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PED2006 Systems Pharmacology > 3. Inflammation and Infection > Flashcards

3. Inflammation and Infection Flashcards

1
Q

What is an antibiotic?

A

A medicine that inhibits the growth (bacteriostatic) or destroys bacteria (bactericidal)

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2
Q

What may antibiotics target?

A

-Cell wall synthesis
-Membrane synthesis
-Protein synthesis
-Metabolic pathways
-Nucleic acid synthesis

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3
Q

Describe the bacterial cell wall structure

A

-Gram positive have thicker peptidoglycan wall, gram negative have thinner and an outer membrane
-Made up of peptidoglycan repeating units, considsting of MurNAc and GlcNAc, transpeptidases catalyse the binding of these repeating units via D-ala-D-ala binding

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4
Q

Describe the mechanism of action of penicillins

A

-Binds to Penicillin-Binding Proteins (PBPs):
PBPs are enzymes involved in the cross-linking of peptidoglycan in bacterial cell walls.
-Inhibits Peptidoglycan Cross-Linking:
Without proper cross-linking, the bacterial cell wall becomes weak and unstable

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5
Q

Give types of penicillins, and examples

A

-β-Lactamase-Resistant Penicillins (eg methicillin)
-Extended-Spectrum Penicillins (eg piperacillin)
-Reverse-Spectrum Penicillins (eg piperacillin-tazobactam)
-Natural Penicillins (eg benzylpenicillin)
-Broad-Spectrum Penicillins (eg amoxicillin)

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6
Q

Describe Cephalosporins

A

-Broad spectrum penicillin
-Used to treat septicaemia
-Most given parenterally, IM or IV, and excretion is largely via kidney
-Can cause nephrotoxicity and diarrhoea

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7
Q

Give examples of cephalosporins

A

-Cefaclor
-Cephalexin
-Cefotaxime

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8
Q

Give some mechanisms that bacteria may develop to resist penicillin

A

-β lactamase production
-Altered PBPs/transpeptidases
-Efflux pumps
-Reducing permeability

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9
Q

Describe how β lactamase production contributes to penicillin resistance

A

-β-lactamase enzymes hydrolyze the β-lactam ring structure of penicillin, rendering it inactive
-Penicillin is broken down before it can bind to penicillin-binding proteins (PBPs) and inhibit cell wall synthesis.

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10
Q

Describe how altered PBPs/transpeptidases contributes to penicillin resistance

A

-Bacteria modify the structure of PBPs, the targets of penicillin.
-The modification reduces the affinity of the antibiotic for these proteins, preventing penicillin from binding effectively.
-Penicillin can no longer inhibit cell wall synthesis

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11
Q

Describe how efflux pumps contribute to penicillin resistance

A

-Some bacteria possess efflux pumps, which actively pump out penicillin and other antibiotics from the bacterial cell before they can exert their effect.
-Penicillin concentrations inside the bacterial cell are kept too low to be effective.

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12
Q

Describe how reduced permeability contributes to penicillin resistance

A

-Bacteria can reduce the penetration of penicillin by modifying the structure or function of their outer membrane proteins
-Reducing influx

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13
Q

What may we administer to prevent β-lactamase function

A

Clavulanic acid

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14
Q

Describe the mode of action of clavulanic acid

A

-Clavulanic acid has a structural similarity to the β-lactam ring of penicillin, which allows it to bind to the active site of β-lactamase enzymes.
-When clavulanic acid binds to β-lactamase, it forms a covalent bond, thereby inactivating the enzyme.

