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7 PATH 1 > 6 HYPERSENSITIVITY REACTIONS > Flashcards

6 HYPERSENSITIVITY REACTIONS Flashcards

1
Q

TYPE I Hypersensitivity reaction, aka:

A

Anaphylactic type, Allergy

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2
Q

What is there a release of in Type 1?

A

Vasoactive amines and other mediators derived from the mast cells or basophils and affecting vascular permeability and smooth muscles in various organs

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3
Q

What is the mechanism of the “First Encounter with allergen (antigen or allergy)” in Type 1 reaction?

A

Most commonly via INHALATION (ex. Pollen) > Blood

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4
Q

What happens after the first encounter with allergen in Type 1 reaction?

A

There is an immune response (IgE) immunoglobulins (antibodies) > bind to receptors on mast cells, which contain granules filled with histamine

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5
Q

Is there a physiological reaction with the first encounter in Type 1 reaction?

A

NO, no physiological reaction

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6
Q

What does an “Allergen” cause activation of?

A

CD4+ T-cells (TH 2 type) > secretion of cytokines IL-4 and IL-5 > IgE production and recruitment of eosinophils

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7
Q

What happens with a “Second Encounter” during a Type 1 reaction?

A

ANTIBODIES PRODUCED from first encounter, bind to the antigen (allergen) forming the *Antigen-antibody complex

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8
Q

What happens to mast cells during a second encounter with allergen in Type 1 reaction?

A

Mast cells undergo degranulation > HISTAMINE released

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9
Q

What does the Second encounter with allergen produce during a Type 1 reaction?

A

Eicosanoids, Leukotriens, and PGD2 are also produced (vasodilation and bronchospastic reactions)

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10
Q

What type of reaction occurs during a Second Encounter with Allergen (Type 1 Reaction)?

A

Pathophysiological Reaction (due to factors released)

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11
Q

What are the functions of Histamine?

A
  • Vasodilation
  • Increased permeability of Blood Vessels
  • Bronchospasm
  • Increased mucus production (submucosal glands) very important in the bronchioles
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12
Q

What are the 2 types of clinical reactions?

A

1) Systemic Anaphylaxis

2) Local Reaction

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13
Q

What is Systemic Anaphylaxis due to?

A

Parental Administration (injection/appearance) of allergen

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14
Q

What does systemic anaphylaxis result in?

A

Itching

- Hives (aka Urticaria) > changes in the skin

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15
Q

What are hives aka?

A

Urticaria

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16
Q

What happens to breathing in Systemic Anaphylaxis?

A
  • Bronchospasm: Due to factors released in bronchospastic reactions
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17
Q

What type of Reaction will you see Laryngeal Edema?

A

Type 1 Systemic Anaphylaxis

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18
Q

What is laryngeal edema?

A

Can develop within a minute after contact with allergen. Causes swelling of larynx leading to closing of the laryngeal opening > Strangulation > Difficulty Breathing > Death (Immediate treatment: puncture above episternal notch)

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19
Q

What type of reaction would you see abdominal cramps, diarrhea, and vomiting?

A

Type 1 Systemic Anaphylaxis

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20
Q

What type of Reaction would you see Vascular (anaphylactic) shock?

A

Type 1 Anaphylactic Type, Allergy

Systemic Anaphylaxis

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21
Q

What is Vascular (anaphylactic) shock?

A

Sudden systemic vasodilation because blood flows (due to gravity) to where there is more concentration of vessels > no blood to brain causes patient to pass out > DEATH.

  • Onset may be immediate or not
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22
Q

What is the #1 cause of death in Type 1 reaction?

A

Vascular Anaphylactic Shock (Systemic Anaphylaxis)

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23
Q

What does a local reaction depend on?

A

How allergen is contacted

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24
Q

What symptoms will you see with Local Reaction Type 1 Anaphylactic Type, Allergy

A

Urticaria (via skin contact) - Same as systemic anaphylaxis = Itch, pain, and swelling (Without inflammatory response)

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25
Q

What Type Hypersensitivity will you see Hay fever?

A

Type 1 Anaphylactic Type, Allergy

LOCAL

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26
Q

Hay fever aka

A

Acute allergic conjunctivitis or acute rhinitis (via inhalation)

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27
Q

What type of reaction would you see Atopic aka Extrinsic Bronchial Asthma?

A

Type 1 Anaphylactic allergy (LOCAL)

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28
Q

What is Atopic aka Extrinsic Bronchial Asthma?

A

Pathogenic reaction in Type 1 local allergic reaction. Important the familiar predisposition for this. Serious, 2 different pathological mechanisms, only 1 of which is associated with allergy

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29
Q

What are the 2 types of Atopic aka Extrinsic Bronchial Asthma

A

Extrinsic Bronchial Asthma

Intrinsic Bronchial Asthma

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30
Q

What are the key features of Extrinsic Bronchial Asthma?

