Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phase 2a > Immunology > Flashcards

Immunology Flashcards

1
Q

What are the 3 polymorphonuclear leukocytes?

A
  1. Neutrophils
  2. Eosinophils
  3. Basophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 mononuclear leukocytes?

A
  1. Monocytes
  2. T-cell
  3. B-cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do monocytes differentiate into?

A

Macrophages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What do T-cells differentiate into?

A
  • T-regs
  • T-helper cells (CD4) (Th1 and Th2)
  • Cytoxic T cells (CD8)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do B-cells differentiate into?

A

Plasma cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What other immune cells should we be aware of?

A
  • Mast cells (migrant granulated cell)
  • Natural killer cell (lymphocyte family)
  • Dendritic cell (antigen-presenting cells in tissues)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is complement secreted?

A

The liver.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 3 modes of action for complement?

A
  1. Direct lysis
  2. Attract more leukocytes to site of infection
  3. Coat invading organisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do antibodies circulate in the blood?

A
  • Bound to B-cells
  • Free in plasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which part of the antibody is responsible for antigen binding?

A
  1. Fab regions
    - Variable in sequence
    - Bind to specific antigens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which part of the antibody is responsible for antigen elimination?

A
  1. Fc region
    - Constant sequence
    - Binds to complement, Fc receptors on phagocytes and natural killer cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 5 classes of antibodies?

A
  1. IgG (most abundant in serum and tissues)
  2. IgA
  3. IgM
  4. IgD
  5. IgE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the structure of IgG antibodies.

A
  • Monomer
  • 2 heavy chains (bind to B cell)
  • 2 light chains (bind to antigen)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the structure of IgA antibodies.

A
  • Mostly a monomer
  • Can be a dimer (20% in humans)
  • Held together by a J chain and a secretory unit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe the structure of IgM antibodies.

A
  • Pentamer (formation dependant on J chains)
  • Monomeric form bound to B cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where are IgG antibodies mainly found?

A

Most abundant serum antibody.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where are IgA antibodies mainly found?

A

Mucous secretions - known as secretory IgA (sIgA).

Also found in serum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where are IgM antibodies mainly found?

A

Largely in blood as they are too large to cross vascular endothelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where are IgD antibodies mainly found?

A

The mature form are mostly found bound to mature B cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where are IgE antibodies mainly found?

A

50% in blood, the rest are bound to mast cells and basophils.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are IgG antibodies responsible for?

A
  • Main antibody in the adaptive immune response
  • Secondary/memory responses
  • Crosses placenta
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are IgA antibodies responsible for?

A
  • First line of defence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are IgM antibodies responsible for?

A
  • Initial contact with antigen (principal immune response)
  • 10 sites for antigen binding (mopping up antigens in blood supply)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are IgD antibodies responsible for?

A
  • No effector functions have been identified (it does bind to antigens)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what are IgE antibodies responsible for?

A
  • Binds to basophils and mast cells which express a high affinity IgE-specific receptor
  • Stimulates histamine release from basophils and mast cells
  • Hypersensitivity reactions and defence against parasitic infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the mechanism of action of antibodies.

A
  • Direct attack on the invader
  • Activation of complement system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the mechanism of action of direct attack (antibodies).

A
  1. Agglutination (antigen-presenting particles are bound together)
  2. Precipitation (molecular complex is so large it comes out of solution)
  3. Neutralisation (antibodies cover the toxic sites)
  4. Lysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are cytokines?

A

Proteins secreted by immune and non-immune cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the action of interferons?

A

Induce a state of viral resistance in uninfected cells and limit the spread of viral infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Give the 3 types of interferons.

A
  1. IFN⍺
  2. IFNβ
  3. IFN𝛾
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Which cells secrete interferons?

A

Virus-infected cells secrete IFN⍺ and β.

Activated Th1 cells secrete IFN𝛾.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What do interleukins do?

A
  • Can be pro-inflammatory (IL1) or anti-inflammatory (IL10)
  • Can cause cells to divide, differentiate and secrete factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What do colony-stimulating factors do?

A

Direct the division and differentiation of bone marrow stem cells (leukocyte precursor).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What do tumour necrosis factors do?

A

Mediate inflammation and cytotoxic reactions (TNF⍺ and β).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are chemokines?