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15
Q

Give some other antibiotics targeting the cell wall, and their mechanism

A

-Cycloserine (inhibits enzymes that catalyse formation of D-Ala, as well as enzymes that catalyse crosslinking)
-Bacitracin (inhibits activity of lipid carrier)
-Vancomycin (Binds D-ala-D-ala, preventing release of building block unit)

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16
Q

Give some antibiotics inhibiting protein synthesis, and their mechanism of action

A

-Chloramphenicol (binds to 50S portion and inhibits formation of peptide bond)
-Erythromycin (binds to 50S portion, prevents translocation-movement of ribosome along mRNA)
-Tetracyclines (interfere with attachment of tRNA to mRNA-ribosome complex)
-Streptomycin (changes shape of 30S portion, causes code on mRNA to be read incorrectly)

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17
Q

Describe tetracycline antibiotics as protein synthesis inhibitors

A

-Competitively binds the A site
-Resistance a growing problem efflux, ribosomal protection, or tetracycline inactivation
-Bacteriostatic
-Can cause decoloration of teeth and photosensitivity
-Broad spectrum of activity (borrelia, chlamydia, rickettsia

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18
Q

Describe aminoglycoside antibiotics as protein synthesis inhibitors

A

-Interferes with mRNA translation
-Poorly absorbed in the gut, must be given IV/IM
-Bactericidal
-Activity enhanced by penicillin
-Adverse effects: Ototoxicity and Nephrotoxicity
-Resistance mechanisms include Aminoglycoside Modifying enzymes, target modification and efflux

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19
Q

Describe macrolide antibiotics as protein synthesis inhibitors

A

-Binds 50S subunit, prevents translocation
-Metabolised by demethylation in liver CYP3A4
-Oral (enteric coated)
-Resistance efflux or methylation of ribosomal targets
-Most effective against Gram positives: Legionella, Chlamydia, Mycoplasma
-Bacteriostatic
-Adverse effects include heart arrhythmias, GI disturbance

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20
Q

Describe chloramphenicol antibiotics as protein synthesis inhibitors

A

-Oral/IV
-Bacteriodstatic/ Bactericidal
-Inhibits transpeptidasation
-Metabolised in liver
-Broad spectrum of activity
-Resistance: enzymatic inactivation via acetyltransferase, efflux, ribosomal mutations
-Side effects include grey baby syndrome, bone marrow suppression

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21
Q

What do sulphonamide antibiotics target?

A

Folate synthesis utilising PABA

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22
Q

What do trimethoprim antibiotics target?

A

Tetrahydrofolate production (using folate) which goes on to be used in DNA replication

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23
Q

Describe the mechanism of action of sulphonamides

A

Sulfonamides act by inhibiting the enzyme dihydropteroate synthase, which is involved in the synthesis of dihydrofolic acid from p-aminobenzoic acid (PABA).

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24
Q

Describe mechanisms of resistance to sulphonamides

A

-Overproduction of PABA: Bacteria can produce more PABA, overwhelming the sulfonamide and reducing its effect.
-Mutations in the dihydropteroate synthase enzyme: Bacteria may acquire mutations in the enzyme that make it less susceptible to inhibition by sulfonamides.
-Efflux Pumps: Some bacteria can pump out sulfonamides, reducing their effectiveness.

