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III > Drug list > Flashcards

Drug list Flashcards

1
Q

What is Zileuton and what is it used for?

A

Used in asthma.

Leukotriene receptor inhibitor which inhibits LTB4.

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2
Q

Monteleukast + Zafirlukast are used to treat what? Why?

A

Asthma.

Leukotriene receptor antagonists.

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3
Q

What is Sofosbuvir? what does it treat?

A

Treats HCV.
NS5B RNA polymerase inhibitor.
Shows antiviral activity against all genotypes and barrier to resistances.

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4
Q

What is Simeprivir?

A

Treatment for HCV.

NS3/4A protease inhibitor.

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5
Q

Faldaprevir is…

A

Treatment for HCV.

NS3/4A protease inhibitor.

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6
Q

Aunaprevir is…..

A

Treatment for HCV.

NS3/4A protease inhibitor.

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7
Q

ABT-450/R is what?

A

Treatment for HCV.

NS3/4A protease inhibitor.

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8
Q

NS5B RNA polymerase inhibitor.

A

Sofosbuvir:

Treat HCV: Shows antiviral activity against all genotypes and barrier to resistances.

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9
Q

Four inhibitors of the NS3/4A protease of HCV?

A

Simeprivir
Faldaprevir
Aunaprevir
ABT-450/R

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10
Q

Daclatasvir is….

A

NS5A protease inhibitor.
Blocks the replication complex formation and assembly.
Only recommended in combination with sofosbuvir +/- ribavirin.

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11
Q

Which anti-HCV medication is recommended in combination with sofosbuvir +/- ribavirin?

A

Daclatasvir.

NS5A protease inhibitor which blocks the replication complex formation and assembly.

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12
Q

ABT-267

A

NS5A protease inhibitor

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13
Q

Ledipasvir

A

NS5A protease inhibitor.

Block the replication complex formation and assembly.

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14
Q

Ribavirin

A

Nucleoside guanosine analogue that interferes with viral replication, dosing is weight based. Used to treat HCV.

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15
Q

ABT-333

A

NNRRIs. Act at a number allosteric sites on the RNA replicase enzyme.

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16
Q

What is one non-specific agent/ immunomodulator that an inert glycol has been added to?

A

PEG-IFN2a.
Used to treat HCV.
A cytokine.
PEGylation can be used to increase the circulating half-life and hide from the immune system.

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17
Q

Three NS5A protease inhibitors:

A

Daclatasvir.
Ledipasvir.
ABT-267

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18
Q

Imidazoles

A

Inhibition of CYP450 enzymes. (CYP51A1) the ERG11 gene product.
Prevent effective ergosterol production and damage accrues to cell wall of fungus.

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19
Q

Fluconazole.

A

nhibition of CYP450 enzymes. (CYP51A1) the ERG11 gene product.
Prevent effective ergosterol production and damage accrues to cell wall of fungus.

Hepatic derangement and QT prolongation.

Orally active.

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20
Q

Terbinafine

A

Squalene epoxidase inhibitor leading to decreased ergosterol production and changed cell permeability causing lysis.

Avoid in pregnancy, LF and renal toxicity.

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21
Q

Griseofulvin

A

Only active against dermatophyte infections.

Should take with or after fatty food.

Accumulates in keratinous tissues and prevents tubulin reorganisation needed for fungal cell to move etc.

Sensitivity testing recommended by PHE.

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22
Q

Caspofungin

A

Echinocandin inhibitor of B-1,3- glucan synthesis in the cell wall.

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23
Q

Anidulafungin

A

Echinocandin inhibitor of B-1,3- glucan synthesis in the cell wall.

Limited license: invasive candidiasis only.
Can be used in renal/hepatic failure patients.

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24
Q

Amphotericin

A

Serious fungal infections.
Targets ergosterol in the membrane and will causes creation of pores.
Fungicidal.
IV use only.

Polyenes lead to renal toxicity, electrolyte disturbances, infusion reactions, cardiotoxicity and hepatotoxicity,

Test dose needed, 1mg over 10mins, crash cart on standy.