A

~40 proteins that direct the movement of cells from the blood stream to the tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Define innate immunity.

A
  • Primitive
  • Instinctive response
  • Does not require immune recognition by lymphocytes
  • No long-lasting memory
  • Integrated with adaptive immunity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are Pattern Recognition Receptors (PRRs)?

A

Receptors on immune cells that detect the presence of PAMPs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are Pathogens Associated Molecular Patterns (PAMPs)?

A

Pathogen-specific molecules that can be detected by PRRs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are toll-like receptors (TLRs)?

A

A type of PRR, that recognise structurally conserved molecules derived from microbes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the components of innate immunity?

A
  1. Physical and chemical barriers (eg. skin)
  2. Phagocytic cells (neutrophils and macrophages)
  3. Blood proteins (complement and acute phase proteins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What are the 3 features of inflammation?

A
  1. Increased blood supply
  2. Increased vascular permeability
  3. Increased leukocyte extravasation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Which cells detect the presence of antigens in the blood?

A

Monocytes and neutrophils.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Which cells detect the presence of antigens in tissues?

A

Macrophages and dendritic cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the 3 activation pathways for complement?

A
  1. Classical (antibody binds to microbe)
  2. Alternative (complement binds to microbe)
  3. Lectin (activated by mannose-binding lectin bound to microbe)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the three ways complement can act on microbes?

A
  1. Lyse microbes directly through the action of MAC (membrane attack complex)
  2. Chemotaxis
  3. Opsonisation (make them easier to phagocytose)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Describe the 3 ways phagocytosis can be initiated.

A
  1. Antibodies bound to antigens on microbe can bind to antibody receptors
  2. C3b opsonised on microbe binds to complement receptor
  3. Mannose receptors bind to carbohydrates on bacteria wall
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the 3 steps to phagocytosis?

A
  1. Binding
  2. Engulfment
  3. Phagosome formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the 2 pathways in neutrophils and macrophages?

A
  1. Oxygen-dependent
  2. Oxygen-independent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Describe the oxygen-dependent pathway in neutrophils and macrophages.

A
  • Uses reactive oxygen intermediates (ROI)
  • Superoxide ions are converted to H2O2 then to a hydroxide free radical
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Describe the oxygen-independent pathway in neutrophils and macrophages.

A
  • Enzymes (eg. lysosome)
  • Proteins (eg. defensins inserted into the membrane of the microbe)
  • pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the 3 possible outcomes after phagocytosis?

A
  • Debris gets secreted by the phagocytic cell
  • Cell components converted to energy
  • Antigens get presented on cell surface via MHC class II receptor

(MHC = major histocompatibility complex)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Why is adaptive immunity required?

A
  • Microbes can evade innate immune responses
  • Intracellular viruses and bacteria evade innate immunity
  • Memory of specific antigens allows a faster response
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the function of T cells and B cells?

A

T cells - intracellular microbes (cell-mediated)
B cells - extracellular microbes (humoral)

53
Q

What’s the link between innate and adaptive immunity?

A

Antigen-presenting cells of the innate immunity activate T cells of the adaptive immunity.

54
Q

What do T lymphocytes respond to?

A

Intracellular presented antigens.

55
Q

What does the T cell receptor do?

A
  • Recognises foreign antigens in association with MHC
  • Activates the T cell
56
Q

Which MHC class presents intrinsic agents and where is it expressed?

A

MHC class I (expressed by all cells except RBCs).

57
Q

Which MHC class presents extrinsic pathogens and where is it expressed?

A

MHC class II (expressed by antigen-presenting cells).

58
Q

How can you remember which CD cells bind to which MHC class?

A

They multiply to equal 8.

CD8 binds to class I and CD4 binds to class II.

59
Q

How can you remember the action of T cells?

A

CD8 is full of hate (Tc killer cells).

60
Q

What must happen for full T-cell activation?

A

Co-stimulatory molecules CD28 on T cells bind to CD80/CD86 on antigen-presenting cell.

61
Q

What happens when a T cell is activated?

A

IL-2 is secreted and binds to IL-2 receptor on the T cells (autocrine).

62
Q

What does T cell activation lead to?

A
  • Division
  • Differentiation (CD4 and CD8)
  • Effector functions
  • Memory
63
Q

What does Tc (CD8) activation lead to?