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25
What are the most common uses of sulphonamides and folate synthesis inhibitors?
-Urinary tract infections (UTIs) -Respiratory tract infections -Gastrointestinal infections, such as shigellosis -Pneumocystis jirovecii pneumonia (PCP) in immunocompromised patients -Toxoplasmosis
26
Describe fluoroquinolone antibiotics
-Inhibits DNA gyrase -Oral and well absorbed -Does not cross BBB -Broad spectrium: gram +ve and -ve and enterobacteria -Inhibits CYP1A2 -Adverse effects: GI effects, prolongation of QT
27
Describe mycobacterial infections, and give an example
-Nonmotile, slow growing -Have very thick, waxy, lipid rich hydrophobic cell walls -Contain mycolic acids in their cell wall -Can survive in macrophages -Major issue in immunocompromised people -eg TB or Leprosy
28
Describe rifampicin antibiotics
-Good against gram positives, negatives and mycobacteria -A semisynthetic derivative of rifamycin -Inhibits prokaryotic DNA-dependent RNA polymerase -Oral crosses BBB -Potent inducer of CYP3A4, increased degradation of glucocorticoids and warfarin
29
Describe Daptomycin antibiotics
-Insertion into the membrane leads to cell death -Gram positive including MRSA, VRSA -Poorly absorbed, must be given IV -Eliminated mainly via renal excretion -Can cause damage to muscoskeletal system, eosinophilic pneumonia and peripheral neuropathy
30
What are the two types of viral families, and give examples
-DNA: Adenovirus, Herpesvirus, Papilomavirus -RNA: Paramyxovirus, Rhabdovirus, Togavirus, Influenza virus, Retrovirus
31
Describe the difficulties surrounding antiviral drugs
-Must penetrate infected cell -High risk of toxicity to healthy cells -Mechanism of action/specificity: Difficult to achieve distributional selectivity, target unique enzymes or metabolic pathways, aiming to interfere with viral nucleic acid synthesis and/or regulation
32
What may antiviral drugs target?
-Viral cell binding and uncoating -Stimulating the host cell immune system -Reverse transcription, DNA or RNA replication -Viral assembly and release
33
What is viral latency
When a virus remains dormant or inactive within a host organism for an extended period, without causing noticeable symptoms or actively replicating
34
What are the types of viral latency, and give examples
-Acute: Rhinovirus, Rotavirus, Influenza -Persistant: Lymphocytic choriomeningitis -Reactivating: Herpes Simplex Virus -Slow: Measles SSPE, HIV
35
Describe the causes of viral latency
-Non replicating cells -Joint replication processes between host and virus -Limited immune detection
36
Give some mechanisms of antiviral resistance
-Mutations in viral enzymes targeted by antiviral drugs -Altered viral target sites -Increased drug efflux -Inhibition of host immune responses
37
Describe Herpesvirus
-Simplex: Cold sores -Varicella zoster: Chicken Pox -Epstein Barr (EBV): Glandular fever -Symptoms include flu-like symptoms (fever, headache, aches and pains) -Infects sensory ganglia where becomes latent, requiring external stimulation of latent infection
38
What is acyclovir an example of?
An antiviral, prodrug nucleoside analogue
39
Describe the mechanism of action of acyclovir
-Viral Thymidine Kinase Activation: Acyclovir is first phosphorylated by viral thymidine kinase (TK), an enzyme encoded by the virus. This step is crucial for the drug's activation, as thymidine kinase is more abundant in infected cells than in uninfected cells, providing some specificity for the drug. -Further Phosphorylation: After the initial phosphorylation, acyclovir is further phosphorylated by host cell enzymes, producing the active form: acyclovir triphosphate. -Inhibition of Viral DNA Polymerase: Acyclovir triphosphate inhibits the viral DNA polymerase, an enzyme essential for viral DNA replication. This blocks the elongation of the viral DNA chain, preventing the virus from replicating. Acyclovir triphosphate also incorporates itself into the viral DNA, leading to chain termination, which stops the DNA replication process.
40
What are the key targets of HIV?
-CD4+ T cells, binding to the CD4 receptor using the gp120 protein -CCR5 and CXCR4 coreceptors on the surface of CD4+ T cells
41
What are the targets for HIV antivirals, and give examples
-Fusion inhibitors (eg enfuvirtide) -CCR5 inhibitors (eg Maraviroc) -Nucleoside Reverse Transcriptase inhibitors (eg Zidovudine) -Non Nucleoside Reverse Transcriptase inhibitors -Protease inhibitors (eg Ritonavir) -Integrase inhibitors (eg Raltegravir)