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25
Q

Flucytosine

A

Systemic fungal infections.
Resistance develops if used as single agent.
Nucleoside analogue.
Synergises well with amphotericin.
Converted to 5-FU leading to inhibition of DNA/RNA synthesis in the nucleus.

Can lead to bone marrow suppression.

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26
Q

Quinine

A

Malaria treatment followed by doxycycline or clindamycin

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27
Q

Atavaquone - Proguanil (malarone)

A

Malaria prophylaxis or treatment.

Inhibits mitochondrial metabolism and anti-folate.

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28
Q

Doxycycline (malaria)

A

Malaria prophylaxis in areas of resistance.

Tetracycline class.

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29
Q

Mefloquine

A

An antimalarial drug consisting of a fluorinated derivative of quinoline. Malaria prophylaxis in areas with resistance.

Inhibits haem detoxification.

Half-life = 2-4 weeks.

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30
Q

Proguanil

A

Malaria prophylaxis in areas with no resistance.
Anti-folate.
12-21 hr half-life.

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31
Q

Chloroquine

A

Malaria prophylaxis in areas with no resistance.

Inhibits haem detoxification.

Half-life: 1-2 months.

Chloroquine + Proguanil are used together in areas with little to no resistance.

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32
Q

Oseltamivir

A

NAi.
Influenza.
NA cleaves sialic acid which facilitates the release of viral particles.
Oral. >1 year olds.
Better absorption than Zanamivir due to addition of hydrophobic groups.

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33
Q

Zanamivir

A

NAi.
Influenza.
NA cleaves sialic acid which facilitates the release of viral particles.

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34
Q

Why are NAi preferred over M2 inhibitors?

A

They are active against all strains of influenza and all serotypes including H5N1.
They are transition state analogues which are administered via Diskhaler

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35
Q

Rimantidine

A

M2 inhibitor. Influenza. Interferes with function of the TM domain of the M2 proteins of influenza A virus.

Less toxic than amantadine.

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36
Q

Amantadine

A

M2 inhibitor. Influenza. Interferes with function of the TM domain of the M2 proteins of influenza A virus.

Resistance is an issue with all M2 inhibitors, neither are NICE recommended any longer.

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37
Q

Raltegravir

A

Integrase inhibitor, HIV treatment.

HIV uses host genetic material to make it’s own DNA (reverse transcriptase) viral DNA has to integrate into the genetic material of host cells with an enzyme known as integrase.

Integrase inhibitors block this entry and prevent the virus from adding its DNA into CD4+ T-cells.

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38
Q

Maraviroc

A

CCR5 antagonist/receptor inhibitor.
For the treatment of CCR5 tropic HIV-1.
Used in combination with other retroviral treatments.

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39
Q

Fuzeon

A

Fusion inhibitor of HIV.

Rationally designed to mimic gp41.

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40
Q

Lopinavir

A

Protease inhibitor.

Stops GAG + POL from being processed into mature proteins needed for HIV function.

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41
Q

Efavirenz + Nevirapine

A

NNRTI: inhibit viral DNA replication by binding at the allosteric site, causing a conformational change of the binding site.

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42
Q

AZT / Tenofovir / Emictabine

A

NRTIs: chain terminators of the binding site who lack the ‘3-OH needed for chain elongation.

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43
Q

Glybera

A

Treatment for familial LPL deficiency. Delivered via adeno-associated virus carrying the gene for LPL.
Restores function. No more accumulation of chylmicrons and triglycerides in plasma.

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44
Q

Clopidogrel

A

Pro-drug atherosclerosis treatment. Block ADP induced platelet activation by blocking the P2Y12 receptor.

Additive effects with aspirin.

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45
Q

Bile Acid Resins

A

ATS. Anion exchange resins.
Sequester bile acids and decrease the reabsorption of bile acids.

Decrease the absorption of cholesterol and increase the use of cholesterol in the synthesis of new bile acids.

Leads to increased expression of LDL receptors also.

Bind to other lipid drugs and taste horrible + give diarrhoea.

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46
Q

Colestyramine

A

ATS. Anion exchange resins.
Sequester bile acids and decrease the reabsorption of bile acids.

