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Immunopharmacology Flashcards

(100 cards)

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1
Q

Why is it important to understand the mediators of the immune response?

A

So we know potential targets for immune therapy

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2
Q

What two events underlie the innate immune response?

A

Vascular events

Cellular events

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3
Q

Examples of vascular events of the innate immune system

A

Vasodilation

Increased permeability of the postcapillary venules

Exudation of fluid

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4
Q

Examples of cells involed in the innate immune system

A

WBC - accumulate in the area of inflammation and are activatedto ingest microbes or kill infected cells

Tissue cells - vascular endothelial cells, mast cells, macrophages

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5
Q

What mediators are released by the immune cells?

A

Eicosanoids

Cytokines

Histamine

Neuropeptides

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6
Q

What two outcomes can arise following an infection?

A

Resolution and healing

Development of a chronic infection

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7
Q

Important enzyme involved in the formation of eicosanoids and platelet-activating factors

A

COX enzyme

Exists in two forms:

  • COX-1
  • COX-2
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8
Q

What is COX-1 important for?

A

Tissue homeostasis

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9
Q

What is COX-2 important for?

A

Induced in activated inflammatory cells

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10
Q

Which drugs target the COX enzyme?

A

Non-steroidal inflammatory drugs

Glucocorticoids

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11
Q

Examples of eicosanoids

A

Prostaglandins

Leukotrienes

Thromboxane

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12
Q

How are COX enzymes involved in the production of eicosanoids?

A

Catalyse the oxidation of arachidonic acids into eicosanoid sub-classes

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13
Q

Effect of bradykinin

A

Vasodilation

Increased vascular permeability

Stimulation of pain nerve endings

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14
Q

Effect of NO

A

Vasodilation

Increased vascular permeability

Stimulates PG release

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15
Q

Which cells produce NO?

A

Most inflammatory cells

Express NO synthase upon activation by cytokines

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16
Q

Examples of cytokines

A

Interleukins

Chemokines

Colony-stimulating factors

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17
Q

How do NSAIDs vary?

A

NSAIDs vary in the degree that they inhibit COX-enzymes

From highly - very - weakly - COX-1 selective

From very - weakly COX2 selective

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18
Q

How selective are aspirin and ibuprofen?

A

Weakly COX-1 selective

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19
Q

Characteristic of weakly COX-2 selective agents

A

They also inhibit COX-1

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20
Q

What are the 3 pharmacological actions of non-steroidal inflammatory drugs?

A

Anti-inflammatory

Analgesic

Antipyretic

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21
Q

Describe the anti-inflammatory action of NSAIDs

A

Inhibit COX-2 actions in inflammation

Promote vasodilation

Vasodilation facilitates increased permeability

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22
Q

Describe the analgesic actions of NSAIDs

A

Reduce pain caused by tissue damage or inflammatory mediators that act on nerve endings

Indirectly decrease the production of prostaglandins which sensitise nerve endings to pain-inducing mediators

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23
Q

Describe the antipyretic actions of NSAIDs

A

Reduce fever

Fever is induced by IL1, which generates E-type prostaglandins in the hypothalamus

This disturbs the natural thermostat and results in an elevation of the set-point

NSAIDs interrupt the synthesis of the relevant PGs

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24
Q

What is the mechanism of action of NSAIDs?

