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B&L Unit 2 > Immunopathology Type 2 (complete) > Flashcards

Immunopathology Type 2 (complete) Flashcards

1
Q

Describe Type II immunopathology

A
  • Ab attacks self

- IgG, IgM, or IgA involved

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2
Q

What are the two types of immunologic mechanisms of tissue damage?

A

1) Complement-mediated damage

2) Stimulatory hypersensitivity

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3
Q

Describe complement-mediated damage

A

Tissues targeted by the autoAbs damaged by:

1) Lysis
2) Phagocytosis
3) Release of phagocytes’ lysosomal enzymes and ROSs

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4
Q

Describe stimulatory hypersensitivity. Give 2 examples.

A

When an autoAb is directed against a cell-surface receptor and then behaves as an … AGONIST (ohhhh hellll nah!)

Examples:

1) Graves Disease
2) “Inappropriate” tachycardia

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5
Q

Describe Graves disease

A
  • When IgG targets the TSH receptor on thyroid cells
  • Mimics TSH and stimulates T3/T4 (thyroid) hormone production
  • There’s a constant (-)ve feedback to the anterior pituitary (that normally releases TSH)

Leads to: HYPERTHYROIDISM

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6
Q

Describe inappropriate tachycardia

A
  • Half of cases have autoAbs target the Beta-adrenergic receptor
  • Stimulatory —» fast heart rate w/o cardiac abnormalities
  • Primarily women
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7
Q

What is an example of a type II mechanism disease of muscle?

A

Myasthenia gravis

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8
Q

What is an example of a type II mechanism disease of the kidney?

A

Goodpasture disease

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9
Q

What is an example of a type II mechanism disease of the heart?

A

1) Rheumatic heart disease

2) Dressler syndrome

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10
Q

What is an example of a type II mechanism disease of red cells?

A

Autoimmune hemolytic anemia

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11
Q

What is an example of a type II mechanism disease of platelets?

A

Autoimmune thrombocytopenia purpura

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12
Q

What is an example of a type II mechanism disease of the thyroid?

A

1) Hashimoto thyroiditis

2) Graves disease

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13
Q

What is an example of a type II mechanism disease of pancreatic islets?

A

Type 1 diabetes

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14
Q

What is an example of a type II mechanism disease of the lungs?

A

Goodpasture syndrome

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15
Q

Describe myasthenia gravis

A
  • Progressive muscle weakness
  • Ab made to alpha subunit of AChR
  • Normally: Aire drives expression of CHRNA1 which has a gene for AChR-alpha
  • Some cases: there are genes that don’t interact w/ Aire —» protein not expressed in thymus —» pre-T cells never see this as self in the thymus

What Cohen said in class:

1) Complement eats neutrophils that respond to autoAb on AChR — can’t eat muscle cells
2) All neutrophil digestive juices released —» damaged neuromuscular end plate

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16
Q

Describe rheumatic heart disease

A
  • Acquired shortly after streptococcal infection (e.g. strep throat)
  • B/c of a cross-rxn btwn a Group-A Streptococccus Ag and structure of heart’s endothelial lining —»> neutrophil-mediated tissue destruction
  • Thought to be related to genetics
  • Though still not sure when and who it will affect
  • More common in areas that do not have rapid treatment for strep throat
17
Q

Describe Dressler syndrome

A
  • After MI, damaged heart muscle cells release proteins not seen by immune system previously —-»> aka “sequestered” Ag
  • Ab attacks these Ag (technically an autoAb)

Symptoms:

1) Persistent cardiac pain
2) Fever
3) Malaise
4) Pericardial effusion

When tx includes anti-inflam agents, gets better as heart heals

18
Q

Describe Goodpasture syndrome

A
  • Uncommon
  • AutoAbs target lung and kidney basement membranes (common Ag in both = Type 4 collagen)

Symptoms:

1) Persistent glomerulonephritis
2) Pneumonitis w/ pulm hemorrhages

19
Q

How would you diagnose Goodpasture syndrome in the kidney indirectly?

A
  • Take normal kidney tissue
  • Add pt’s serum
  • Add labeled anti-IgG
  • Visualize where IgG is near the glomeruli

Will be linear if GPS

20
Q

How would you diagnose Goodpasture syndrome in the kidney directly?

A
  • Add labeled anti-IgG to pt’s kidney tissue
  • Visualize where IgG is near the glomeruli

Will be linear if GPS

21
Q

Describe “linear” immunofluorescent patterns. What type of immunopathology does it show? Why is that?

A

In GPS: Anti-IgG goat sera attaches to IgG along basement membrane in glumeruli —> that’s why the fluorescence is linear

Type II

22
Q

Describe “lumpy, bumpy” immunofluorescent patterns. What type of immunopathology does it show? Why is that?

A

Anti-IgG binds to IgG which are in clumps throughout glumeruli

Type III

IMPORTANT: Seen in systemic lupus erythematosus

23
Q

Describe autoimmune thrombocytopenia purpura

A
  • Bleeding abnormalities b/c of platelet destruction (autoAb targets them)
  • Platelets are opsonized — destruction is rapid (mainly in spleen)
  • May follow viral infection

Requires immunosuppression and splenectomy for TX

24
Q

Describe autoimmune hemolytic anemia

A
  • May follow a viral infection
  • Can be associated w/ another autoimmune syndrome or cancer
  • Many drugs can induce this

Cold version: when exposed to cold —»> red cell hemolysis b/c of autoAb which only binds at 15 Celcius

25
Q

Describe systemic lupus erythematosus

A
  • AutoAb targets dsDNA
  • Cell membrane normally protects cell from this autoAb
  • But cells die all the time and release dsDNA
26
Q

Describe rheumatoid arthritis

A
  • Most common autoimmune disease (1 in 100 Americans)
  • Rheumatoid factor (RF) detected in pts
  • It is IgM anti-IgG’s Fc
  • IgG beads mixed w/ pt serum cause beads to agglutinate)

Overall: anti-IgG attacks joints

27
Q

Describe Hashimoto thyroiditis

A
  • Inflammatory disease of the thyroid
  • Thought to be T and B cell immunity to thyroid Ags

Causes: hypothyroidism

28
Q

What is the innocent bystander effect?

A

Damage to normal tissue which is infected with truly foreign antigen

You see this in TB a lot —» macros go crazy and eat everything including normal lung tissue

29
Q

Describe the foreign + self hybrid Ag and its mechanism

A
  • anti-self B cell binds to self plus foreign epitope
  • Ingest and digest time
  • Foreign epitope presented to Tfh on Class II MHC
  • Then activated and makes more Ab that is anti-self
  • Also instructed to class-switch by Tfh —» more problems

BE SURE THAT YOU KNOW THIS

30
Q

Describe the emergence of the forbidden clone

A

When a clone escapes normal clonal deletion mechanisms and mature —» seen as an Ag

Ex: myasthenia gravis

31
Q

What is the function of the Aire gene?

A
  • Drives thymic exposure of self-Ags —» negative selection process of pre-T cells
  • Encodes a transcription factor that drives transciption of genes for these self-Ag

Remember myasthenia gravis? Aire can’t interact with CHRNA promotor —» no AChR alpha subunit shown to pre-T cells

32
Q

What role do Treg cells play in Type II immunopathology?

A

Treg cells may not ensure appropriate immune responses

Allows self-non-self discriminatory process to break down somehow

B&L Unit 2 (9 decks)

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