Decrease the absorption of cholesterol and increase the use of cholesterol in the synthesis of new bile acids.

Leads to increased expression of LDL receptors also.

Bind to other lipid drugs and taste horrible + give diarrhoea.

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47
Q

Cholestipol

A

ATS. Anion exchange resins.
Sequester bile acids and decrease the reabsorption of bile acids.

Decrease the absorption of cholesterol and increase the use of cholesterol in the synthesis of new bile acids.

Leads to increased expression of LDL receptors also.

Bind to other lipid drugs and taste horrible + give diarrhoea.

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48
Q

Fibrates

A

ATS.
Agonists at the gene regulatory elements (PARR). PPARalpha esp.
Increase gene expression for Lipoprotein Lipase (LPL) ApoA1 and ApoA5.

Decrease VLDL secretion, increase hepatic uptake of LDL, decrease CRP + fibrinogen levels, increase glucose tolerance and limit smooth muscle inflammation.

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49
Q

Statins.

A

HMG-CoA reductase inhibitors.
Prevents mevalonate being converted into cholesterol and prevents LDL uptake.

Cell adhesion molecule expression is reduced, decreased ashesion and transendothelial migration, inhibition of chemokine and
MMP secretion.

Effect of statins on the cytoskeleton also alters leukocyte migration.

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50
Q

Amiloride.

A

CF. Blocks sodium resorption.

Others may be more effective but they pose a hyperkalaemia risk.

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51
Q

Ivacaftor

A

CF. Class 3 regualtion (G551D) and class 4 regulation (R117H)

Potentiator.

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52
Q

Denufosol

A

P2Y12 agonist, not effective at maintaining lung function and a risk of enhancing the mucus secretion by activating goblet cells.

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53
Q

Ezetimibe

A

ATS/Anti-cholesterol drug.

Targets Nieman Pick C1 cholesterol absorption channels at the enterocyte jejunal brush border.

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54
Q

Penicillins

A

Inhibitors of cell wall synthesis.
Bind to PBPs a type of transpeptidase involved in crosslinking.

Mimic the D-ala D-ala residues on the peptide chain and stimulate autolysins to break down the cell wall.

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55
Q

Cephalosporins.

A

Inhibitors of cell wall synthesis, contain a beta-lactam ring just like penicillins.

Increased activity against gram negative bacteria.

Affinity for PBPs and resistance to beta-lactamases.

Penetration through the outer membrane gives rise to the activity against gram negative bacteria.

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56
Q

Monobactams

A

Inhibitors of cell wall synthesis.
Beta-lactam containing.
Less likely to cause hypersensitivity.

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57
Q

Vancomycin

A 
Glycopeptide. 
Inhibitor of cell wall synthesis. 
Binds to terminal D-ala-D-ala. 
Resistance arises due to D-ala --> D-lactate. 
5hbonds vs 4 hbonds.
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58
Q

Teicioplanin

A

Glycopeptide.
Cell wall synthesis inhibitor.

Binds the terminal D-ala D-ala peptide preventing transglycosylase enzyme from adding the PG monomer onto the glycan chain and prevents cross linking.

Penetrates into CSF.

59
Q

Polymyxins

A

Bind tightly to Lipid A component of cell membrane causing the leakage of cytoplasmic contents.

Neurotoxic and nephrotoxic. Can cause contact dermatitis.

60
Q

Sulphonamides

A

Inhibitors of nucleic acid synthesis:

Dihydropterate synthetase inhibitor.

61
Q

Carbapenems

A

Highly resistant to BLs including ESBL.

Inhibit cell wall synthesis

62
Q

Trimethoprim

A

Inhibitor of nucleic acid synthesis.

Inhibits dihydrofolate reductase.

63
Q

Co-trimoxazole

A

Trimethoprim and sulphamethazole for pneumocystitis’s pneumonia.

64
Q

Rifamycins

A

RNA Polymerase inhibitors.

Orally active for treatment of TB and against meningitis/infections involving prosthetics.

65
Q

Nitroimidazoles

A

Affect DNA

66
Q

Ciprofloxacin

A

Inhibit DNA replication.
Type II DNA gyrase
Type IV topoisomerases.

