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My Respiratory > Immunity > Flashcards

Immunity Flashcards

1
Q

What are the hallmarks immune deficiency?

A
  • serious infections
  • persistent infections
  • unusual infections
  • recurrent infections
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2
Q

What are secondary immunodeficiency disorders?

A

common, subtle, involve more than one component of the immune system

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3
Q

What are the associated conditions to secondary immunodeficiency disorders?

A

HIV, immunosuppressive therapy, chemotherapy, cancers of the immune system and malnutrition

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4
Q

What are the common upper respiratory complications?

A

sinusitis, otitis media or laryngeal angioedema

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5
Q

What are the common lower respiratory complications?

A

malignancies, ILDs, pneumonia, bronchitis or bronchiectasis

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6
Q

What are the four ways that the cycle of a neutrophil can go wrong?

A

1- neutrophil development (leading to severe congenital neutropenia)
2- neutrophil trans endothelial migration (leads to recurrent infections, high neutrophil counts in the blood due to leukocyte adhesion deficiency)
3- neutrophil phagocytosis and killing (eg chronic granulomatous disease where free radical can’t be generated)
4- defects in macrophage killing (intracellular bacteria)

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7
Q

What is the treatment for phagocyte deficiencies?

A
  • immunoglobin replacement therapy
  • aggressive management of infection using oral/IV antibiotics and antifungals or surgical drainage of abscesses
  • definitive therapy so stem cell transplants or gene therapy
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8
Q

What are the four ways that there can be defects in leukocyte development?

A
  • defects in hamatopoetic stem cells
  • defects in lymphoid precursor cells
  • defects in thymocyte development
  • defects in B cell developments
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9
Q

What are the effects of having defects in hematopoetic stem cells?

A

there is disruption in the mitochondrial membrane potential so no leukocytes are made so this is fatal

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10
Q

What happens when there are defects in lymphoid precursor cells?

A

SCID can occur as the patient can’t produce leukocytes, the child will have many infections and it is treated prophylactically (avoid infections and aggressive treatment of infections) and definitively (stem cell)

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11
Q

What is the result of defects in thymocyte development?

A

DiGeorge syndrome where there are no CD4+ (so no antibody so bacteria infections) or CD8+ (so viral infections) T cells and no CD4+ Th cells (fungal infections)

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12
Q

What is the result of defects in B cell development?

A

X-linked agammaglobulinaemia

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13
Q

What re the two ways that leukocyte effector functions can be defected?

A
  • T cell effector functions (infections)

- B cell effector functions (hyper IgM syndrome and selective IgA deficiency)

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14
Q

What are the clinical features of T cell deficiencies?

A
  • recurrent infections
  • opportunistic infections
  • malignancies at young age
  • autoimmune disease
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15
Q

What are the clinical features of B cell deficiencies?

A
  • recurrent infections
  • opportunistic infections
  • antibody-mediated autoimmune disease
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16
Q

What is a hypersensitivity disorder?

A

an immune response that results in bystander damage to the self which is usually an exaggeration of normal immune mechanisms

17
Q

What is type 1 hypersensitivity?

A

Immediate/allergy (eg asthma or anaphylaxis)

18
Q

How does type 1 hypersensitivity work?

A
  • IgE mediated antibody response to external antigen triggered by allergens
  • B cells recognise antigen and make IgE antibody, Th2 cells provide help and vasoactive substances are realised by mast cells
  • mast cells and eosinophils express receptors for the Fc region of the IgE antibody and the leftover IgE antibody on the B cell bins to the mast cells
  • allergen binds to IgE on mast cell so histamine is released and there is increased expression of pro-inflammatory cytokines and leukotrienes
19
Q

What are the clinical features of type 1 hypersensitivity?

A
  • muscle spasm (bronchoconstriction so wheeze)
  • mucosal inflammation (mucosal oedema and increased secretions)
  • inflammatory cell infiltrate
    it occurs quickly
20
Q

What is the management of type 1 hypersensitivity?

A
  • avoidance of allergen
  • blocking mast cell activation
  • preventing mast cell activation
21
Q

What is type 2 hypersensitivity?

A

direct cell effects, cell surface antigen eg good pastures syndrome

22
Q

How does type 2 hypersensitivity work?

A
  • involves IgM or IgG antibodies to cell surface antigens
  • antibody binds to host cells causing cell death through activation of complement, natural killer cells and macrophages (opsonisation)
23
Q

What is type 3 hypersensitivity?

A

immune complex mediate, soluble antigens eg acute hypersensitivity pneumonitis

24
Q

How does type 3 hypersensitivity work?

A
  • excess soluble antigen , antibody binds forming small immune antibody-antigen completes that deposit in tissue and cause inflammation
  • opsonisation (antibody-mediated phagocytosis) and activation of neutrophils and macrophages so tissue damage
25
Q

What is the management of type 3 hypersensitivity?

A

decrease inflammation with corticosteroids and to decrease antibody production with immunosuppresion

26
Q

What is type 4 hypersensitivity?

A

delayed type eg sarcoidosis

27
Q

How does type 4 hypersensitivity work?

A
  • antigen recognition by CD4 Th1 or Th2 cells and cytotoxic CD8 cells
  • independent of antibody
  • 2-14 days to develop
28
Q

What are examples of type 4 hypersensitivity?

A

sarcoidosis and tuberculosis

29
Q

What is the treatment for type 4 hypersensitivity?

A

systemic corticosteroids to block T cell and macrophage activation

30
Q

What is the pneumonic for the four types of hypersensitivity?

A

1- Allergic, Anaphylaxis and Atopy
2- antiBody
3- immune Complex
4- Delayed

31
Q

What is harmless autoimmunity?

A

low titres of auto-antibodies or auto-reactive T cells

32
Q

What is harmful autoimmunity?

A

high titre of auto-antibodies or auto-reactive T cells leading to significant tissue or organ damage and chronic inflammation

33
Q

What are the two tolerance mechanisms for how the immune system deals with auto reactive T and B cells?

A
  • deletion of self-reactive lymphocytes in primary lymphoid tissues
  • inactivation of self-reactive lymphocytes in peripheral tissues that escape central tolerance
34
Q

What are the two ways that autoimmune diseases can be classed?

A
  • clinical classification so organ-specific diseases or non-organ specific diseases
  • pathological classification so Gel and Coombs
35
Q

What is an example of a type 2 hypersensitivity?

A

Goodpasture’s and graves’ disease

36
Q

What is an example of a type 3 hypersensitivity?

A

SLE

37
Q

What is an example of a type 4 hypersensitivity?

A

rheumatoid arthritis

38
Q

What is a mast cell degradation product that can be measured in acute anaphylaxis?

A

serum tryptase

My Respiratory (15 decks)

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