A
  • Apoptosis
  • Secretion of IFN𝛾 (inhibiting viral invasion)
  • Secretion of chemokines
  • Kills cells directly
64
Q

What does Th1 (CD4) activation lead to?

A
  • Travel to secondary lymphoid tissue (eg. lymph nodes)
  • Th1 cells recognise antigen on infected cells via T cell receptor
65
Q

What does Th2 (CD4) activation lead to?

A
  • Bind to B cells which are presenting antigens
  • T cell secretes cytokines
  • These cause the B cell to divide and differentiate
66
Q

Which membrane bound antibodies do B cells express?

A

IgM or IgD monomers.

67
Q

How many types of antibodies can an individual B cell make?

A
  • 1 antibody specific to 1 antigen
  • We are born with all the B cells required to identify any pathogen
68
Q

What happens when a B cells recognises self?

A

Its killed in the bone marrow.

69
Q

How do B cells present antigens to T cells?

A
  • Phagocytose pathogen
  • Present antigen on MHC II
  • T cell receptor binds to MHC II
  • Lots of co-stimulatory molecules required
70
Q

What happens when B cells become activated?

A

B cell becomes a plasma cell and produces immunoglobulins.

71
Q

What do B cells differentiate into?

A
  • Plasma cells (antibody forming cell)
  • Memory cells
72
Q

What is the function of memory cells?

A
  • Long lasting immunity
  • Responds quickly next time it detects the same antigen
  • Vaccination
73
Q

What is the immunological theory?

A

Infection leads to the production of ‘protective substances’ in serum which can neutralise and kill pathogens.
- Protection persists (memory)
- Protection transfers to other individuals

74
Q

Define passive immunisation.

A

The transfer of pre-formed antibodies.

75
Q

What are the 2 types of passive immunisation?

A
  • Natural immunisation
  • Artificial immunisation
76
Q

Describe natural passive immunity.

A

Transfer of preformed maternal antibodies across placenta or through breast milk.

Provides protection against:
- Diptheria
- Tetanus
- Rubella
- Mumps
- Poliovirus

77
Q

Describe artificial passive immunity.

A

Treatment with pooled human IgG (immunoserum).

Effective for:
- Immunocompromisation
- Pathogens with a short incubation time
- Acute danger of infection (eg. rabies)
- Anti-toxins or anti-venoms

78
Q

What are the disadvantages of passive immunisation?

A
  • Does not provide immunological memory
  • No long term protection
  • IgG is cleared from circulation
79
Q

How do toxins act on a nerve cell to produce toxic effects?

A

Toxin prevents fusion of vesicles at the synapse so the neurotransmitters cannot get into the synapse.

80
Q

How does a tetanus toxin act on the synapse?

A

Tetanus toxin vesicles contain lysine and GABA which prevents muscle relaxation, causing muscle contraction (spasticity).

81
Q

How does a botulinum toxin act on the synapse?

A

Botulinum vesicles contain ACh which prevents muscle contraction, causing muscle relaxation.

82
Q

Define active immunisation.

A

Manipulation of the immune system to generate a persistent protective response against pathogens by mimicking natural infection.

83
Q

How does inoculation differ from active immunisation?

A

Inoculation refers to the introduction of viable microorganisms into an individual to evoke an immune response.

84
Q

What are the advantages of active immunisation?

A
  • Antigen specificity and diversity
  • Mobilises immune system to generate memory
  • Learned immunological behaviour (fast response)
  • Specific self/non-self recognition
85
Q

What are the 4 stages of active immunisation?

A
  1. Engage innate immune system
  2. Mimicking agent elicits danger signals, triggering PAMPs and TLRs
  3. Activation of specialist antigen-presenting cells
  4. Engage adaptive immune system to generate memory T and B cells
86
Q

Describe the polysaccharide antigen response. (Pnemovax vaccine)

A
  • Produces T-cell independent B-cell response
  • Produces the required antibody
  • Cannot be used in children under 2 as they do not have T-cell-independent B-cell response
87
Q

Describe the protein antigen response.
(Men-C vaccine)

A
  • Requires both T-cell and B-cell to process and produce immune response
  • Combines polysaccharide and protein structure
  • Effective in children
88
Q

How does the onset of influenza affect the activation of immunological memory?