A
  • Via Type I allergic Reaction
  • Common in KIDS, familial predisposition to localized type I hypersensitivity reactions
  • Genetic predisposition
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31
Q

What are the key features of Intrinsic Bronchial Asthma? **

A
  • NOT ASSOCIATED WITH TYPE I HYPERSENSITIVITY **

- AUTOIMMUNE

32
Q

What minor symptoms will you see with LOCAL REACTION Type 1 Hypersensitivity?

A

Diarrhea, vomiting, contact allergic dermatitis - blistering

33
Q

Who has predispositions to Type 1 Anaphylactic Reactions?

A

More likely in children who are not fed breast milk for at least 3 months

  • Family predisposition
34
Q

Type II Reaction aka

A

Anti body Dependent (dependent on the presence of Ab)

35
Q

What is the definition of Type II - Antibody Dependent (dependent on the presence of Ab) ?

A

Mediated by antibodies directed against target antigens on the surface of cells or other tissue components. Complement system work with humoral activity not cell - mediated

36
Q

What are the 3 subtypes of Type II Antibody Dependent (dependent on presence of Ab)?

A

1) Complement Dependent Reactions
2) Antibody-Dependent Cell-Mediated Cytotoxicity
3) Antibody-Mediated Cellular Dysfunction

37
Q

Complement Dependent Reactions are seen in ______

A

Glomerulonephritis

38
Q

What disease would you see Complement Dependent Reactions?

A

Autoimmune Disease - antibodies for target (self) cells

39
Q

How does the Complement dependent reaction activate?

A

Complement activation via Classical Pathway (DIRECT LYSIS)

40
Q

What is the “Classical Pathway”?

A

DIRECT LYSIS

Antigen-antibody complex formed (Ab binds to the Ab receptor at the allergen surface) > complement activation (via classical pathway) > MAC (Membrane Attack Complex = makes holes in the target antigen cell) > Releases enzymes and target cell is destroyed

41
Q

Complement activation via Alternative Pathway =

A

OPSONIZATION

42
Q

What is the Alternative Pathway?

A

After antigen-antibody complex formation > Via C3b (aka opsonin) > complex binds to target tissue making it more easily phagocytized by phagocytic cells

43
Q

What are the Disorders associated with Alternative Pathway OPSONIZATION?

A
  • Glomerular Pathology
  • Hemotransfusin Reactions
  • Erythroblastosis Fetalis
44
Q

What happens during Glomerular Pathology?

A

Body starts producing Ab against Ag in the basement membrane, this forms the Ab-Ag complex and complement activation

> Disruption of BM, Hydrolytic enzymes and activated oxygen causes attraction of PMN cells (Phagocytosis)

45
Q

What is Frustrated Phagocytosis associated with?

A

Glomerular Pathology

46
Q

What is Frustrated Phagocytosis?

A

Occurs when the phagocytic cells cannot engulf the large sized antigen

47
Q

What is Hemotransfusin Reactions?

A

Associated with blood transfusions between a donor and a recipient where the blood types are not matched (blood types: O, A, B, AB)

> Leads to HEMOLYSIS

48
Q

What is Erythroblastosis Fetalis?

A

Associated with the other 2 antigens found on RBC’s Rh factor. 85% of people have Rh antigen on their RBC’s > Rh (+) individuals. The other 15% are Rh (-)

49
Q

What happens during the First Exposure: First Pregnancy?

A

Rh (+) dad + a Rh (-) mom > during delivery blood is mixed through the placenta. Mom is exposed to Rh (+) blood type, no pathological reaction occurs.

Mom produces anti-Rh antibodies after the first delivery

50
Q

Second Pregnancy of the Rhesus Conflict:

A

With a second Rh (+) fetus > mother plasma goes to the blood circulation of the fetus through the placenta:

51
Q

What can the Second Pregnancy of the Rhesus Conflict cause?

A
  • RBC lysis & clumping (hemolysis) > Jaundice and Death
  • In fetus anti-Rh antibodies into fetus
  • Transfusion needed
52
Q

What are examples of complement - dependent reactions?

A
  • Autoimmune Hemolyitic Anemia
  • Certain Drug Reactions
  • Pemphigus Vulgaris
53
Q

What is Autoimmune Hemolytic Anemia?

A

Agranulocytosis and thrombocytopenia Ex. Hemosiderosis

54
Q

What are Certain drug reactions associated with Examples of Complement Dependent Reactions?

A

Can lead to production of anti-neutrophil antibodies > Decreased Neutrophils > DEATH

55
Q

What is Pemphigus Vulgaris?

A

Antibodies against Desmosomal proteins > Ab bind to the desmosomal proteins > Interference with complement - dependent reactions > Causes blisters

56
Q

What is the function of Antibody-Dependent Cell-Mediated Cytotoxicity?