42
Describe fusion inhibitor HIV antivirals
-Inhibits fusion of cellular and viral membranes -Given by subcutaneous injection -Most effective as combination therapy -Mild injection site reactions due to hypersensitivity -Emergence of resistance due to mutations in outer envelope Glycoprotein GP41
43
Describe CCR5 inhibitor HIV antivirals
-Maraviroc binds to the CCR5 receptor on the membrane of human CD4 cells -This binding prevents the interaction of HIV1 GP120 and human CCR5 receptor which is necessary for entry into the cell
44
Describe NRTIs (nucleoside reverse transcriptase inhibitors) HIV antivirals
-Potent inhibitor of HIV replication in vitro, active when phosphorylated intracellularly to its triphosphate, inhibits viral reverse transcriptase, as triphosphate competes for proviral synthesis, leading to premature termination of viral DNA elongation. -Life long therapy, with a risk of toxicity as it also inhibits mammalian DNA polymerases. -Headaches, nausea, anaemia, leucopenia, neutropenia associated, with resistance growing
45
Describe NNRTI (Non-nucleoside reverse transcriptase inhibitors) HIV antivirals
-Bind to the NNRTI binding pocket, inducing a conformational change inhibiting its ability to convert HIV RNA to DNADe
46
Describe Protease inhibitor HIV antivirals
-HIV replication involves the translation of its RNA into long polyproteins (Gag and Gag-Pol). These polyproteins must be cleaved by HIV protease to produce functional viral proteins. -Protease inhibitors bind to the active site of the protease enzyme and prevent it from performing this crucial cleavage -Inhibits CYPs
47
Describe integrase inhibitor HIV antivirals
-Integrase enzyme facilitates the integration of viral DNA into the host cell's genome. Once integrated, the virus can begin the process of replication, creating new viral particles. -Integrase inhibitors block this crucial step by binding to the active site of the integrase enzyme. This binding prevents the viral DNA from integrating into the host genome, which stops the virus from replicating.
48
What does Highly Active Antiretroviral Therapy consist of?
HAART typically includes following classes: -Nucleoside reverse transcriptase inhibitors (NRTIs) -Non Nucleoside Reverse transcriptase inhibitors (NNRTIs) -Protease inhibitors
49
What is inflammation?
-Protective response of vascularised tissues to infections and damaged tissues -Brings cells and molecules of host defence from the circulation to the sites where they are needed -in order to eliminate the offending agents
50
What are the steps of the inflammatory response?
-Recognition of the offending agent / injury -Recruitment of leukocytes -Removal of the offending substance -Regulation of the response -Repair of damaged tissue
51
What are the two types of inflammation?
-Acute inflammation -Chronic inflammation
52
Describe acute inflammation
-Rapid onset -Short duration -Mainly neutrophils -Prominent characteristic response
53
Describe chronic inflammation
-Slow onset -Long duration -Monocytes/macrophages/lymphocytes -Less characteristic response
54
Give the local clinical aspects of acute inflammation
-Redness (rubor) -Heat (calor) -Swelling (tumor) -Pain (dolor) -Loss of function
55
What are the three major components of acute inflammation?
-Dilation of small vessels, slowing blood flow (vascular) -Increased vascular permeability of the microvasculature (vascular) -Emigration of the leukocytes (cellular)
56
Give some key inflammatory mediators
-Histamine -Plasma proteins -Prostaglandins -Leukotrienes -Cytokines -Chemokines
56
Describe Bradykinin
-Made from kininogens (plasma proteins) -Increases vascular permeability by gap junction dissociation -Increases histamine release from mast cells -Increased local endothelial eicosanoid production
57
Name and describe the effect of two eicosanoids
-Prostaglandin: vasodilation and increased permeability -Leukotrienes: Leukocyte recruitment and vascular permeability
58
What are the two main cellular mediators of chronic inflammation
-Macrophages (secreting cytokines, propagating inflammation) -Lymphocytes (Secreting antibodies and cytokines, propagating inflammation)
59
Give drug classes used to reduce inflammatory and immune responses
-Steroidal anti inflammatory agents -Disease modifying antirheumatoid drugs (DMARD) -Immune checkpoint inhibitors -Antihistamines -Immunosuppressants -Nonsteroidal anti inflammatory agents (NSAIDs)
