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I&D > week 5 allergies, hypersensitivities, vaccines > Flashcards

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
Q

Mechanisms of Pathogenesis of Autoimmune Hemolytic Anemia?

A

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
Q

Mechanisms of Pathogenesis of Goodpasture syndrome?

A

Its a cytotoxic Type II Hypersensitivity Reactions

Abs to Type IV collagen in basement membrane of lungs & kidneys

27
Q

Mechanisms of Pathogenesis of Pemphigus Vulgaris?

A

Its a cytotoxic Type II Hypersensitivity Reactions

Autoantibodies to desmosomal proteins in skin cells Blisters in oropharynx & skin

28
Q

Mechanisms of Pathogenesis of Rheumatic Fever?

A

Its a cytotoxic Type II Hypersensitivity Reactions

Antibodies to Streptococcus cell-wall Ag Preceded by pharyngitis

29
Q

What are the 3 non cytotoxic type 2 hypersensitivity reactions?

A

Transplant Rejection

Graves Disease (Thyroid disease – Thyrotoxicosis)

Pernicious Anemia

30
Q

Whats the disease of type 3 Hypersensitivity she wants us to focus on? Describe it.

A

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
Q

Whats the type of GAS immunologic disease?

A

Post-streptococcal glomerulonephritis (PSGN)

  • Not reduced by antibiotic therapy
  • Follows skin or pharyngeal infections
  • More common in children • Good prognosis
32
Q

Type 4 Hypersensitivity important things?

A
  • 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
Q

Type IV Hypersensitivity diseases?

A

The only one that involves T lymphocytes

Tuberculin TB Skin Test

Contact Dermatitis

Rheumatoid Arthritis

34
Q

What are the 5 different types of vaccines?

A
  1. Inactivated/Killed
  2. Toxoid (inactivated toxin)
  3. Subunit
  4. Conjugate
  5. Live, attenuated
35
Q

Inactivated/Killed Vaccines - what do they contain? How are they inactivated? examples?

A
  • 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
Q

Inactivated/Killed Vaccines - what do they contain? How are they inactivated? examples?

A
37
Q

toxoid - what do they contain? How are they inactivated? lifelong protection?examples?

A

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
Q

What kind of response does the toxoid vaccine elicit?

A

drive immune responses to create protective Abs

39
Q

Subunit Vaccine - what do they contain? examples?

A

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
Q

Conjugated Vaccines - what do they contain?

A

polysaccharide (intended for encapsulated bacteria) coupled to a protein carrier (- diphtheria toxoid). Why? T cells of some patients dont recognize polysaccharides

41
Q

Conjugated Vaccines - examples

A

Examples: Haemophilus influenzae (HiB), Pneumococcal conjugate, Meningococcal conjugate

42
Q

Which types of vaccines Adjuvants used in?

A

Toxiod, inactivates, subunit

43
Q

What kind of reactions conjugated vaccines elicit?

A

Elicit immunological memory

Reduce asymptomatic carriage of the bacteria, resulting in marked herd immunity

44
Q

What immunoglobulin is produced due to conjugated vaccine?

A

T cell-dependent B cell activation → IgG

45
Q

Which types of vaccines use specific protein, sugar, capsid, etc? Why is it good?

A

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
Q

Examples of Live/Attenuated Vaccines?

A

Measles, Mumps, Rubella (MMR), Varicella (Chickenpox), Rotavirus, Influenza (nasal spray), Polio (oral – OPV), Yellow Fever, Bacille Calmette Guérin (BCG)

47
Q

How are live/attenuated vaccines administered?

A

live, attenuated organisms that are either injected (MMR, Varicella, BCG), ingested (Rotavirus, OPV), or sprayed into nose

48
Q

Do Live/Attenuated Vaccines provide log lasting immunity?

A

Yes. Similar to natural infection so they create a strong, long-lasting immunity (1-2 doses for lifetime of protection)

49
Q

How is immunity developed in live/attenuated vaccines?

A

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

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