67
Q

Macrolides

A

50S subunit binders which inhibit protein synthesis.

Decrease translation and the release of tRNA.

68
Q

Streptogramins

A

50S subunit

69
Q

Lincosamides

A

50S subunit.

Staphylococcal bone and joint infections. RTI, peritonitis, septiceamia.

70
Q

Oxazildonones

A

Bind 23s in 50s subunit decreasing the assembly of the initiation complex.

71
Q

Chloramphenicol

A

50S subunit, prevents formation of peptide bonds.

Can cause bond marrow suppression, aneamia, blood disorders.

72
Q

Aminoglycosides

A

30s subunit, decreasing the assembly of the initiation complex and decreasing the binding of tRNA in the A site.

Single daily doses are the least toxic.

73
Q

Clavulanic acid, Tazobactam, sulbactam.

A

Beta-lactamase inhibitors.

74
Q

Cycloserine

A

As a cyclic analogue of D-alanine, cycloserine acts against two crucial enzymes important in the cytosolic stages of peptidoglycan synthesis.

Broad spectrum antibiotic, used in TB treatment.

75
Q

Bacitracin

A

Skin and eye infections, can cause contact dermatitis. Prevents wound infections.
Cell wall synthesis inhibitor.

Bacitracin interferes with the dephosphorylation of C55-isoprenyl pyrophosphate, a molecule that carries the building-blocks of the peptidoglycan bacterial cell wall outside of the inner membrane.

76
Q

Daptomycin

A

Lipopeptide.
IV for SSTIs, endocarditis, MRSA.
Targets cytoplasmic membrane and causes rapid depolarisation and loss of function.

May cause myopathy, nephrotoxicity etc.

77
Q

Tetracyclines

A

30S subunit, decreases RNA binding in the A site.

78
Q

Ketolides

A

Subset of the macrolides, derived from erythromycin.

According to a recent study comparing the action of the classic macrolides erythromycin and azithromycin with ketolides, which are used to treat serious infections, the more powerful drugs (ketolides) were the more “leaky” in blocking the production of proteins. The researchers were surprised to discover that ketolides, which are known to be better antibiotics, allow for many more proteins to be made compared to the older, less efficient macrolides. As a result, it is now believed that allowing cells to make some proteins could be much more damaging for a microbe than not letting it make any proteins at all.

The only ketolide on the market at this moment is telithromycin, which is sold under the brand name of Ketek.

79
Q

Fusidic acid

A

Narrow spectrum.
Target: EFG-GDP complex.
Affects the EFG which supplies the energy for translocation, binds EFG-GDP complex to the ribosome and decreases the translocation of tRNA.

80
Q

Rifampicin

A

RNA Polymerase inhibitor.

Intracellular activity and used against TB. Red-coloured fluids.

81
Q

Isoniazid

A

TB. Mycolic acid synthesis inhibitors.

82
Q

Pyranizamide

A

Mycolic acid of TB synthesis inhibitor.

83
Q

Ethambutol.

A

TB. Increases permeability of the cell wall and inhibits cell wall synthesis.

84
Q

Streptomycin/capreomycin

A

Macrolides that are 2nd line against TB.

85
Q

Azithyomycin

A

Newer macrolide for 2nd line use against TB.

86
Q

Chlorpheniramine, Loratadine, Astemizole

A

The H1 receptor is Gq coupled to a GPCR. Activation of the receptor triggers activation of PLC which causes Ca2+ release from vesicles, which causes endothelial cell contraction and oedema. Airway and smooth muscle contraction & neuropeptide release – vasodilation. H1 antagonists stop this action.

87
Q

Cimetidine, Ranitidine

A

The H2 receptor is a Gs coupled GPCR. The binding of histamine to the H2 receptor activates adenylyl cyclase which produces cAMP. This leads to vascular smooth muscle relaxation. By antagonising this, we increase SM contraction and act on the parietal cells, so block gastric acid secretion.

