MECHANISM OF ACTION Flashcards
causes degenerative alterations in the tegument and intestinal cells of the worm by binding to the colchicine-sensitive site of tubulin, thus inhibiting its polymerization or assembly into microtubules.
MEBENDAZOLE
The loss of the cytoplasmic microtubules leads to impaired uptake of glucose by the larval and adult stages of the susceptible parasites and depletes their glycogen stores.
The loss of the cytoplasmic microtubules leads to impaired uptake of glucose by the larval and adult stages of the susceptible parasites and depletes their glycogen stores.
Degenerative changes in the endoplasmic reticulum, the mitochondria of the germinal layer, and the subsequent release of lysosomes result in decreased production of adenosine triphosphate (ATP), which is the energy required for the survival of the helminth.
Due to diminished energy production, the parasite is immobilized and eventually dies.
Adverse Effects
Diarrhea, abdominal pain
Symptoms of overdose include** elevated liver enzymes, headaches, hair loss, low levels of white blood cells (neutropenia)**, fever, and itching
By promoting the release of acetylcholine, inhibiting cholinesterase, and stimulating ganglionic neurons, serves as a depolarizing neuromuscular blocking agent in helminths
PYRANTEL PAMOATE
This causes extensive depolarization of the helminth muscle membrane, resulting in tension to the helminth’s muscles, leading to paralysis and release of their attachment to the host organism’s intestinal walls
GABA receptor agonist
PIPERAZINE
binds directly and selectively to muscle membrane GABA receptors, presumably causing hyperpolarization of nerve endings, resulting in flaccid paralysis of the worm.
PIPERAZINE
While the worm is paralyzed, it is dislodged from the intestinal lumen and expelled live from the body by normal intestinal peristalsis.
Mechanism of action is thought to involve sensitizing the microfilariae to phagocytosis
is an inhibitor of arachidonic acid metabolism in microfilariae.
DIETHYLCARBAMAZINE
This makes the microfilariae more susceptible to innate immune attack but does not kill the parasites outright
Host destruction of parasites results, depending on the parasite, in severe but reversible reactions, including leukocytosis, retinal hemorrhages and ocular complications, tachycardia, rash, fever, encephalitis, and lymph node enlargement and swelling.
binds selectively and with high affinity to glutamate-gated chloride ion channels in invertebrate muscle and nerve cells of the microfilaria.
also is believed to act as an agonist of the neurotransmitter gamma-aminobutyric acid (GABA), thereby disrupting GABA-mediated central nervous system (CNS) neurosynaptic transmission
IVERMECTIN
works by causing severe spasms and paralysis of the worms’ muscles. This paralysis is accompanied - and probably caused - by a rapid Ca 2+ influx inside the schistosome
Secondary effects are inhibition of glucose uptake, lowering of glycogen levels, and stimulation of lactate release
PRAZIQUANTEL
Inhibits parasite respiration.
It is an alternative for Fasciola hepatica (sheep liver fluke infection) and an alternative to praziquantel for acute pulmonary paragonimiasis
BITHIONOL
Acts by the uncoupling of the electron transport chain to ATP synthase.
The disturbance of this crucial metabolic pathway prevents the creation of adenosine triphosphate (ATP), an essential molecule that supplies energy for metabolism.
NICLOSAMIDE
inhibits oogenesis and spermatogenesis.
The compound also inhibits thephosphofructokinaseenzyme, leading to glycogen depletion.
NIRIDAZOLE
Niridazole hascentral nervous systemtoxicity and can cause hallucinations.
Also, it may cause allergic reactions in sensitive people.
Agonistic activity towards the L-subtype nicotinic acetylcholine receptors in nematode muscles
This agonistic action reduces the capacity of the males to control their reproductive muscles and limits their ability to copulate.
LEVAMISOLE
Levamisole is an immunostimulant that has been shown to increase NK cells and activated T-cells in patients receiving this adjuvantly along with 5FU for Stage III colon cancer.
An antibiotic that binds to ergosterol, a major component of fungal cell membranes. It forms pores that alter membrane stability and allow leakage of cellular contents.
AMPHOTERICIN B
selectively inhibit the cytochrome P–450-mediated sterol demethylation of lanosterol to ergosterol in fungal membranes
inhibits the transformation of yeast cells into hyphae, the invasive and pathogenic form of the parasite
AZOLE ANTIFUNGALS
Prevents the synthesis of ergosterol, the fungal equivalent of cholesterol, thereby increasing membrane fluidity and preventing growth of the fungus
KETOCONAZOLE
noncompetitively inhibit the synthesis of a major fungal cell wall component, β-(1,3)-d-glucan, which is not present in mammalian cell walls.
ECHINOCANDINS
CASPOFUNGIN, ANIDULAFUNGIN, AND MICAFUNGIN
intrafungally converted into the cytostatic fluorouracil which undergoes further steps of activation and finally interacts as 5-fluorouridinetriphosphate with RNA biosynthesis thus disturbing the building of certain essential proteins
also undergoes conversion into 5 fluorodeoxyuridinemonophosphate which inhibits fungal DNA synthesis
FLUCYTOSINE
The drug binds to tubulin, interfering with microtubule function, thus inhibiting mitosis.
It binds to keratin in keratin precursor cells and makes them resistant to fungal infections.
GRISEOFULVIN
Inhibit squalene epoxidase, resulting in the accumulation of squalene inside the fungal cells.
Decrease the ability of fungi to make sterols
TERBINAFINE, TOLNAFTATE
exerts its effects by reversibly inhibitingDNA-dependent RNA polymerase, which further inhibits bacterial protein synthesis and transcription.
Rifampin
pro-drug that is converted to its active form metabolite by catalase-peroxidase and exerts its action by further inhibiting the biosynthesis of mycolic acid.
Isoniazid