A

Inhibit the COX enzyme

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25
Which NSAID is irreversible?
Aspirin
26
What is the difference between COX-1 and COX-2?
Both are found in the site of inflammation But COX-1 is constitutively expressed, and is necessary for the production of the protective mucosa in the GI and kidneys COX-2 has no endogenous role and is only found in sites of inflammation
27
How are newer COX drugs different from the classical forms of the drug?
Newer COX drugs are selective to COX-2, leading to fewer side effects since COX-1 is required for the formation of protective mucosa
28
Suppression of which COX enzyme leads to most of the side-effects of NSAIDs?
COX-1
29
Side-effects of NSAIDs
GI disturbances Skin reactions Adverse renal effects Bone marrow depression and liver disorders Encephalitis Bronchospasms Adverse cardiovascular effects
30
How do COX-1 NSAIDs lead to mucosal damage?
COX-1 is involved in the formation of PGs that play a role in stimulating the formation of the protective mucosal lining of the stomach
31
How do NSAIDs cause adverse renal effects?
Decrease local renal PG levels PGs are used to increase blood flow and promote natriuresis
32
What is gout?
Chronic disease Caused by the overproduction of purines Crystals of sodium urate precipitate in the joints causing an inflammatory response
33
Strategies for gout therapy
Reducing uric acid synthesis Inhibiting migration of immune cells to the site Reduce pain
34
What are the two phases of the immune response?
Induction phase Effector phase
35
What does the effector phase consist of?
Antibody-mediated component Cell-mediated component
36
What controls the phases of the immune response?
Cytokines
37
Describe the maturation of the adaptive immune response
ThP cells give rise to Th0 cells Th0 cells develop into Th1 and Th2 cells
38
Which part of the immune system are Th1 cells involved in?
Cell-mediated immunity
39
Which part of the immune system are Th2 cells involved in?
Humoral immunity
40
What do Th1 cells do once activated by pathogen peptides presented on the MHC of APCs?
Produce cytokines that activate macrophages which kill intracellular organisms Stimulate CD8+ T cells to proliferate, driving the production of cytotoxic T cells which kill virally infected host cells
41
How does the humoral immune response effectively fight a pathogen?
Antibodies contain two Fab and one Fc portion Fab = recognise and interact with parts of the pathogen Fc = trigger host defences
42
Which cells contain receptors for the Fc portion of the antibodies?
Many inflammatory host cells
43
What do antibodies represent?
A direct link between the invading pathogen and the host
44
Which interleukin is important in Th1 development?
IL-2
45
What immune defect do inappropriate Th1 responses trigger?
RA MS Anaemia Insulin-dependent diabetes Allograft rejection
46
What immune defect do inappropriate Th2 responses trigger?
Hypersensitivities
47
3 classes of drugs used for unwanted immune responses
Antihistamines Anti-rheumatoid agents Immunosuppressants
48
What is the importance of histamine in the immune response?
Mediator of both acute inflammation and hypersensitivity Released by granulocytes and mast cells
49
What are the two types of histamine receptor?
H1 - ileum contraction, systemic vasodilation, bronchoconstriction, vestibular nucleus and vomiting center H2 - gastric acid secretion, smooth muscle relaxation
50
How can histamine responses be targeted for therapy in hypersensitivities?
H1-receptor antagonists Unwanted effects include: sedative CNS actions, GI disturbances and antimuscarinic effects
51
What are DMARDs?
Disease modifying anti rheumatoid agents Alleviate symptoms of RA without stopping the progress of disease
52
How do glucocorticoids target the immune response?
Decrease transcription of genes for IL-2 and macrophage-activating cytokines
53
What is the main action of immunosuppressants?
Inhibit clonal expansion
54
What is the main target for most immunosuppressants?
IL-2 signal transduction/gene transcription
55
Clinical uses of immunosuppressants
Inhibit rejection of transplanted organs and tissues Suppress graft-versus-host disease Treatment of autoimmune conditions
56
What are pathogens?
Bacteria that cause disease
57
Which aspect of a healthy host prevents pathogens from causing infection?
The immune inflammatory response
58
What are the two effects of antibacterial drugs?
Bactericidial Bacteriostatic
59
What are bactericidial antibiotics?
Kills the bacterium
60
What are bacteriostatic antibiotics?
Stops the bacterium from growing through the use of the host's defense mechanisms
61
Are antibacterial agents and antibiotics the same thing?
No Antibacterial agents are chemicals produced by one microorganism that kills or prevents the growth of another agent
62
How are antibacterial agents specific?
Target metabolic processes that are different in bacteria So no major side effects due to ineffectiveness in host cells
63
How are antibacterial agents and antibiotics different?
Antibiotics inhibits the replication or survival of cellular pathogens Antibacterial agents actively and selectively kill bacteria
64
What are the targets for antibacterial drugs?
Cell wall Plasma membrane Protein synthesis Nucleotide metabolism Bacterial genome
65