A
  • Rapid onset so the infection can become established before immunological memory can be activated
  • Requires repeated, annual immunisation
89
Q

How does the onset of polio affect the activation of immunological memory?

A
  • Takes up to three days to establish infection of the nervous system
  • Provides opportunity for immunological memory activation
90
Q

What are the different antigen options used in vaccines?

A
  • Whole organism (live attenuated or killed/inactivated)
  • Subunit
  • Peptides
  • DNA/RNA
  • Engineered virus
91
Q

Give an example of whole organism vaccinations.

A
  • Live attenuated pathogen (eg. TB, typhoid, MMR)
  • Killed, inactivated organism (eg. influenza, Hep A, anthrax)
92
Q

What are the advantages of live-attenuated vaccination?

A
  • Causes transient infection
  • Activates full, natural immune response
  • Prolonged contact with the immune system
  • Produces memory response
  • Long and comprehensive protection
93
Q

What are the disadvantages of live-attenuated vaccination?

A
  • Immunocompromised individuals at risk of infection
  • Complications
  • Risk of reverting to virulent form
  • Can lead to outbreaks in areas with poor sanitation
94
Q

What are the advantages of dead/inactive pathogen vaccination?

A
  • No risk of infection
  • Storage is less critical
  • Strong immune response possible due to different antigenic components
95
Q

What are the disadvantages of dead/inactive pathogen vaccination?

A
  • Tend to just activate humoral response (lack of T cell involvement)
  • Immune repsonse is weaker
  • Booster vaccination required
96
Q

Give examples of subunit vaccinations.

A
  • Inactivated exotoxins (eg. diptheria and tetanus)
  • Antigenic extracts (eg. Men C)
  • Recombinant microbial antigens
97
Q

What are the advantages of subunit vaccinations?

A
  • No risk of infection
  • Easier to store and preserve
98
Q

What are the disadvantages of subunit vaccinations?

A
  • Produce weaker immune response
  • Repeated vaccinations and adjuvants required
  • Must consider genetic heterogeneity of the population by choice of antigen
99
Q

Give an example of synthetic peptide vaccinations.

A
  • Therapeutic cancer vaccines (peptides from tumour associated antigens)
  • No current vaccines
100
Q

What is a major disadvantage of peptide vaccinations?

A

Not efficient due to the heterogeneity of the HLA molecules in the population.

101
Q

How does DNA vaccination work?

A
  • Transient expression of pathogenic genes into host cells in order to generate immune responses
  • Involves injecting a genetically engineered plasmid containing the DNA sequence encoding the antigen
  • No current vaccines
102
Q

What are the advantages of DNA vaccination?

A
  • No risk of infection
  • Cost effective
  • Stability in shipping and storage
  • In vivo expression
103
Q

What are the disadvantages of DNA vaccination?

A
  • No transient infection (mild response)
  • Require booster vaccinations
  • Limited to protein imunogens
  • Small risk of affecting genes controlling cell growth
104
Q

How does recombinant vector vaccination work?

A
  • Combining the physiology of a pathogenic organism with the DNA of a non-pathogenic
  • Imitates the effect of transient infection
  • Used to make Ebola vaccine for 2018 outbreak
105
Q

What are the advantages of recombinant vector vaccinations?

A
  • Ideal stimulus to immune system
  • Produces immunological memory
  • Flexible (different components can be engineered)
  • Safe (relative to live attenuated vaccination)
106
Q

What are the disadvantages of recombinant vector vaccinations?

A
  • Require refrigeration for transport
  • Can cause illness in immunocompromised individuals
  • Immune response to virus in subjects can negate effectiveness.
107
Q

What is an adjuvant?

A

Any substance added to a vaccine to stimulate an enhanced immune response.

108
Q

Give an example of an adjuvant and how it enhances immune response.

A

Aluminium salts:
- Activates macrophages and lymphocytes
- Help the antigen-presenting cells absorb antigen
- Extend presence of antigen in the blood
- Potentiate opsonised phagocytosis

109
Q

What cells are involved in cell-mediated immune response?

A
  • Neutrophils and monocytes (phagocytes)
  • Lymphocytes (antibody production)
110
Q

What is involved in non-cellular (humoral) immune response?

A
  • Immunoglobulins (antibodies)
  • Complement
  • Surfactant proteins
111
Q

When are humoral response antibodies made during the immune response?

