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Disease Processes > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Mechanism of statins

A
  • Lipid/cholesterol lowering agents
  • Inhibit HMG-coA reductase which plays a role in cholesterol production
  • Increases LDL (bad cholesterol) uptake by the liver
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2
Q

Mechanism of fibrates

A
  • Lipid/cholesterol lowering agents
  • Activate PPAR
  • Induces transcription of genes that facilitate lipid metabolism
  • Increases HDL levels (good cholesterol)
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3
Q

Class and mechanism of penicillin

A
  • Broad spectrum, bactericidal beta-lactam
  • Inhibit bacterial cell wall synthesis by preventing cross linking of peptides by binding to the transpeptidase enzyme (PBPs), preventing bacterial cell wall formation
  • Cell walls are improperly made, this allows water to flow into the cell, causing it to burst (cytolysis)
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4
Q

Different examples of macrolides

A

Macrolides are a class of antibiotic that includes erythromycin, roxithromycin, azithromycin and clarithromycin

  • Used for patients with penicillin allergy
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5
Q

First-line indications for macrolides

A

First-line indications for macrolides include the treatment of atypical community acquired pneumonia, H. Pylori (as part of triple therapy), chlamydia and acute non-specific urethritis.

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6
Q

Cephalosporin class?

A

Beta lactam, bactericidal

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7
Q

Mechanism of cephalosporin

A
  • Mimic the D-Ala-D-Ala site, irreversibly inhibiting the PBP cross-linking of the peptidoglycan bacterial cell wall
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8
Q

Indications of cephalosporin

A 
Septicaemia
Pneumonia
Meningitis
Biliary-tract infections
Peritonitis
Urinary-tract infections
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9
Q

Examples of nucleoside reverse transcriptase inhibitors

A

Abacavir
Tenofovir
Emtricitabine

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10
Q

Mechanism of nucleoside reverse transcriptase inhibitors

A

Stop HIV changing ssRNA to dsDNA

- They cause chain termination after they have been incorporated into DNA

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11
Q

Examples of NNRTIs

A

Nevirapine
Efavirenz
Etravirine

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12
Q

Mechanism of NNRTIs

A

Stop HIV from changing ssRNA into dsDNA

  • They have a high affinity for the hydrophobic binding pocked located near the active site of HIV reverse transcriptase, so it cannot catalyse DNA polymerisation
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13
Q

Mechanism of protease inhibitors

A

Block new HIV from being cut into smaller pieces and from being reassembled into new, infectious particles
- Mimic the natural peptide substrate of HIV called aspartyl protease enzyme

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14
Q

Mechanism of integrase inhibitors

A

Block HIV from being integrated into the cell DNA
- They target HIV integrase, responsible for the integration of viral genetic material into human DNA, a crucial step in the replication cycle of HIV

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15
Q

Mechanism of entry inhibitors

A

CCR5 antagonists
- Bind to CCR5 receptor which blocks HIV protein gp120 from association with the receptor, so it is unable to enter human macrophages and T cells, but it can use CXCR4 instead

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16
Q

Mechanism of attachment and post-attachment inhibitors

A
  • Bind to the gp120 portion of HIV envelope protein that makes up the spikes of the virus
  • Prevents HIV from attaching to CD4 receptor on T cells, which it uses to gain entry to the cell plasma membrane
17
Q

Class and mechanism of clotrimazole

A

Anti fungal - lanosine demethylase inhibitor

Inhibition of yeast 14-alphademethylase, a cytochrome p450 enzyme which converts lanosterol to ergosterol, an important component of the fungal cell membrane
- Causes increased membrane permeability and possibly disruption of membrane bound enzymes

18
Q

Class and mechanism of fluconazole

A
  • Lanosine demethylase inhibitor
  • Anti-fungal
  • Inhibits 14-alpha-demethylase, a cytochrome p450 enzyme which converts lanosterol into ergosterol, an important component of the fungal cell membrane
19
Q

Class and mechanism of nystatin

A
  • Ionophore
  • Anti-fungal
  • Binds ergosterol in fungal cell membranes, causes formation of pores in the membrane, leading to potassium and other cellular constituents leakage, causing cell death
20
Q

Class and mechanism of Amphotericin

A
  • Ionophore
  • Binds ergosterol in fungal cell membranes
  • Pore formation in membrane
  • Leakage of contents, e.g. K+ and other constituents
  • Cell death
21
Q

Class and mechanism of betamethasone & clobetasone

A
  • Glucocorticoid receptor agonist
  • Anti-inflammatory, anti-pruritic and vasoconstrictive properties
  • Binds to receptor, which then translocates to the nucleus and binds to glucocorticoid response elements, causing the increase or decrease of specific target genes, having anti-inflammatory actions:
    1. Induction of lipocortin-1 synthesis
    2. Cox-1 and Cox-2 expression is suppressed, decreasing eicosanoid production
22
Q

