DRUGS BLOCK 13 Flashcards
ISONIAZID
- In order to covert when given isoniazid is first converted by a mycobacterial enzyme called peroxidase, into its active metabolite: IPRONIAZID
- Iproniazid inactivates enzymes associated with MYCOLIC ACID synthesis, and mycolic acid is needed to build bacterial cell walls
- It also INHIBITS MYCOBACTERIAL PEROXIDASE preventing the bacteria from metabolizing hydrogen peroxide, which accumulates inside the cell causing serious damage.
PACLITAXAL
Interfering with the formation of microtubules will cause mitosis to fail and the cell will eventually die without replicating.
All anticancer microtubule inhibitors are given intravenously.
DRUG CLASS: TAXANE – microtubule inhibitor
INDICATION: lung cancer (metastatic– small cell lung cancer), breast and ovarian cancer.
MOA: So they act like cement that overstablizes the microtubules and prevents them from depolymerizing and breaking down.This is a problem because the microtubules need to break down during anaphase so the cell can divide
Impaired degradation of the polymerised microtubules
CISPLATIN
DRUG CLASS: Chemotherapy drug
INDICATION: testicular tumours, ovarian tumours and bladder cancer
MOA: DNA Alkylating agent > DNA crosslinking > decrease DNA replication
RIFAMPICIN
DRUG CLASS: Antibiotic
INDICATION: Myobacterial infections including latent or active TB
MOA:
Rifampin acts via the inhibition of DNA-dependent RNA polymerase, leading to a suppression of RNA synthesis and cell death.
Side Effects: Rifampicin can cause red/orange discolouration of secretions, such as urine and tears.
ISONIAZID
Indication: active or latent TB
MOA: Isoniazid > Iproniazid.
- Iproniazid prevents the formation of mycolic acid which is needed to build the bacterial cell walls.
- Also inhibits myobacterial peroxidase which would usually metabolise hydrogen peroxidase so it doesn’t harm the bacteria. By preventing it from metabolising we are allowing it to accumulate and cause serious cell damage.
Side effect: Isoniazid can cause peripheral neuropathy. Pyridoxine (vitamin B6) is co-prescribed to reduce the risk.
ETHAMBUTOL
DRUG CLASS: TB med
Indication: Treatment and prophylaxis of TB
MOA: blocking arabinosyltransferase, which synthesizes the arabinogalactan that’s used in the bacterial cell wall.
SIDE EFFECT:
optic neuritis, which decreases visual acuity and the ability to differentiate between red and green ( colour blindness)
PYRAZINAMIDE
INDICATION: TB
MOA: converted to its active form PYRAZINOIC ACID.
This medication inhibits mycobacterial fatty acid synthase which is an enzyme that also participates in the synthesis of mycolic acid.
SIDE EFFECT:
Decreases the renal excretion of uric acid - HYPERURICEMIA- gout
CIPROFLOXACIN
Drug class: second generation fluoroquinolone. It is an antibiotic
Indication: bacterial infections including resp infections and UTI
Mechanism of action:
- acts on bacterial topoisomerase II ( DNA gyrase) and topoisomerase IV
- Ciprofloxacin’s targeting of the alpha subunits of DNA gyrase prevents it from supercoiling the bacterial DNA which prevents DNA replication
SALBUTOMOL
Drug class: Beta 2 agonist
Indication: Asthma, Bronchitis, COPD
MOA:
Bind to b2 receptors on the lungs
SALMETEROL
Drug Class: B2 agonist
Indication: Asthma and COPD
MOA:
- is a long-acting beta-2 adrenergic receptor agonist used to treat asthma and COPD.
BUDESONIDE
Drug Class: Steroid
Indication: Asthma, Crohn’s disease, ulcerative collitis, COPD
MOA:
- decreased leukocyte migration to sites of inflammation
Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days
MONTELUKAST
Drug Class: Leukotriene receptor antagonist
Indication: as part of asthma regime, ASTHMA PROPHYLAXIS especially really good at preventing exercise induced bronchoconstriction and also relieve seasonal allergic rhinitis
ONLY TAKEN ORALLY
MOA:
IPRATROPIUM
Drug Class: Anticholinergic drug
Indication: severe asthma flares
Usually given with b2 agonist in an inhaler
MOA:
muscarinic acetylcholine receptor antagonist
The function of the parasympathetic system in the airway is to generate bronchial secretions and constriction and hence, the inhibition of this action can lead to bronchodilation and fewer secretions.
Leukotrine Antagonists
Leukotriene receptor antagonists like montelukast and zafirlukast are peroral medications that bind to the leukotriene receptors in the smooth muscles of the respiratory airways and prevent leukotriene from binding.
This weakens smooth muscle contraction in the respiratory tract, decreases mucus secretion, and reduces inflammation
HOW leukotrines cause inflammation
Allergens from environmental triggers, like air pollutants or cigarette smoke, are picked up by dendritic cells which present them to a type 2 helper T cell or Th2 cell in the lamina propria. These cells then produce cytokines like IL-4 and IL-5 which causes the inflammatory response.
IL-4 is especially important because it leads to the production of IgE antibodies by B cells, and these antibodies bind to FcεR1 receptors on mast cells to activate them.
These mast cells use an enzyme called phospholipase A2 to take membrane phospholipids and make a 20 carbon polyunsaturated fatty acid called arachidonic acid.
Arachidonic acid is then metabolized by two important enzymes: one is cyclooxygenase-2 or COX-2, which makes prostaglandins, another one is 5-lipoxygenase or 5-LOX, which makes leukotrienes.
Now, IL-5 on the other hand, activates eosinophils, which promote an immune response by releasing more cytokines and leukotrienes.
Minutes after exposure to the allergen, phospholipase A2 gets activated inside the mast cells, which results in the synthesis and release of leukotrienes and the prostaglandins.
Leukotrienes bind with the leukotriene receptors on the bronchial smooth muscles and cause them to contract. They also bind to receptors on the mucous glands to increase mucus secretion.
Similarly, prostaglandins also bind to their receptors in smooth muscles and mucus glands to cause a similar effect. These mediators also increase the vascular permeability in the airways and attract more immune cells to the area.
The combination of inflammation and bronchospasm cause obstruction of the airway which leads to symptoms like coughing, chest tightness, dyspnea, or difficulty breathing, and wheezing, which is a high-pitched whistling sound during exhalation.