A

Monocytes/Macrophages, neutrophils, eosinophils, and natural killer cells (NK) cells are known as non-T and non-B lymphocytes > Don’t have specific receptors

  • These cells have receptors for Fc fragment of IgE (IgG & IgM, rarely IgE)
57
Q

What is the mechanism of Antibody-Dependent Cell-Mediated Cytotoxicity ?

A

Antigen-Antibody complex formed (F AB fragment of IgE binds to target cell)

  • Non T/ non B cells bind to the free Fc portion > cell death WITHOUT PHAGOCYTOSIS OR COMPLEMENT SYSTEM ACTIVATION**
58
Q

Why is the mechanism in Antibody-Dependent Cell-Mediated Cytotoxicity important?

A

Important in parasites, virus-infected cells, tumor cells (antiviral and anti-tumerous activity). But this is not the primary action against viruses because it involves time due to Ab production

59
Q

What is distinct about Antibody Mediated Cellular Dysfunction?

A

No phagocytosis nor complement activation

60
Q

What are the diseases associated with Antibody Mediated Cellular Dysfunction?

A

1) Myasthenia Gravis
2) Hashimoto’s Thyroiditis
3) Grave’s Disease
4) Pernicious Anemia

61
Q

What is Myasthenia Gravis characterized as?

A

Progressive Muscle Weakness. As the day continues muscle becomes very fatigued.

62
Q

What is the normal function of Ach?

A

Motor end plate: Neuron Synaptic terminal contains vesicles containing Ach, when impulse is transmitted, degranulation occurs, releasing Ach into synaptic cleft. Ach binds to its receptor on the muscle to induce contraction

63
Q

What happens in Myasthenia Gravis?

A

Antibodies against Ach receptors on the muscle prevent muscle contraction (blocking of receptors)

64
Q

What are the symptoms of Myasthenia Gravis?

A

Symptoms of muscle weakness progresses through the day especially in muscles most used: Eye lids, pharyngeal, laryngeal muscles…accumulation of antibodies through the day > increasing weakness, leads to death if untreated as it will affect the diaphragm and pharyngeal muscles > CANT BREATHE

65
Q

What is Hashimoto’s Thyroiditis?

A

Most common cause of Hypothyroidism in USA (Where iodine levels in the diet are normal - non deficient areas)

66
Q

What is the 1st described autoimmune disease, 1912 by Hashimoto

A

Hashimoto’s Thyroiditis

67
Q

What is the mechanism of The thyroid/TRH?

A

Hypothalamus releases TRH (thyroid releasing
hormone) —> simulates the anterior pituitary to release
TSH (thyroid stimulating hormone) —> stimulates the
thyroid to release thyroid hormones (T3, T4) —> increased
thyroid hormones in blood cases negative feedback onto
anterior pituitary and hypothalamus (normal regulation)

68
Q

What happens in Hashimoto’s Thyroiditis?

A

there is an overproduction of auto-
antibodies against TSH receptors on thyroid gland —>
antibodies bind to the receptors, preventing TSH from
binding to thyroid gland (blocking antibody) Lack of
stimulation (TSH)—> the thyroid gland atrophies->
hypothyroidism

69
Q

What is an autoimmune diseases more common in females 8:1?

A

Graves Disease

70
Q

What is the Mechanism of Grave’s Disease?

A

same as Hashiomoto´s but Ab do not block the
TSH receptors. Instead, overproduction of auto-antibodies
bind and stimulate TSH receptors (mimic TSH) —>
overproduction of thyroid hormones —> hyperthyroidism

71
Q

What is “Bulging eyes” associated with Grave’s Disease?

A

Exopthalmus (bulging eyes)

72
Q

What is Pernicious Anemia?

A

Autonomic binding antibody against the intrinsic factor receptors

73
Q

What is Type III Hypersensitivity reaction?

A

Immune Complex Mediated Type: Binding of Ab to a fixed tissue (Type I and II binding is to the free target)

74
Q

How is Type III - Immune Complex Mediated Type actually mediated?

A

Hypersensitivity is Mediated by deposition of antigen-antibody (immune) complexes, followed by complement activation and accumulation of polymorphonuclear leukocytes.

75
Q

What is the major characteristic of Type III - Immune Complex Mediated Type?

A

Antibody/Antigen are usually NOT fixed in the tissue, they are in the blood circulation

76
Q

What is Phase I of Type III - Immune Complex Mediated Type?

A

Immune Complex formation

  • Antigen is present in blood
  • Production of antibodies
  • Antigen and antibody bind to form immune complex
77
Q

What is Phase II of Type III - Immune Complex Mediated Type?

A

Immune Complex DEPOSITION

  • Immune complex attaches to the vessel wall

7 PATH 1 (11 decks)

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