutaneous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Type 1: wheel and flare

A

Where the allergins like insect bites enter subcutaneous causing swelling and redness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Type 1: hay fever

A

if allergens like pollen, mite feces are inhaled they may cause oedema,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Type 1: Bronchial asthma

A

allergens like pollen, and feces causing airway inflammation and bronchial constriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Type 1: Food allergy

A

digesed orally can cause vomiting, diarrhea, itching, hives and anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What do INHALED allergens share

A

They are proteins, often protease in low doses. These can be broken down into peptide that are presented by MHC II.
They have a low molecular weight do they can diffuse rapidly.
They are stable and highly soluble.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What do INHALED allergens share

A

They are proteins, often protease in low doses. These can be broken down into peptide that are presented by MHC II.
They have a low molecular weight do they can diffuse rapidly.
They are stable and highly soluble.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How do individuals become sensitized to an INHALED allergen

A

1) Upon first exposer, the allergen leach along epithelial layer and is taken up by APC in the airway mucosa.
2) APC activate naive T cells to become Th2 cells.
3) Th2 cells secrete IL4
4) IL4 binds to B cell IL4R.
5) B cell swiches isotope to IgE
6) IgE binds to FceR1 on mast cells.-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Where does predisposition to allergic disease come from?

A

genetic polymorphisms make an individual more susceptible to allergic reaction.

Such polymorphisms are found in MCHII genes, T cell receptor genes, TIM, IL4 gene allele.

31
Q

Where does predisposition to allergic disease come from?

A

genetic polymorphisms make an individual more susceptible to allergic reaction.

Such polymorphisms are found in MCHII genes where there is enhanced presentation, T cell receptor genes causing enhanced recognition, TIM gene, IL4 receptor gene allele causing more signalling .

32
Q

What is the bi-phase aspect of a reaction?

A

1 )Inital immediate phase: localised wheel and flare within 15 minutes.
2) Late phase: after 6 hours there is generalized swelling in the surrounding tissue.

33
Q

Describe asthmatic response to inhaled pathogen

A

before allergen max air into lungs is high. Antigen challenge causes immediate decrease in rate of flow of air in/out of lungs. In late phase 6 hours later, there is another drop.

34
Q

What are the physical effects of IgE

A

Activated mast degranulation which influences

i) GI tract to increase fluid and peristalsis

35
Q

What are the physical effects of IgE on the GI, airways and blood vessels?

A

Activated mast degranulation which influences

i) GI tract to increase fluid and peristalsis
ii) airways to decrease diameter and increase mucus
iii) blood vessels to increase blood flow and increase permeability

36
Q

What are the physical effects of IgE on the GI, airways and blood vessels?

A

Activated mast degranulation which influences

i) GI tract to increase fluid and peristalsis. Leading to vomiting expulsion.
ii) airways to decrease diameter and increase mucus. coughing expulsion.
iii) blood vessels to increase blood flow and increase permeability. Leading to swelling and inflammation to try carry allergen to lymph node.

37
Q

What is systemic anaphylaxis?

A

When allergen in blood activate mast cells in the whole body:

  • in heart circulation can be comprimised and lack of consciousness.
  • in respiratory tract there is cotraction of smooth muscle, leading to difficulty breathing
  • in GI tract there is contraction of smooth muscle causing cramps and vomiting.
38
Q

What is systemic anaphylaxis that kills 160 US people every year.

A

When allergen in blood activate mast cells in the whole body:

  • in heart circulation can be comprimised and lack of consciousness.
  • in respiratory tract there is cotraction of smooth muscle, leading to difficulty breathing
  • in GI tract there is contraction of smooth muscle causing cramps and vomiting.
39
Q

What is the treatment of systemic anaphylaxis?

A

Administered epinephrine/adrenaline. this increases arterial blood pressure

40
Q

What causes allergic rhinitis (running nose)

A

Allergens in the respiratory tract; allergen enters mucosa and activated mast cells in mucosal.
Mast cells degranulation, causing increase permeability and nasal epithelial to make mucus.
Eosinophils move out into airways from blood with the increased mucus
Eosinophils are activated at the tissues and release inflammaion mediators.

41
Q

What is allergic asthma? What is acute response and what is chronic response?

A

This is the result of chronic inflammation of the airways.
Accute response where mucosal mast cell captures antigen and inflammatory mediators contract smooth muscle, increase mucus so airways are obstructed.

Elevated blood permablity means more eosinophils which degranulate and Th2 cells which cause more damage.
Chronic response:

42
Q

What is allergic asthma? What is acute response and what is chronic response?

A

This is the result of chronic inflammation of the airways.
Accute response where mucosal mast cell captures antigen and inflammatory mediators contract smooth muscle, increase mucus so airways are obstructed.

