Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Immunopharmacology > Flashcards

Immunopharmacology Flashcards

1
Q

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

A

So we know potential targets for immune therapy

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

What two events underlie the innate immune response?

A

Vascular events

Cellular events

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

Examples of vascular events of the innate immune system

A

Vasodilation

Increased permeability of the postcapillary venules

Exudation of fluid

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

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

What mediators are released by the immune cells?

A

Eicosanoids

Cytokines

Histamine

Neuropeptides

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

What two outcomes can arise following an infection?

A

Resolution and healing

Development of a chronic infection

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

What is COX-1 important for?

A

Tissue homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is COX-2 important for?

A

Induced in activated inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which drugs target the COX enzyme?

A

Non-steroidal inflammatory drugs

Glucocorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Examples of eicosanoids

A

Prostaglandins

Leukotrienes

Thromboxane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How are COX enzymes involved in the production of eicosanoids?

A

Catalyse the oxidation of arachidonic acids into eicosanoid sub-classes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Effect of bradykinin

A

Vasodilation

Increased vascular permeability

Stimulation of pain nerve endings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Effect of NO

A

Vasodilation

Increased vascular permeability

Stimulates PG release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which cells produce NO?

A

Most inflammatory cells

Express NO synthase upon activation by cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Examples of cytokines

A

Interleukins

Chemokines

Colony-stimulating factors

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

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

How selective are aspirin and ibuprofen?

A

Weakly COX-1 selective

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

Characteristic of weakly COX-2 selective agents

A

They also inhibit COX-1

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

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

A

Anti-inflammatory

Analgesic

Antipyretic

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

Describe the anti-inflammatory action of NSAIDs

A

Inhibit COX-2 actions in inflammation

Promote vasodilation

Vasodilation facilitates increased permeability

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the mechanism of action of NSAIDs?

A

Inhibit the COX enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which NSAID is irreversible?

A

Aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the difference between COX-1 and COX-2?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

How are newer COX drugs different from the classical forms of the drug?

A

Newer COX drugs are selective to COX-2, leading to fewer side effects since COX-1 is required for the formation of protective mucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Suppression of which COX enzyme leads to most of the side-effects of NSAIDs?

A

COX-1

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

Side-effects of NSAIDs

A

GI disturbances

Skin reactions

Adverse renal effects

Bone marrow depression and liver disorders

Encephalitis

Bronchospasms

Adverse cardiovascular effects

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

How do COX-1 NSAIDs lead to mucosal damage?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How do NSAIDs cause adverse renal effects?

A

Decrease local renal PG levels

PGs are used to increase blood flow and promote natriuresis

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

What is gout?

A

Chronic disease

Caused by the overproduction of purines

Crystals of sodium urate precipitate in the joints causing an inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Strategies for gout therapy

A

Reducing uric acid synthesis

Inhibiting migration of immune cells to the site

Reduce pain

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

What are the two phases of the immune response?

A

Induction phase

Effector phase

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

What does the effector phase consist of?

A

Antibody-mediated component

Cell-mediated component

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What controls the phases of the immune response?

A

Cytokines

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

Describe the maturation of the adaptive immune response

A

ThP cells give rise to Th0 cells

Th0 cells develop into Th1 and Th2 cells

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

Which part of the immune system are Th1 cells involved in?

A

Cell-mediated immunity

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

Which part of the immune system are Th2 cells involved in?

A

Humoral immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What do Th1 cells do once activated by pathogen peptides presented on the MHC of APCs?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How does the humoral immune response effectively fight a pathogen?

A

Antibodies contain two Fab and one Fc portion

Fab = recognise and interact with parts of the pathogen

Fc = trigger host defences

42
Q

Which cells contain receptors for the Fc portion of the antibodies?

A

Many inflammatory host cells

43
Q

What do antibodies represent?

A

A direct link between the invading pathogen and the host

44
Q

Which interleukin is important in Th1 development?

A

IL-2

45
Q

What immune defect do inappropriate Th1 responses trigger?

A

RA

MS

Anaemia

Insulin-dependent diabetes

Allograft rejection

46
Q

What immune defect do inappropriate Th2 responses trigger?

A

Hypersensitivities

47
Q

3 classes of drugs used for unwanted immune responses

A

Antihistamines

Anti-rheumatoid agents

Immunosuppressants

48
Q

What is the importance of histamine in the immune response?

A

Mediator of both acute inflammation and hypersensitivity

Released by granulocytes and mast cells

49
Q

What are the two types of histamine receptor?

A

H1 - ileum contraction, systemic vasodilation, bronchoconstriction, vestibular nucleus and vomiting center

H2 - gastric acid secretion, smooth muscle relaxation

50
Q

How can histamine responses be targeted for therapy in hypersensitivities?

A

H1-receptor antagonists

Unwanted effects include: sedative CNS actions, GI disturbances and antimuscarinic effects

51
Q

What are DMARDs?

A

Disease modifying anti rheumatoid agents

Alleviate symptoms of RA without stopping the progress of disease

52
Q

How do glucocorticoids target the immune response?

A

Decrease transcription of genes for IL-2 and macrophage-activating cytokines

53
Q

What is the main action of immunosuppressants?

A

Inhibit clonal expansion

54
Q

What is the main target for most immunosuppressants?

A

IL-2 signal transduction/gene transcription

55
Q

Clinical uses of immunosuppressants

A

Inhibit rejection of transplanted organs and tissues

Suppress graft-versus-host disease

Treatment of autoimmune conditions

56
Q

What are pathogens?