60
What do pattern recognition receptors bind?
-Pathogen associated molecular patterns (PAMPs): eg LPS, peptidoglycan -Damage associated molecular patterns (DAMPs): released by host cells when they are damaged or stressed
61
Give some key pattern recognition receptors
-Toll like receptors (TLR) -NOD like receptors (NLR) -RIG I like receptors (RLR) -C type lectin receptors (CLR)
62
Describe how PPR binding leads to inflammatory response
-Bionding activates transcription via NFKB, IRF3/7, MAPK -This leads to secretion of pro inflammatory cytokines -Recruiting macrophages, dendritic cells and neutrophils (inflammation)
63
Describe the steps of the arachidonic acid pathway
-Membrane phospholipids are converted to arachidonic acid by phospholipase A2 -Cyclooxygenase (COX) converts this to prostaglandins or thromboxanes -5 lipooxygenase (5LOX) converts this to Leukotriene A4 -Which are then converted to leukotriene C4 or Leukotriene B4
64
What is lipocortin, and what can it be used for?
-Inhibitor of phospholipase A2 -Glucocorticoids eg dexamethasone stimulate lipocortin expression
65
Give the differences in expression and function of COX1 and COX2
-COX1 has constitutive expression, COX2 has inducible (activated by inflammation, injury) -COX1 main function is homeostasis (gastric protection, platelet function) COX2 main function is inflammatory response
66
What are the products of COX1?
-Thromboxane A2 (promotes platelet aggregation, vasoconstriction) -PGE2, PGE2 (maintains mucosal blood flow and stimulates mucus production)
67
What are the products of COX2
-PGE2 in joints (main driver of joint inflammation, leading to pain, swelling) -PGI2 (opposes TXA2, preventing excessive clotting and keeping vessels dilated)
68
What is the use of naproxen?
-NSAID -Strong antiinflammatory response -Including chronic inflammation -Short term analgesic
69
What is the use of ibuprofen?
-NSAID -Moderate antiinflammatory response -Used initially against chronic inflammation -Short term anaglesia
70
What is the use of piroxicam?
-NSAID -Strong anti-inflammatory response -Long term treatment of chronic inflammation -Long term analgesia
71
Describe the mechanism of actions of NSAIDs
-Reversible competitive inhibition eg ibuprofen -Reversible non competitive inhibition eg paracetamol (not NSAID though) -Irreversible inhibition eg aspirin
72
What causes the side effects associated with NSAIDs?
Inhibition of COX1 housekeeping enzymes
73
Describe what causes fever/pyrexia in inflammation
-Cytokines migrate to the brain, binding to receptors on endothelial cells -Activating prostaglandin E2 synthesis -Which activates the hypothalamus, leading to fever
74
What are the gastrointestinal adverse effects surrounding COX1 inhibition?
-Dyspepsia, nausea, vomiting from mucosal damage and bleeding in stomach -Inhibitiom of synthesis of stomach PGE2, decreasing gastric acid and increasing mucus
75
What are the renal adverse effects surrounding COX1 inhibition?
-Renal insufficiency and continued treatment can lead to renal damage -Inhibition of synthesis of PGI2 (COX2) and PGE2 (vasodilation and transport of sodium, leading to natriureisis)
76
What are the respiratory adverse effects surrounding COX1 inhibition?
-Bronchospasm -Seen in viral infection patients using aspirin
77
What is the issue surrounding COX2 inhibitors?
Increased risk of: -Thrombotic events -Heart attack -Stroke With prolonged use
78
What causes the issues surrounding COX2 inhibition?
-Imbalances between anti and pro-thrombotic prostanoids -As COX2 produces PGI2 which decreases platelet aggregation and causes vasodilation -Meaning platelet thromboxanes lead to thrombosis and vasoconstriction
79
How does cortisol mediate anti-inflammatory effects
-Induces lipocortin which inhibits phospholipase A2 -Inhibiting all levels of inflammation (acute, chronic)
80
Give the action of inducing lipocortin and hence inhibiting phospholipase A2
-Decreases inflammatory mediators -Decreases capillary permeability -Decreases phagocytic action of leucocytes -Decreases histamine release -Decreases activity of mononuclear cells and proliferation/repair of tissue -Decreases thromboxanes
81
What are hypersensitivity reactions?
Exaggerated or inappropriate immunologic responses occurring in response to an antigen or allergen
82
Give the 4 main types of hypersensitivity reactions