Elevated blood permablity means more eosinophils which degranulate and Th2 cells which cause more damage.
Chronic response results where constant, irreversible damage to the airways.

43
Q

What is allergic asthma? What is acute response and what is chronic response?

A

This is the result of chronic inflammation of the airways.
Accute response where mucosal mast cell captures antigen and inflammatory mediators contract smooth muscle, increase mucus so airways are obstructed via a mucous plug.

Elevated blood permablity means more eosinophils which degranulate and Th2 cells which cause more damage.

Chronic response results where constant, irreversible damage to the airways.

44
Q

What are uricaria, angioedema and eczema examples of?

A

skin allergic reactions

45
Q

What are uricaria, angioedema and eczema examples of?

A

skin allergic reactions. Allergen into skin where mast cells degranulate in the connective tissue so blood vessels dilate locally and swelling from influx of proteins, cells, fluids to skin.

46
Q

What are uricaria, angioedema and eczema examples of? How are they caused?

A

skin allergic reactions. Allergen into skin where mast cells degranulate in the connective tissue so blood vessels dilate locally and swelling from influx of proteins, cells, fluids to skin.

47
Q

What are vomiting, diarrhea, urticaria examples of?

A

Ingested allergen where mucosal mast cells are activated, and their degranulated histamine acts on intestinal epithelium, blood vessels and smooth muscles.

Contraction of the smooth muscles causes diarrhea and vomiting.
When antigen goes into blood and carried to skin this causes urticaria

48
Q

What are the treatments of type 1 hypersensitivity?

A

1) Avoidance
2) Anti-histamines: blocks histamine binding
3) Corticosteriods: supress leukocyte function to stop inflammation
4) Cromolyn sodium: stabilises/prevents mast cell degranulate
5) Epinephrine
6) Desensitisation

49
Q

What are the treatments of type 1 hypersensitivity?

A

1) Avoidance
2) Anti-histamines: blocks histamine binding
3) Corticosteriods: supress leukocyte function to stop inflammation
4) Cromolyn sodium: stabilises/prevents mast cell degranulate
5) Epinephrine
6) Desensitisation: introduce small quantities of allergen.

50
Q

How does Type 2 Hypersensitivity work?

A

After 18 hours of antigen exposer, IgG/IgM binds to self/foreign antigen on an cell surface. The antibody triggers phagocytosis, or complement lysis of cell which will damage the tissue.

51
Q

What are two examples of Type 2?

A

1) Blood transfusion reactions with incompatible blood

2) Haemolytic disease in newborn.

52
Q

Describe Type 2 blood transfusion reactions.

A

A group has extra N-acetyl galactosamine. The B type has an extra galactose. O type has neither.

53
Q

Describe Type 2 blood transfusion reactions.

A

A group has extra N-acetyl galactosamine. The B type has an extra galactose. O type has neither.
Therefore, O group people make ANTI-A and ANTI-B antibodies and so can only be transfused with O type blood. Type A can be transfused with O type and A type. And AB type, with both A and B antigens can be transfused with all blood types.

54
Q

How does Haemolytic disease in newborns arise? “Blue babies”

A

An incompatibility of Rhesus D blood antigens.
If mother does not have the RhD antigen, but partner does, baby has RhD+.
Mother becomes sensitised to RhD+ to see it as foreign.
Second baby is also RhD+ the mother can react to this as it is a second exposer; mother makes IgG antiRhD antibodies which cross placenta and attack baby.

55
Q

How is Haemolytic disease in newborns avoided “Blue babies”

A

Mothers are tested for RhD positive or negative. If negative, they are infused with anti-RhD IgG after delivery of the first child.
This means the RhD+ blood from first child is eliminated and mother is not sensitised to it.

56
Q

How does Haemolytic disease in newborns arise? “Blue babies”

A

An incompatibility of Rhesus D blood antigens.
If mother does not have the RhD antigen, but partner does, baby has RhD+.
Mother becomes sensitised to RhD+ to see it as foreign.
Second baby is also RhD+ the mother can react to this as it is a second exposer; mother makes IgG antiRhD antibodies which cross placenta and attack baby.

This causes swollen abdomen: enlarged liver, spleen due to destruction of RBC
Blue skin as heamoglobin breakdown
Bloachyness (facial petechia) caused by haemorrhage from platelet damage.

57
Q

Why does pencillin cause type 2 reactions? What is the pathway?

A

Human cells altered.
Penicillin has a reactive group in its structure which allows it to bind to blood cells. This complex of pencillin and RBC can be recognised as a foreign molecule.

RBC are then phagocytosed by macrophage, and presented to helper T cells which are activated in to Th2 cells.

Th2 cells stimulated B cells to make IgG Ab aginst penicillin-RBC causing pahgocytosis/lysis via complement C1-3/C1-C9

58
Q

Describe Type 3 Hypersensitivity.