A

Bacteria that cause disease

57
Q

Which aspect of a healthy host prevents pathogens from causing infection?

A

The immune inflammatory response

58
Q

What are the two effects of antibacterial drugs?

A

Bactericidial

Bacteriostatic

59
Q

What are bactericidial antibiotics?

A

Kills the bacterium

60
Q

What are bacteriostatic antibiotics?

A

Stops the bacterium from growing through the use of the host’s defense mechanisms

61
Q

Are antibacterial agents and antibiotics the same thing?

A

No

Antibacterial agents are chemicals produced by one microorganism that kills or prevents the growth of another agent

62
Q

How are antibacterial agents specific?

A

Target metabolic processes that are different in bacteria

So no major side effects due to ineffectiveness in host cells

63
Q

How are antibacterial agents and antibiotics different?

A

Antibiotics inhibits the replication or survival of cellular pathogens

Antibacterial agents actively and selectively kill bacteria

64
Q

What are the targets for antibacterial drugs?

A

Cell wall

Plasma membrane

Protein synthesis

Nucleotide metabolism

Bacterial genome

65
Q

What is the specificity of antibacterial drugs targeting protein synthesis?

A

30s and 50s subunits of bacterial ribosomes are different from those in human hosts

66
Q

What is the specificity of antibacterial drugs targeting nucleotide metabolism?

A

Unlike humans which take up dietary folates, bacteria synthesise folic acid required for nucleotide synthesis using PABA

This can be targeted by drugs

67
Q

What is the specificity of antibacterial drugs targeting the bacterial genome?

A

Bacterial topoisomerase II differs from that of humans and is a good target

Bacterial RNA polymerase inhibitors

68
Q

What is the difference between gram positive and gram negative bacteria?

A

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
Q

Why is the composition of the cell wall important?

A

Determines the effects of antibiotics on them

70
Q

Do gram positive or gram negative bacteria have more complex cell walls?

A

Gram negative bacteria

Contain transmembrane water-filled channels called porins which hydrophilic antibacterial agents can move freely through

71
Q

What two categories of resistance exist?

A

Genetic determinants of resistance

Biochemical mechanisms of resistance

72
Q

Examples of genetic determinants of resistance

A

Chromosomal determinants - mutations of chromosomal genes

Extrachromosomal determinants

Transfer of resistance genes between bacteria

73
Q

Describe extrachromosomal determinants of resistance

A

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
Q

How can resistance genes be transferred between bacteria?

A

Conjugation

Sex pili connect two bacteria, allowing transfer of plasmids between them

Also transferred by phages

75
Q

Examples of biochemical mechanisms of resistance

A

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
Q

Example of enzymes that inactivate a drug

A

Beta-lactamases

77
Q

What are b-lactams examples of?

A

Drugs that affect peptidoglycan synthesis

Bactericidial

78
Q

Mechanism of action of b-lactams

A

Inhibit the synthesis of the peptidoglycan corset by inhibiting the enzyme that inserts the cross-links

79
Q

Examples of b-lactams

A

Penicillins

Cephalosporins

80
Q

How do bacteria develop resistance to penicillins?

A

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
Q

Main type of drugs affecting DNA synthesis in bacteria

A

Fluoroquinolones

Inhibit topoisomerase II

Essential for transcription and replication

82
Q

Main problem with antituberculosis drugs

A

Development of multi-drug resistant strains

83
Q

What is the prevalence of TB?

A

World’s main cause of death from a single agent

84
Q

First-line drugs of TB

A

Isoniazid

Rifampicin

Pyrazinamide

85
Q

What is done to reduce the emergence of resistant organisms in TB?

A

Compound therapy

Long-term

86
Q

What disease, apart from TB, does rifampicin also treat?

A

Leprosy

87
Q

Structure of viruses

A

DNA or RNA

Protein coat

Some contain enzymes

88
Q

How do viruses replicate?

A

By taking over the metabolic processes of the host

Virtually become part of the host cells

Therefore, selective chemotherapy is difficult

89
Q

Where can a virus bind to its host cell through?

A

Receptors for cytokines

Neurotransmitters

Ion channels

Membrane glycoproteins

90
Q

Describe the pathogenic life cycle of viruses

A

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
Q

How do many viruses enter the host cell?

A

Through receptor-mediated endocytosis

92
Q

How are RNA retroviruses special?

A

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
Q

What are the two main groups of anti-HIV drugs?

A

Reverse transcriptase inhibitors

Protease inhibitors

94
Q

What are the two main types of reverse transcriptase inhibitors?

A

Nucleoside RTIs

Non-nucleoside RTIs

95
Q

Mechanism of action of nucleoside RTIs

A

Inhibit the action of viral reverse transcriptase

96
Q

Mechanism of action of non-nucleoside RTIs

A

Denature the catalytic site of reverse transcriptase

97
Q

Mechanism of action of protease inhibitors

A

Protease cleaves the precursor polyproteins to make the structural and functional proteins of the new virions

Protease inhibitors prevent this step

98
Q

What are targets of antiviral drugs?

A

Inhibit penetration of host cell

Inhibit transcription of the viral genome

99
Q

What type of immunomodulators can be used in treating viral infections?

A

Interferon-a - induces host cell enzymes with antiviral activity

Immunoglobulins - specific for viruses

100
Q

Clinical uses for non-anti-HIV antiviral agents

A

Aciclovir = herpes

Foscarnet = CMV

Pharmacology (13 decks)

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