88
Q

Aspirin (low Dose)

A

Post: acute MI, coronary artery bypass, after angioplasty and stenting, acute thrombotic stroke, PE and thrombosis

89
Q

Aspirin targets what residue in COX-1?

A

SER530 in COX-1 and SER516 in COX-2.
Aspirin irreversibly acetylates serine residues on COX, preventing platelet TxA2 synthesis. Endothelial cells make new COX so PGI2 is still released and inhibition of platelet aggregation and vasodilation can occur.

90
Q

Meloxicam,

Celecoxib

A

Anti-inflammatory, analgesic and antipyretic.

Inhibition of COX-2 gives rise to the anti-inflammatory effects of NSAIDs.

91
Q

Natalizumab

A

Anti-A4 integrin.
Against MS.
Monoclonal antibody that targets the a4 integrin molecule. This inhibits T-cell interactions with the brain endothelium decreasing trafficking in the brain.

92
Q

Marimastut

A

MMP substrate inhibitor.
Small Hydrozamic acid based molecule that mimics the MMP substrate collagen.

Non-specific tho, prinomastat is better.

93
Q

Aspirin targets what residue in COX-2?

A

SER530 in COX-1 and SER516 in COX-2.
Aspirin irreversibly acetylates serine residues on COX, preventing platelet TxA2 synthesis. Endothelial cells make new COX so PGI2 is still released and inhibition of platelet aggregation and vasodilation can occur.

94
Q

Doxycycline at sub-antibiotic levels.

A

Treatment of periodontal disease.

Inhibits MMP synthesis and activity.

95
Q

TIMPs

A

Endogenous inhibitors of MMPs, if we can upregulate their synthesis we can inhibit MMPs.

Easily inactivated by oxidation.
Non-specific.

96
Q

Methotrexate

A

Folate antagonist used in RA.
Inhibits dihydrofolate reductase, giving rise to anti-proliferate effect.

May block proliferation of EC required for angiogenesis in the synovium.

Suppression of IL-1 induced IL-6 so decreased synovial cell proliferation and decreased RONs.

Resistance develops and can cause bone marrow suppression and GIT damage.

97
Q

Sulfasalazine

A

RA & IBD.

Affects macrophage biochemistry to favour the production of anti-inflammatory cytokines.

98
Q

Peniclliamine

A

RA.
Decreases joint swelling, RF and concentration of APP.

Prevents maturation of newly synthesized collagen.

99
Q

Treatment of periodontal disease.

Inhibits MMP synthesis and activity.

A

Doxycycline at sub-antibiotic levels.

100
Q

Folate antagonist used in RA.

Inhibits dihydrofolate reductase, giving rise to anti-proliferate effect.

A

Methotrexate

May block proliferation of EC required for angiogenesis in the synovium.

Suppression of IL-1 induced IL-6 so decreased synovial cell proliferation and decreased RONs.

Resistance develops and can cause bone marrow suppression and GIT damage.

101
Q

Hydroxychloroquinine

A

Used in Malaria, RA.
Reduced joint swelling and decreases RF levels. Similar to Gold.
Lysosomotrophic and inhibits PLA2 to reduce cytokine transcription.

102
Q

Leflunomide

A

RA. Orotate dehydrogenase inhibitor. Prevents synthesis of pyrimidine and suppresses B-cell activity + autoantibody production.

103
Q

How do DMARDs appear to alleviate RA symptoms?

A

Mainly by dampening down the innate immune system. Inhibition of macrophage activation, cell proliferation and decrease of pro-inflammatory cytokines and ROS.

104
Q

Decreases joint swelling, RF and concentration of APP.

Prevents maturation of newly synthesized collagen.

A

Peniclliamine.

Taste disturbances, rashes, autoimmune diseases.

105
Q

Used in Malaria, RA.
Reduced joint swelling and decreases RF levels. Similar to Gold.
Lysosomotrophic and inhibits PLA2 to reduce cytokine transcription.

A

Hydroxychloroquinine

106
Q

Glucocorticoids

A

RA, chronic inflammation.
Enter cells, bind to cytoplasmic receptors. Complex translocates to the nucleus and acts as a transcription factor.
Can bind to response elements and activate gene transcription.
Can bind and repress gene activation such as AP1 and NFKB.