A
  • IgM - made at the beginning of infection
  • IgG - targets single epitomes
  • IgE - specific to allergens
112
Q

What are the common features of anaphylaxis?

A
  • Rapid onset
  • Blothcy rash
  • Swelling of face and lips
  • Wheeze
  • Hypotension
  • Cardiac arrest (if severe)
113
Q

What drugs most commonly cause hypersensitivity reactions?

A
  • Amiodarone
  • Bleomycin
  • Methotrexate
  • NSAIDs
  • Nitrofurantoin
  • Novel Ig-based treatments
114
Q

Describe Type 1 Hypersensitivity.

A
  1. B cells are stimulated to produce IgE antibodies
  2. IgE binds to mast cells and basophils (sensitisation)
  3. Second exposure causes IgE cross-linking, anaphylactic degranulation of mast cells and release of inflammatory mediators
  4. Leads to acute anaphylaxis
115
Q

Give examples of Type 1 Hypersensitivity reactions.

A
  • Allergic rhinitis (hayfever)
  • Asthma
  • Nut, food and drug allergies
116
Q

What is atopy?

A

An inherited tendency to produce an exaggerated IgE response to an antigen.

117
Q

How is Type 1 Hypersensitivity diagnosed?

A

Skin Prick Tests (SPTs)

(Or Radioallergosorbent Tests (RASTs), serum is exposed to bed of suspected allergen)

118
Q

What is the treatment for hayfever?

A
  • Prevent exposure
  • Anti-histamines
  • Steroids (reduce local inflammation)
  • Desensitisation therapy
119
Q

What is the treatment for acute anaphylaxis?

A
  • Avoid exposure
  • Anti-histamines (prevent/ease acute symptoms)
  • Acute resuscitation (adrenaline, fluids etc)
  • Decrease ongoing inflammation
120
Q

Give examples of extrinsic asthma.

A
  • Atopy-related asthma (IgE driven)
  • Occupation asthma induced by acute irritants (or long term exposure to allergens or endotoxins)
121
Q

Give examples of intrinsic asthma.

A

Late-onset asthma caused by conditions, eg. nasal polyposis and aspirin sensitivity.

122
Q

Describe Type 2 Hypersensitivity.

A

Antibody mediated process by which IgM and IgG are directed against allergen cell surface antigens.

Leads to cell lysis, tissue damage or loss of function (through classical complement pathway and antibody-dependent cell-mediated cytotoxicity).

123
Q

Give examples of Type 2 Hypersensitivity reactions.

A
  • Transplant rejection
  • Autoimmune diseases
124
Q

Describe Type 3 Hypersensitivity.

A

Immune complex accumulation.

Occurs when immune complexes have not been cleared by innate immune cells, increasing activation and leukocyte recruitment.

125
Q

Give examples of Type 3 Hypersensitivity reactions.

A
  • Systemic Lupus Erythematosus
  • Post-streptococcal glomerulonephritis
  • Rheumatoid arthritis
126
Q

Describe Type 4 Hypersensitivity.

A

Delayed T-cell mediated hypersensitivity.

  1. CD4 and T-helper cells recognise antigens in complex with MHC class II
  2. The APC secretes IL-12 (stimulates proliferation of CD4 and TH1 cells)
  3. IL2 and INF induce further TH-1 cytokine release
  4. Immune response leads to the activation of CD8 T cells and macrophages
127
Q

What is a key presentation of Type 4 Hypersensitivity reactions?

A

Granulomas - collection of T-cells and macrophages formed during inflammation to wall-off foreign substances that the body is unable to eliminate.

128
Q

Give examples of Type 4 Hypersensitivity reaction.

A
  • TB
  • Contact dermatitis
  • Sarcoidosis
129
Q

What drugs most commonly cause hypersensitivity reactions?

A
  • Amiodarone
  • Bleomycin
  • Methotrexate
  • NSAIDs
  • Nitrofurantoin
  • Novel Ig-based treatments
130
Q

What is involved in the diagnosis and treatment of drug hypersensitivity?

A

Diagnosis:
- Lung function tests
- CT scans
- Chest X-rays

Treatment:
- Withdraw offending drug
- Steroids for severe respiratory failure

Phase 2a (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions