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Transition block 1 > Immunology > Flashcards

Immunology Flashcards

1
Q

What are some causes of secondary immune deficiency?

A
  • Infections - HIV, measles
  • Drugs - immunosuppressants, anti-cancer drugs, corticosteroids
  • Malignancy - lymphoma, leukaemia, myeloma, metastasis
  • Biochemical and nutritional disorders - malnutrition, T1DM, T2DM, renal insufficiency/dialysis
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2
Q

What is a granuloma?

A

An organised collection of activated macrophages and lymphocytes

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3
Q

What is the underlying pathology/immunology of a granuloma?

A
  • Non-specific inflammatory response
  • Results in activation of T lymphocytes and macrophages
  • Failure of removal of the stimulus results in persistent production of activated cytokines
  • End result is organised collection of persistently activated cells
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4
Q

What are some of the differential diagnoses for a lung granuloma?

A

Sarcoidosis, TB, leprosy, silicosis, chronic stage of hypersensitivity pneumonitis, foreign bodies

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5
Q

How can antibody deficiencies present?

A
  • Recurrent bacterial infections e.g. recurrent URTI and LRTI
  • Antibody mediated autoimmune diseases e.g. thrombocytopenia, autoimmune haemolytic anaemia
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6
Q

Common variable immune deficiency (CVID) is a primary antibody deficiency, what are the features of CVID?

A
  • Low IgG, IgA and IgM
  • Recurrent bacterial infections esp respiratory
  • Often associated with autoimmune disease
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7
Q

What is another example of a common primary antibody deficiency?

A
  • Selective IgA deficiency
  • 2/3rds are symptomatic
  • 1/3rd have recurrent RT infections
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8
Q

What are some secondary causes of recurrent bacterial infections and hypogammaglobulinaemia?

A
  • Protein loss - nephrotic syndrome
  • Failure of protein synthesis - lymphoproliferative disease e.g. CLL
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9
Q

In basic terms, what is complement?

A

Protein constantly secreted by the liver to act as a sticky coat for intruders in order to turbo-boost immediate immune defence

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10
Q

What does complement deficiency result in?

A

Predisposes to bacterial infection especially meningitis

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11
Q

What is the function of natural killer cells?

A
  • Kill cells that lack MHC
  • Natural means that they have no need for antigen specificity
  • No long term memory
  • NK cells are an innate immunity feature that eliminate cancer cells
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12
Q

What can NK cell defects result in?

A

Predispose to recurrent VZV, HSV, CMV, HPV

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13
Q

What receptors are involved in innate recognition of invaders and what do these respond to?

A
  • Toll like receptors are expressed on phagocytes and dendrities as built in burglar alarm for microbes
  • Respond to PAMPs (pathogen-associated molecular patterns)
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14
Q

What happens as a result of TLR activation?

A

Pro-inflammatory cytokines and type 1 interferon secretion

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15
Q

What can TLR dysfunction cause and what can be used to remedy this?

A
  • Dysfunction can lead to immunodeficiency (too little) or autoimmunity (too much)
  • TLR-activators are used to boost immunity (anti-skin cancer creams e.g. imiquimod)
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16
Q

What do TNF inhibitors do?

A
  • Block pro-inflammatory cytokines
  • These drugs are foreign proteins so the immune system can form antibodies against them
17
Q

How do most biologic drugs work and what are some examples?

A
  • Most are artificial antibodies that block the body’s own proteins so they act just like passive immunisation and have to be injected every couple of weeks
  • Since they are normal proteins, their metabolism is not dependent on liver or renal function
  • Adalimumab = anti-TNF
  • Pembrolizumab = anti-PD1
  • Secukinumab = anti-interleukin 17
18
Q

Name the types of transplant rejection

A
  • Hyperacute rejection minutes-hours
  • Acute cellular rejection 5-30 days
  • Acute vascular rejection 5-30 days
  • Chronic allograft failure >30 days
19
Q

What is the pathology and mechanism behind hyperacute rejection?

A
  • Thrombosis and necrosis, type II hypersensitivity
  • Preformed antibody and complement fixation
20
Q

What is the pathology and mechanism behind acute cellular rejection?

A
  • Cellular infiltration, type IV hypersensitivity
  • CD4 and CD8 T cells
21
Q

What is the pathology and mechanism behind acute vascular rejection?

A
  • Vasculitis, type II hypersensitivity
  • De novo antibody and complement fixation
22
Q

What is the pathology and mechanism behind chronic allograft rejection?

A
  • Fibrosis and scarring
  • Immune and non-immune mechanisms
23
Q

What do memory B cells do and how do they form?

A
  • They are generated during primary immune responses and can survive for many years even after the antigen has been eliminated
  • Memory B cells rapidly re-activate in response to a second encounter with that specific antigen
24
Q

Vaccination stimulates rare naive T cells, what happens as a result of this?

A
  • Induces a strong T cell response in 14-21 days
  • Some become effector T cells which mostly die by apoptosis but some become memory T cells
25
Q

What are some of the advantages of inactivated vaccines?

A
  • Quick/easy
  • Can be made quickly (prevent epidemics)
  • Elicit good antibody responses
  • Easy to store
  • Usually safe
26
Q

What are some of the disadvantages of inactivated vaccines?

A
  • Not very potent
  • Many killed organisms don’t stimulate good immune response because they don’t replicate or disseminate
  • Doesn’t stimulate clonal expansion of B and T cells, thereby requiring multiple injections
27
Q

What are some examples of inactivated vaccines?

A
  • Whole cell vaccines e.g. polio, hep A, rabies
  • Fractional vaccines;
    • subunit vaccines e.g. hep B, pertussis
    • toxoid e.g. diphtheria, tetanus
    • pure polysaccharide vaccines e.g. haemophilus influenzae type B
28
Q

What diseases are included in the 6-in-1 vaccine?

A
  1. Polio
  2. Hep B
  3. Pertussis
  4. Diphtheria
  5. Tetanus
  6. Haemophilus influenzae type B
29
Q

What are some of the advantages of live attenuated vaccines?

A
  • All relevant effector mechanisms elicited
  • Localised, strong response
  • Usually only one single dose required
30
Q

What are some of the disadvantages of live attenuated vaccines?

A
  • Safety - may revert to virulence, may cause infection in immune-compromised host
  • Fragile - must be stored and handled carefully
31
Q

Name some examples of live attenuated vaccines

A
  • Viruses - measles, mumps, rubella, chickenpox, yellow fever, rotavirus, small pox
  • Bacterial - BCG, oral typhoid

Transition block 1 (11 decks)

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