Immunosuppresants increase likelihood of infection.

107
Q

Infliximab

A

Anti-TNFalpha.
Chimeric Ab. Just the constant region in the mAb is humanised and the mAb binds TNFa decreasing the amount of circulating pro-inflammatory cytokine.

Given at 0, 2, 6 and 8 weekly with MTX to reduce immunogenic reactions.

108
Q

Adalimumab

A

MTX resistant patients. IBD.
Anti-TNFa.
Risk of reccurence of TB.
Fully humanized.

109
Q

Side effects of glucocorticoids.

A

Metabolic.
Osteoporosis: decrease in collagen synthesis leads to a decrease in osteoblast function and Ca2+ absorption by the inhibition of vitamin D action.

PTH hormone then increases calcium resorption from bone.

Diabetogenic + increased appetite,

sodium and water retention, HT, oedema + CV events.

110
Q

Certolizumab

A

Anti RA, Anti -TNFa.
PEGylated.
Chimeric.
Only the hypervariable regions are murine.

111
Q

SIL-1R

A

Soluble receptor targeting pro-inflammatory cytokines.

Problems:
SIL-1R also bound IL-1Ra which can lead to exacerbation of disease.

Natural soluble receptors are rapidly cleared by the circulation.

Homotrimeric TNF can still crosslink with membrane receptors even when bound to a soluble receptor.

Soluble receptors may also facilitate signal transduction by ligand passing.

112
Q

Enlinomab

A

Anti-ICAM (murine)

Blocked cellular adhesion molecules, T-cell migration and decreased IL-6.

113
Q

Risk of recurrence of TB.

A

Adalimumab.

114
Q

Given at 0, 2, 6 and 8 weekly with MTX to reduce immunogenic reactions.

A

Infliximab

115
Q

RA, chronic inflammation.
Enter cells, bind to cytoplasmic receptors. Complex translocates to the nucleus and acts as a transcription factor.
Can bind to response elements and activate gene transcription.
Can bind and repress gene activation such as AP1 and NFKB.

A

Glucocorticoids

116
Q

Methods of producing humanised mAbs.

A

Immunizing transgenic mice carrying the human genes or by in-vitro recombination in bacteriophages.
Reduces the immunogenic reactions.

117
Q

Anti-TNFa mAb that is pegylated.

A

Certolizumab.

118
Q

What is the theory behind and challenges associated with using soluble receptors to treat inflammatory conditions?

A

The theory is to increase the circulating concentration of soluble receptors to mop up the free cytokine.

The challenges are:
1. Natural receptors are rapidly cleared from circulation by the body.

  1. Homotrimeric TNF is still able to bind to membrane bound receptors even when bound by soluble receptor. (Overcome by use of soluble receptors that have been modified so that this interaction is sterically prevented, Etanercept?)
  2. Soluble receptors themselves may facilitate signal transduction by ligand passing.
119
Q

Etanercept

A

anti-TNFa.
Dimerisation of two soluble receptors using PEG so that they can target vasculature or link the soluble receptors to the Fc domain of an antibody.

Extends the half-life, can bind two molecules of TNF preventing membrane bound receptor activation.

Twice weekly sc injections.

Can be used in juvenille arthritis and 1st choice after DMARD failure.

120
Q

IL4, 10 and 13

A

Anti-inflammatory cytokines that can downregulate TNF, IL-1 and IFNg to boost the host defence

Non-immunogenic.

121
Q

What is Gancyclovir?

A

(Thymidine kinase)
Gene therapy - delivery of anti-inflammtory genes to the required site.

Requires rapid transient effects and the use of tissue promoters e.g. macrophages and lysosyme.

122
Q

What are the advantages of treating RA with gene therapy such as Gancyclovir?

A

Constant high concentration at the required site. Not degraded like an injected protein.

Disadvantages: Can’t switch off if an infection occurs.

123
Q

Can be used in juvenille arthritis and 1st choice after DMARD failure.

A

Etanercept:
anti-TNFa.
Dimerisation of two soluble receptors using PEG so that they can target vasculature or link the soluble receptors to the Fc domain of an antibody.