-Type I: Reaction mediated by IgE antibodies -Type II: Cytotoxic reaction mediated by IgG or IgM antibodies -Type III: Reaction mediated by immune complexes -Type IV: Delayed reaction mediated by cellular response
83
Describe the stages of mast cell degranulation during type I hypersensitivity
SENSITISATION: -Upon first exposure to allergen, APC processes antigen and presents it to TH2 cell -TH2 cells release IL4 and IL12, activating B cell -B cells proliferate into plasma cells, secreting IgE -IgE binds to mast cells by Fc region, sensitising the mast cells RE-EXPOSURE -Upon exposure, mast cells with IgE bind to antigen and release inflammatory molecules, resulting in allergy symptoms
84
What may mast cells release during degranulation
-HISTAMINE (most important) -Prostaglandin -Platelet activating factor -Leukotrienes -Heparin -Tryptase
85
What may inflammatory mediators released by mast cell degranulation lead to?
-Bronchospasm -Rhinitis -Erythema -Cutaneous and pulmonary oedema -Eosinophilia
86
Give examples of localised type I hypersensitivity reactions
-Hay fever -Hives/uticaria -Asthma -Angioedema
87
Give an example of a systemic type I hypersensitivity reaction
Anaphylaxis
88
Describe symptoms of allergic rhinitis
-Red and itchy, watery eyes -Sneezing, congestion, runny nose -Itchy or sore throat, post nasal drip, cough -Fatigue
89
Describe how antihistamines mediate their effects
Most clinical antihistamines are H1 receptor inverse agonists
90
Give the difference between first and second generation antihistamines (and give examples)
-First-generation antihistamines (e.g., diphenhydramine, chlorpheniramine) are sedating because they cross the blood-brain barrier, leading to drowsiness and sedation. -Second-generation antihistamines (e.g., loratadine, cetirizine) are non-sedating as they do not cross the blood-brain barrier (or do so minimally), resulting in fewer CNS effects
91
What are the mechanisms of action of immunosuppressants?
Primarily by blocking the expression and activity of T cell growth factor and activating cytokine IL2
92
Give types of immunosuppressants, and example compounds
-Glucocorticoids: Prednisolone -Calcineurin inhibitors: Tacrolimus or Cyclosporine -Dual Calcineurin/mTOR inhibitors: Sirolimus -IL2 receptor antagonists: Daclizumab/Basiliximab -Nucleic acid synthesis antagonists: MMF -T cell receptor antagonists: Muromonab
93
What do glucocorticoids target?
-Costimulation signals -IL2 Gene expression -GR complexes directly bind to p65 of NFKB, preventing activation of these inflammatory genes -GR promotes IKBa synthesis, preventing p50/p65 nuclear translocation, preventing activation
94
What do calcineurin inhibitors target?
-Calcineurin -An enzyme crucial for activating T cells -Preventing Calcineurin from removing phosphate group from NFAT -Meaning it cannot activate IL2 gene
95
What do TCR inhibitors target?
-T cell receptor -Blocking its interaction with antigen-presenting cells and preventing T-cell activation and proliferation.
96
What do IL2 receptor inhibitors target?
-IL2 receptor -By blocking these, they prevent T cell activation and proliferation
97
What do mTOR inhibitors target?
-mTOR (mechanistic target of rapamycin) pathway Which is essential for cell growth and proliferation. -Inhibiting mTOR suppresses T-cell activation and reduces immune responses.
98
What do nucleic acid synthesis inhibitors target?
-Synthesis of purines or pyrimidines -Which are necessary for DNA and RNA production. -This inhibition prevents the proliferation of immune cells like T and B cells, thereby suppressing the immune response.
99
Describe immunotherapy
-immune cells can be stimulated or inhibited by a range of immune cell checkpoint protein interactions -PD1 receptor antagonists prevent tumour cells from binding to and inactivating PDL1, enabling T cells to remain active
100
Give examples of targets of antibiotics
-Cell wall synthesis -Membrane synthesis -Protein synthesis -Metabolic pathways -Nucleic acid synthesis
101
Give examples of penicillins
-Amoxicillin -Flucloxacillin -Benzylpenicillin -Mecillinam
102
Give examples of non-penicillin cell wall targeting antibiotics
-Cycloserine -Vancomycin -Cefaclor -Cephalexin
103
Give examples of protein synthesis inhibiting antibiotics
-Chloramphenicol -Erythromycin -Tetracycline -Streptomycin
104
Give examples of antibiotics that inhibit folate synthesis or utilisation
-Trimethoprim -Sulfamethoxazole -Sulfacetamide -Sulfanitran

PED2006 Systems Pharmacology (5 decks)

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