What is the specificity of antibacterial drugs targeting protein synthesis?
30s and 50s subunits of bacterial ribosomes are different from those in human hosts
66
What is the specificity of antibacterial drugs targeting nucleotide metabolism?
Unlike humans which take up dietary folates, bacteria synthesise folic acid required for nucleotide synthesis using PABA This can be targeted by drugs
67
What is the specificity of antibacterial drugs targeting the bacterial genome?
Bacterial topoisomerase II differs from that of humans and is a good target Bacterial RNA polymerase inhibitors
68
What is the difference between gram positive and gram negative bacteria?
Gram positive bacteria = stain with Gram's stain Main difference is the structure of cell wall - negative = single layer - positive = can be up to 40 layers thick
69
Why is the composition of the cell wall important?
Determines the effects of antibiotics on them
70
Do gram positive or gram negative bacteria have more complex cell walls?
Gram negative bacteria Contain transmembrane water-filled channels called porins which hydrophilic antibacterial agents can move freely through
71
What two categories of resistance exist?
Genetic determinants of resistance Biochemical mechanisms of resistance
72
Examples of genetic determinants of resistance
Chromosomal determinants - mutations of chromosomal genes Extrachromosomal determinants Transfer of resistance genes between bacteria
73
Describe extrachromosomal determinants of resistance
Many bacteria have genetic elements that can replicate on their own These are called plasmids Plasmids can carry resistance genes Some stretches of plasmid DNA can be transported from one plasmid The stretches are called transposons and can spread resistance
74
How can resistance genes be transferred between bacteria?
Conjugation Sex pili connect two bacteria, allowing transfer of plasmids between them Also transferred by phages
75
Examples of biochemical mechanisms of resistance
Production of enzymes that inactivate the drug Modification of the drug-binding sites Decreased accumulation of the drug in the bacterium - efflux mechanisms Alteration of the target enzymes
76
Example of enzymes that inactivate a drug
Beta-lactamases
77
What are b-lactams examples of?
Drugs that affect peptidoglycan synthesis Bactericidial
78
Mechanism of action of b-lactams
Inhibit the synthesis of the peptidoglycan corset by inhibiting the enzyme that inserts the cross-links
79
Examples of b-lactams
Penicillins Cephalosporins
80
How do bacteria develop resistance to penicillins?
B-lactamases disrupt the b-lactam ring Can overcome this using b-lactamase inhibitors But there are also other mechanisms of resistance = modification of binding sites, reduced permeability to the outer membrane
81
Main type of drugs affecting DNA synthesis in bacteria
Fluoroquinolones Inhibit topoisomerase II Essential for transcription and replication
82
Main problem with antituberculosis drugs
Development of multi-drug resistant strains
83
What is the prevalence of TB?
World's main cause of death from a single agent
84
First-line drugs of TB
Isoniazid Rifampicin Pyrazinamide
85
What is done to reduce the emergence of resistant organisms in TB?
Compound therapy Long-term
86
What disease, apart from TB, does rifampicin also treat?
Leprosy
87
Structure of viruses
DNA or RNA Protein coat Some contain enzymes
88
How do viruses replicate?
By taking over the metabolic processes of the host Virtually become part of the host cells Therefore, selective chemotherapy is difficult
89
Where can a virus bind to its host cell through?
Receptors for cytokines Neurotransmitters Ion channels Membrane glycoproteins
90
Describe the pathogenic life cycle of viruses
Virus binds to receptor Entry Uncoating Reverse transcription to make double stranded DNA copy of viral RNA DNA copy enters nucleus and integrates with host cell Transcription of provirus Translation by host ribosomes Protease action Assembly and budding New virions
91
How do many viruses enter the host cell?
Through receptor-mediated endocytosis
92
How are RNA retroviruses special?
Use reverse transcriptase that makes a DNA of the viral RNA This DNA copy is integrated into the host genome and directs the generation of new viral particles
93
What are the two main groups of anti-HIV drugs?
Reverse transcriptase inhibitors Protease inhibitors
94
What are the two main types of reverse transcriptase inhibitors?
Nucleoside RTIs Non-nucleoside RTIs
95
Mechanism of action of nucleoside RTIs
Inhibit the action of viral reverse transcriptase
96
Mechanism of action of non-nucleoside RTIs
Denature the catalytic site of reverse transcriptase
97
Mechanism of action of protease inhibitors
Protease cleaves the precursor polyproteins to make the structural and functional proteins of the new virions Protease inhibitors prevent this step
98
What are targets of antiviral drugs?
Inhibit penetration of host cell Inhibit transcription of the viral genome
99
What type of immunomodulators can be used in treating viral infections?
Interferon-a - induces host cell enzymes with antiviral activity Immunoglobulins - specific for viruses
100
Clinical uses for non-anti-HIV antiviral agents
Aciclovir = herpes Foscarnet = CMV

Pharmacology (13 decks)

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