week 5 allergies, hypersensitivities, vaccines Flashcards

1
Q

What is the name of the peptide that is released from mast cells and causes hypersensitivity and edema?

A

Bradykinin

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2
Q

What is another peptide that leads to production of Bradykinin?

A

Kallikrein

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3
Q

What are the effects of Bradykinin?

A

Edema. Released from mast cells -→ inflammation

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4
Q

What can inhibit Bradykinin production and how?

A

C1 Inhibitor - Inhibit coagulation Protein (?) and production of Kallikrein (C1-INH blocks generation of Bradykinin at 2 levels)

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5
Q

What are the causes of hypersensitivity?

A
  • When the immune reactions are strong enough to induce immune pathology and are clinically manifest
  • Excessive response to pathogens
  • Some are initiated by environmental Ags (latex)
  • Some are initiated by self Ags and cause autoimmune diseases
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6
Q

What are the two phases of hypersensitivity?

A
  1. Sensitization -asymptomatic, don’t know how it happens
  2. Elicitation - disease presentation - dont know the sensitizing Ag. modulated by memory immune response. Happens repeatedly
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7
Q

4 types of Hypersensitivity? what are they mediated by?

A

Type 1 -Immediate - Mediated by IgE (mast cells)

Type 2 - Ab mediated (IgG or IgM)

Type 3 - Immune complex (Ag-Ab complex circulating before going to tissues)

Type 4 - T cell mediated

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8
Q

4 main steps of type 1 hypersensitivity sensitization?

A
  1. 1st exposure to allergen
  2. Activation of follicular T cells (Tfh) and stimulation of IgE class switching in B cells
  3. Production of IgE
  4. Binding of IgE to FcεRI on mast cells
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9
Q

What are the two phases of the elicitation type 1 hypersensitivity? Clinical signs of each?

A
  1. Immediate hypersensitivity
  • Rashes
  • Sinus congestion
  • Bronchial constriction
  • Abdominal pain/Diarrhea
  • Systemic shock
  • Anaphylaxis
  1. late phase reaction
  • Due to the accumulation of inflammatory leukocytes, including neutrophils, eosinophils, basophils, and TH2 cells, PGN, LTN
  • May occur without a detectable immediate hypersensitivity reaction
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10
Q

What are the effectors of elicitation step of type 1 hypersensitivity?

A

Mast cells, Basophils, Eosinophils

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11
Q

What are the mediators of type 1 hypersensitivity?

A

Mast cells (or basophils): Vasodilation, Vascular leak, Broncho-constriction, Intestinal hypermotility, Inflammation, Tissue damage

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12
Q

For the type 1 hypersensitivity one of the effectors is Eosinophils. How do they lead to killing of parasites?

A

She wants us to know that eosinophils dont bind IgE, its the Granule protein who kill parasites

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13
Q

you are seeing while elevated roundish patches on the skin of a patent that has been given allergen markers. Explain your findings

A

Wheel and flare - result of type 1 immediate hypersensitivity

Wheel - patch on the skin thats elevated

Flare - erythema/redness

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14
Q

List the diseases of type 1 hypersensitivity?

A
  • Systemic Anaphylaxis
  • Bronchial Asthma
  • Urticaria (Hives)
  • Atopic Dermatitis
  • Allergic rhinitis (Hay fever)
  • Food allergies
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15
Q

Symptoms and tx of Systemic Anaphylaxis?

A

Type 1 hypersensitivity.

Massive release of histamine, leukotrienes, prostaglandins, & cytokines

Constriction of the airways, laryngeal edema, hives in the skin, nausea

Treatment: Epinephrine; Antihistamines; Cortisone

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16
Q

Symptoms and tx of Bronchial astma?

A

Type 1 hypersensitivity.

  • Airway obstruction; Chronic bronchial inflammation with eosinophils
  • Increased production of thick mucus
  • Treatment: Inhaled corticosteroids (Long-term); Albuterol (Rescue inhalers)
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17
Q

Symptoms and tx of Urticaria (Hives)?

A

Type 1 hypersensitivity.

  • Mediated largely by histamine
  • Treatment: Avoidance of known triggers; Antihistamines
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18
Q

Symptoms and tx of Atopic dermatitis?

A

Type 1 hypersensitivity.

  • Can be blocked by corticosteroids, which inhibit cytokine synthesis
  • As a late-phase inflammatory reaction, it is not inhibited by antihistamines
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19
Q

Symptoms and tx of Allergic rhinitis (Hay fever)?

A

Type 1 hypersensitivity.

– Edema, irritation, mucus in nasal mucosa

  • Treatment: Corticosteroids; Antihistamines; Pseudoephedrine (Decongestants)
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20
Q

Symptoms and tx of Food allergies?

A
  • Hives and GI problems
  • Treatment: Antihistamines; Epinephrine
21
Q

Special thing about Type II Hypersensitivity Reactions?

A

They are not systemic. Specific to the tissues where AGs are present (AB mediated - IgG, IgM)

22
Q

What are the two main mechanisms by which the pathology is caused in type 2 hypersensitivity?

A
  1. Activation of complement
  2. Antibody-Dependent Cellular Cytotoxicity (ADCC) - hemolytic disease of the newborn - HDNB
23
Q

What are the 5 cytotoxic type 2 hypersensitivity reactions?

A

Transfusion Reactions

Autoimmune Hemolytic Anemia

Goodpasture syndrome

Pemphigus Vulgaris

Rheumatic Fever - Untreated GAS pharyngitis

24
Q

Mechanisms of Pathogenesis of Transfusion Reactions?

A

Its a cytotoxic Type II Hypersensitivity Reactions

  • Abs to proteins on transfused, incompatible RBCs (hemolysis)
25
Mechanisms of Pathogenesis of Autoimmune Hemolytic Anemia?
Its a cytotoxic Type II Hypersensitivity Reactions Autoantibodies to one’s own RBCs (mother rH- and fathers rH+ → kid can have rH+ → reaction from mom with second 🤰 )
26
Mechanisms of Pathogenesis of Goodpasture syndrome?
Its a cytotoxic Type II Hypersensitivity Reactions Abs to Type IV collagen in basement membrane of lungs & kidneys
27
Mechanisms of Pathogenesis of Pemphigus Vulgaris?
Its a cytotoxic Type II Hypersensitivity Reactions Autoantibodies to desmosomal proteins in skin cells Blisters in oropharynx & skin
28
Mechanisms of Pathogenesis of Rheumatic Fever?
Its a cytotoxic Type II Hypersensitivity Reactions Antibodies to Streptococcus cell-wall Ag Preceded by pharyngitis
29
What are the 3 non cytotoxic type 2 hypersensitivity reactions?
Transplant Rejection Graves Disease (Thyroid disease – Thyrotoxicosis) Pernicious Anemia
30
Whats the disease of type 3 Hypersensitivity she wants us to focus on? Describe it.
Systemic Lupus Erythematosus * Inflammation in connective tissues and the lining of blood vessels * Inheritance pattern unknown * Nephritis, Arthritis, Butterfly facial rash Also GAS immunologic disease
31
Whats the type of GAS immunologic disease?
Post-streptococcal glomerulonephritis (PSGN) * Not reduced by antibiotic therapy * Follows skin or pharyngeal infections * More common in children • Good prognosis
32
Type 4 Hypersensitivity important things?
* Macrophage activation; Cytokine-mediated inflammations; Cell lysis * Attracts cytotoxic CD8+ T cells or release cytokines from CD4+ lymphocytes, which act through mediator cells (primarily macrophages) to produce chronic inflammatory reactions
33
Type IV Hypersensitivity diseases?
The only one that involves T lymphocytes Tuberculin TB Skin Test Contact Dermatitis Rheumatoid Arthritis
34
What are the 5 different types of vaccines?
1. Inactivated/Killed 2. Toxoid (inactivated toxin) 3. Subunit 4. Conjugate 5. Live, attenuated
35
Inactivated/Killed Vaccines - what do they contain? How are they inactivated? examples?
* contain all antigens to which the host immune response can generate protective T and B cell response (cant replicate) * Made by inactivating the whole pathogen by **heat** or by **chemicals** * **Polio (IPV) Hepatitis A, Rabies**
36
Inactivated/Killed Vaccines - what do they contain? How are they inactivated? examples?
37
toxoid - what do they contain? How are they inactivated? lifelong protection?examples?
toxin thats been inactivated made from inactivated toxin - by heat or chemicals no lifelong protection - need booster (10 years for the Td-tetanus/diphtheria booster) Tetanus, Diphtheria
38
What kind of response does the toxoid vaccine elicit?
drive immune responses to create protective Abs
39
Subunit Vaccine - what do they contain? examples?
contain isolated/specific component of a pathogen Examples: Hepatitis B (HBsAG expressed in yeast- **surface antigen**) , Human Papilloma Virus (HPV), Pertussis, Influenza (shot), Pneumococcal polysaccharide (mixed polysaccharides isolated from the outer **capsule** of 23 different serotypes), Meningococcal polysaccharide
40
Conjugated Vaccines - what do they contain?
polysaccharide (intended for encapsulated bacteria) coupled to a protein carrier (- diphtheria toxoid). Why? T cells of some patients dont recognize polysaccharides
41
Conjugated Vaccines - examples
Examples: Haemophilus influenzae (HiB), Pneumococcal conjugate, Meningococcal conjugate
42
Which types of vaccines Adjuvants used in?
Toxiod, inactivates, subunit
43
What kind of reactions conjugated vaccines elicit?
Elicit immunological memory Reduce asymptomatic carriage of the bacteria, resulting in marked herd immunity
44
What immunoglobulin is produced due to conjugated vaccine?
T cell-dependent B cell activation → IgG
45
Which types of vaccines use specific protein, sugar, capsid, etc? Why is it good?
Subunit and Conjugate Vaccines Provide strong immune responses to the parts Suitable for everyone, including people with weakened immunity and/or longterm health issues
46
Examples of Live/Attenuated Vaccines?
Measles, Mumps, Rubella (MMR), Varicella (Chickenpox), Rotavirus, Influenza (nasal spray), Polio (oral – OPV), Yellow Fever, Bacille Calmette Guérin (BCG)
47
How are live/attenuated vaccines administered?
live, attenuated organisms that are either injected (MMR, Varicella, BCG), ingested (Rotavirus, OPV), or sprayed into nose
48
Do Live/Attenuated Vaccines provide log lasting immunity?
Yes. Similar to natural infection so they create a strong, long-lasting immunity (1-2 doses for lifetime of protection)
49
How is immunity developed in live/attenuated vaccines?
Host cells process and present viral Ags in context of host MHC to allow protective T cell and B cell immune response to be generated