Class and mechanism of imatinib

A
  • Tyrosine kinase inhibitor
  • Targets the Bcr-Abl tyrosine kinase (oncoprotein - CML)
  • Inhibits cell proliferation driven by Bcr-Abl positive cells
  • Induces apoptosis
23
Q

Class and mechanism of dacarbazine & cyclophosphamide

- Which stage of the cell cycle does it act on

A
  • Alkylating agent (chemotherapy)
  • Bind covalently to DNA via their alkyl group to guanine, preventing the strands from linking as they should
  • Causes the breakage of DNA strands and then death of the cancer cell as it cannot multiply
  • CELL CYCLE INDEPENDENT - works at any point
24
Q

Class and mechanism of vinblastine

A
  • Anti-microtubule agent
  • Block cell division by preventing microtubule function
  • Prevents cancer cells from completing mitosis, leading to apoptosis
25
Q

Class and mechanism of etoposide

- Which stage of the cell cycle does it act on

A
  • DNA topoisomerase II inhibitor
  • Inhibits DNA topo II, thereby inhibiting DNA re-ligation
  • Causing errors in DNA synthesis, leading to apoptosis
  • S and G2
26
Q

Class and mechanism of 5-fluorouracil

- Which stage of the cell cycle does it act on

A
  • Anti-metabolite
  • Pyrimidine analogue
  • Anti-metabolites masquerade as purine or pyrimidine and become incorporated into DNA.
  • Acts on the S phase of the cell cycle, stopping normal development and division
27
Q

Ciprofloxacin class and mechanism

A
  • Quinolone = topo II inhibitor
  • Inhibits topo II (DNA gyrase) which are required for bacterial DNA replication, transcription, repair, strand supercoiling repair, and recombination
28
Q

Class and mechanism of vancomycin

A
  • DRUG OF LAST RESORT
  • Not active against gram-negative bacilli, mycobacteria or fungi
  • Inhibition of NAM-NAG peptide subunits into the peptidoglycan matrix, which is a major structural component of the Gram-positive cell walls
29
Q

Class and mechanism of sulfamethoxazole.

- Indications

A
  • PABA analogue
  • Competes with PABA in binding to dihydrofolate synthetase
  • Inhibition of dihydrofolate synthetase will inhibit the synthesis of tetrahydrofolic acid (THF)
  • THF is required for the synthesis of purines and dTMP
  • Inhibition of THF synthesis inhibits bacterial growth
  • Similar to trimethoprim
  • Indications: bronchitis, prostatitis, UTIs
30
Q

Class and mechanism of trimethoprim

A
  • Used for UTI and acute/chronic bronchitis
  • Folate antagonist
  • Binds to dihydrofolate reductase, inhibiting the reduction of dihydrofolic acid to tetrahydrofolic acid
  • THF is an essential precursor in the thymidine synthesis pathway and therefore inhibition of this will inhibit bacterial DNA synthesis
31
Q

Class and mechanism of rifampicin

A

Broad spectrum anti-biotic - RNA/DNA polymerase inhibitor
- Antimycobacterial

  • Its mode of action is via the inhibition of DNA-dependent RNA polymerase, leading to a suppression of RNA synthesis and cell death
32
Q

Class and mechanism of gentamicin

A
  • Aminoglycoside antibiotic
  • 30S/50S inhibitor
  • Broad-spectrum
  • Bind to bacterial 30S ribosomal subunit, inhibiting protein synthesis
  • Treat TB and gram-positive infections
  • Can cause significant ear and kidney damage
33
Q

Class and mechanism of erythromycin

- Indications

A
  • Macrolide antibiotic
  • 50S inhibitor
  • Reversibly binds 50S subunit of bacterial ribosomes at the donor binding site, blocking the translocation of peptides from the acceptor site to the donor site, inhibiting protein synthesis
  • Respiratory infections
  • Syphillis
  • Skin infections
  • Chronic prostatitis
  • ONLY EFFECTIVE AGAINST DIVIDING ORGANISMS
34
Q

Class and mechanism of oxytetracycline

A
  • Broad spectrum antibiotic - 30S inhibitor
  • Mechanism: inhibition of bacterial cell wall growth by binding to the 30S ribosomal subunit. Preventing amino-acyl tRNA from binding to the A site of the ribosome, causing inhibition of translation
35
Q

Class and mechanism of benzylpenicillin / penicillin G

A
  • Transpeptidase inhibitor
  • Use for gram-positive organisms
  • Binds to PBP, causing the inhibition of bacterial cell wall synthesis

Disease Processes (31 decks)

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