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Immunology #2 > Hypersensitivities 2 > Flashcards

Hypersensitivities 2 Flashcards

1
Q

Clinical signs of Type II hypersensitivities

A
  • Agglutination
  • Spherocytes- cells without central pallor, RBC lysis
  • Hemolysis- RBC break down
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2
Q

Type II hypersensitivity

A
  • Destruction of cells due to the binding of antibodies (IgG/IgM) to the cell surface
  • Results in damage and cell destruction mediated by NK cells, complement, phagocytic cells
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3
Q

Type II hypersensitivity reactions

A

Antibody mediated cell lysis occurs as normal to kill infected cells, but the hypersensitivity begins when we start to destroy cells due to antibody binding
- The Antibody binds to cell, activates Complement, phagocytic cells or NK cells

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4
Q

Immune-mediated destruction of RBCs or platelets

A
  • Occurs due to antibody binding to the RBC
  • Two means of destruction: phagocytosis in the spleen or complement-mediated lysis in blood
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5
Q

Extra-vascular hemolysis

A

Phagocytosis of RBCs in the spleen in immune-mediated destruction

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6
Q

Intra-vascular hemolysis

A
  • Complement-mediated lysis during immune mediated destruction of RBCs
  • Occurs mainly in bloodstream
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7
Q

Immune mediated hemolytic anemia (IMHA)

A
  • Form of immune mediated destruction of RBCs
  • Most seen in dogs, middle aged, females, strong breed associations/genetics
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8
Q

Antibody targets for immune mediated hemolytic anemia (IMHA)

A
  1. Self RBC antigens- autoimmune
  2. Alloantigen antigens- occur from transfusions of RBCs
  3. Foreign antigens absorbed to the cell surface- innocent bystander for example during infections)
  4. Altered self (RBC) antigen- can be caused by drugs, microbes, toxins altering the normal protein structure or create new epitopes in the altered self-antigens
  5. Exposed cryptic antigens- epitopes are normally hidden but become visible during inflammation
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9
Q

Blood groups

A

RBCs express cell surface molecules (glycoproteins and glycolipids) that can act as antigens
- Many different genes that encode for these antigens and result in different blood groups

EA= erythrocyte antigens

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10
Q

Blood transfusion potential issues

A
  • Antibodies in the serum of the donor can recognize recipient RBCs but this usually has milder effects
  • Antibodies in the recipient can react with the antigens on the RBCs from the donor
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11
Q

Effects of issues with blood transfusions

A

Since RBCs all have their own antigens, when we do blood transfusions there are antibodies that can bind to these different antigens, cause lysis via complement or opsonization
- If large amounts of RBCs are being lysed, it can cause serious disease (blood clotting, disseminated intravascular coagulation)

Complement system in large amounts can result in anaphylaxis and shock etc.

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12
Q

Cross-matching

A
  • testing for antibodies against different blood groups
  • overall don’t want agglutination
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13
Q

Major vs. minor cross matching

A

major
- mix recipient serum with donor cells. Don’t want any of the recipient antibodies to be up against the donors RBCs

minor
- mix donor serum with recipient cells
- looks at whether there are antibodies in the donor serum that will react to the recipients RBCs

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14
Q

Hemolytic disease of the newborn (HDN) or Neonatal isoerythrolysis

A

Newborn has both alloantigens from mother and father. Memory responses can cause worsening with repeated pregnancies

  1. Disease often occurs when there are tears in the placenta
  2. Allow fetal cells to enter the maternal blood and cause the mother to mount an immune response to the foreign blood group antigens
  3. Mother is sensitized to the antigen and therefore makes antibodies against it
  4. Antibodies concentrate in the colostrum and are passed on to the neonate
  5. Colostral antibodies cause RBC lysis in newborn
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15
Q

Clinical signs of HDN

A
  • Anemia
  • Jaundice
  • Lethargy
  • Anorexia
  • Death
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16
Q

Diagnosis of immune mediated hemolytic anemia

A
  • Clinical signs: anemia, jaundice
  • CBC: usually has regenerative responses with spherocytes and ghost cells
  • Direct Coombs or direct anti-globulin test (DAT): test to demonstrate antibodies bound to RBCs
17
Q

Immune mediated thrombocytopenia (ITP)

A
  • Mechanisms similar to IMHA
  • Occurs in conjunction with RBC disease in some patients (Evans syndrome)
  • Clinical signs: hemorrhage (often petechial hemorrhages on skin and mucus membranes)
  • Diagnosis: often difficult to find sufficient platelets to do testing. Want to measure either antibodies bound to the platelets or serum antibodies binding to normal platelets
    **ELISA, immunofluorescence flow cytometry
18
Q

Type II hypersensitivities

A
  • Pemphigus and pemphigold
  • Addisons disease
  • Diabetes mellitus
  • Myasthenia gravis
19
Q

Pemphigus and Pemphigold diseases

A
  • Type II hypersensitivity skin diseases
  • Damage to the skin due to antibody and complement-mediated destruction of antigens in skin
  • Blisters in the skin that depend on the location of the target antigens. If antigen is superficial then blister is superficial, etc.
20
Q

Pemphigus foliaceus

A

Antigens superficial

21
Q

Pemphigus vulgaris

A

Deep ulcers of muco-cutaneous junctions

22
Q

Bullous pemphigold

A
  • Deep ulcerative lesions
  • “deepest”
23
Q

Addisons disease

A
  • Type II hypersensitivity
  • Antibodies target cells in adrenal cortex
  • Results in low levels of glucocorticoids and mineralocorticoids
24
Q

Diabetes mellitus

A
  • Type II hypersensitivity
  • antibodies target insulin producing cells (beta cells) of the islets of Langerhans in the pancreas
25
Q

Myasthenia gravis

A
  • Type II hypersensitivity
  • Disease characterized by muscle weakness
  • Antibodies target the acetylcholine receptor blocks the receptor and initiates complement mediated injury to the post-synaptic membrane
26
Q

Combinations of hypersensitivities

A
  • Type II damage in immune-mediated disease does not always occur in isolation from other forms of immune mediated damage

Ex. immune-mediated thyroid disease with lymphocytic inflammation. Often involves Type II, Type III, and type IV mechanisms

Immunology #2 (17 decks)

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