Extends the half-life, can bind two molecules of TNF preventing membrane bound receptor activation.

Twice weekly sc injections.

124
Q

Anakinra

A

IL-1RA.
Recombinated non-glycosylated form of IL-1RA, which decreases the signs and symptoms of RA in a rapid and sustained fashion. Decreases the progressive bone destruction.

Not effective in all patients.

125
Q

Tocade

A

Targeted Collagenases but trials were stopped due to decrease in efficacy.

126
Q

Anti-inflammatory cytokines that can downregulate TNF, IL-1 and IFNg to boost the host defence

Non-immunogenic.

A

IL4, 10 and 13

127
Q

What are the disadvantages of treating RA with gene therapy such as Gancyclovir?

A

Disadvantages: Can’t switch off if an infection occurs.

Constant high concentration at the required site. Not degraded like an injected protein.

128
Q

IL-1RA

A

Anakinra

129
Q

Cyclosporine and Tacrolimus

A

Fungal peptides with selective effects on T-cells and which prevent clonal expansion of IL-2 and IL-2R.

Bind immophillins and inhibit gene transcription.

Used in organ transplantation to prevent rejection.

130
Q

Rolipram

A

Type 4 phosphodiesterase inhibitor that binds to and inhibits PDE4, stimulating adenylyl cyclase and increasing the production of cAMP, which suppresses the TNF transcription.

131
Q

Azathioprine, Cyclophosphamide

A

Cytotoxic agents.

132
Q

Omega 3

A

High doses change amino acid metabolites into PGF3 and LTB5 which are less inflammatory.

133
Q

Type 4 phosphodiesterase inhibitor that binds to and inhibits PDE4, stimulating adenylyl cyclase and increasing the production of cAMP, which suppresses the TNF transcription.

A

Rolipram

134
Q

Used in organ transplantation to prevent rejection.

A

Cyclosporine and Tacrolimus

Fungal peptides with selective effects on T-cells and which prevent clonal expansion of IL-2 and IL-2R.

Bind immophillins and inhibit gene transcription.

135
Q

Anti-IL-17

A

IL-17 is produced by Th17 (see what they did there?) cells and is present in inflamed joints and synergies and enhances the effects of TNF and can upregulate NFKB, MAPK, IL-6, COX-2 and NO.

136
Q

Treg

A

Upregulates T-reg.
Dampen downs the immune cell activation and causes secretion of anti-inflammatory cytokines. IL-10
TGFB.

Decreases the function of APC.

137
Q

Fungal peptides with selective effects on T-cells and which prevent clonal expansion of IL-2 and IL-2R.

A

Cyclosporine and Tacrolimus

Bind immophillins and inhibit gene transcription.

Used in organ transplantation to prevent rejection.

138
Q

Rituximab

A

To treat severe RA in comb with MTX.
Anti-CD20 chimeric mAb.
B - cell depleting growth arresting drug.

IV injection x2 spaced two weeks apart but repeated every 6m-3y.

Fc-receptor mediated antibody cytotoxicity. Complement mediated cell lysis.

139
Q

Abatercept.

A

Anti-T cell.
Soluble receptor composed of CTLA4 and Fc fragment of IgG. Blocks the interaction of CD80 with CD28 on T-cell.

May also have CD28 independent action to inhibit lymphocyte action and cause cell death.

140
Q

Drug used to treat severe RA in comb with MTX.
Anti-CD20 chimeric mAb.
B - cell depleting growth arresting drug.

A

Rituximab

141
Q

Anti-T cell.

Soluble receptor composed of CTLA4 and Fc fragment of IgG. Blocks the interaction of CD80 with CD28 on T-cell.

A

Abatercept.

May also have CD28 independent action to inhibit lymphocyte action and cause cell death.

142
Q

Tocilizumab

A

Anti-IL6R.

Increases the concentration of IL-6, an anti-inflammatory cytokine.

143
Q

JAK inhibitor

A

Tofacitinib. Specific inhibitor of JAK3 so will block IL2, 3, 5 and 21.

III (24 decks)

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