A

This is caused by the deposition of small IgG antigen immune complexes in the blood vessel walls. They accumulate and fix complement causing inflammation.
C3a stimulaes mas cells to release histamine
C5a recruits inflammatory cells to site.
Platelets accumulate causing clots and bursting blood vessels resulting in skin heamorrhage.

59
Q

Describe Type 3 Hypersensitivity.

A

Takes 1-2 hours
This is caused by the deposition of small IgG antigen immune complexes in the blood vessel walls. They accumulate and fix complement causing inflammation.
C3a stimulaes mas cells to release histamine
C5a recruits inflammatory cells to site.
Platelets accumulate causing clots and bursting blood vessels resulting in skin heamorrhage.

60
Q

Describe Type 3 Hypersensitivity.

A

Takes 1-2 hours
This is caused by the deposition of small IgG antigen immune complexes in the blood vessel walls. They accumulate and fix complement causing inflammation; C5a binds to mast cell C5a receptor;C5a recruits inflammatory cells to site. IgG binds to Fc receptor RIII on mast cell stimulates mast cells to release histamine

Platelets accumulate causing clots and bursting blood vessels resulting in skin heamorrhage.

61
Q

Give some examples of type 3 reactions in various places in the body.

A 
In blood vessel wall causes vasculitis
In renal glomeruli causes nephritis.
In joint spaces cause arthritis
In skin causes arthus reaction.
In alveolar interface causes farmer's lung.
62
Q

Give some examples of type 3 reactions in various places in the body.

A

In blood vessel wall immune complexes (IC) causes vasculitis
In renal glomeruli causes nephritis.
In joint spaces cause arthritis
In skin causes arthus reaction.
In alveolar interface causes farmer’s lung.

63
Q

Describe the symptoms of Type 3 hypersensitivity

A

Fever, vasculitis, arthritis, nephritis.
However, serum sickness is brief and only persist around the time of Immune complex formation. Once the foreign antigen is cleared, and here is a prevalence (high) level of antibodies in the plasma the symptoms resolve

64
Q

Describe Type 4 hypersensitivity

A

It takes a long time/called delayed hypersensitivity, taking 1-3 days. This is caused by T cells that need alot more antigen to cause this reaction than other hypersensitivities.

65
Q

Type 4: Contact

A

Itch reaction to metals (nickel, chromate) or haptens like poison ivy.
This can cause intraepidermal abscesses and erthema

66
Q

Type 4: Delayed type

A

This is the response to antigens like insect venom or microbacterial proteins.

It causes local skin swelling, erthema, dermatitis, induration (hardening)

67
Q

What is the tuberculin test? (type 4 example)

A

reaction where person is injected in the skin with tuberculin bacilli to see whether they have tuberculosis disease if they swell.

68
Q

How does type 4 work? Why does it take longer?

A

1) uptake antigen, and presented on APC
2) Specific MEMORY T cells from previous exposure migrate to site and become activated
3) It takes longer as there needs to be a T cell of correct specificity to arrive at site.
4) T cell releases mediators
5) activate local endothial cells, recruit infiltrate of macrophages
6) overall there is protein and fluid accumualtion

69
Q

How does Type 2 Hypersensitivity work?

A

After 18 hours of antigen exposer, IgG/IgM binds to self/foreign antigen on an human cell surface. The antibody triggers phagocytosis, or complement lysis of cell which will damage the tissue.

70
Q

What are two examples of Type 2?

A

1) Blood transfusion reactions with incompatible blood
2) Haemolytic disease in newborn.
3) Abs specific for cell components altered by penicillin.

71
Q

Describe Type 3 Hypersensitivity.

A

Takes 1-2 hours
This is caused by the deposition of small IgG antigen immune complexes (IC) in the blood vessel walls. They accumulate and fix complement causing inflammation; C5a binds to mast cell C5a receptor;C5a recruits inflammatory cells to site. IgG binds to Fc receptor RIII on mast cell stimulates mast cells to release histamine

Platelets accumulate causing clots and bursting blood vessels resulting in skin heamorrhage.

72
Q

Give some examples of type 3 reactions in various places in the body.

A

THE SITE DEtERMINES THE PATHOLOGY:
In blood vessel wall immune complexes (IC) causes vasculitis
In renal glomeruli causes nephritis.
In joint spaces cause arthritis
In skin causes arthus reaction.
In alveolar interface causes farmer’s lung.

73
Q

What are the influences of T cells in Type 4?

A

1) chemokine recruit macrophages
2) cytokine IFN-gamma activates macrophages increase proinflammatory
3) cytotoxin TNFalpha kills tissue
4) cytokine IL3 produces monocyte in bone marrow.

Immunology (19 decks)

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