Drug list Flashcards
Paracetamol
Drug class: NSAID
Indication: pain, fever
Contraindications:
Side effects:
Amoxicillin
(ANTIBIOTIC CHOICE FOR PREGNANT WOMEN)
Drug class: Penicillin antibiotic (Broad Spectrum)
Indication: Treatment of infections.
H. pylori infections - Peptic ulcers
Haemophillius influenza - Resp infections and Pneumonia
Salmonella, Listeria Sp. -
Diarrhea
Used for infections caused by gram positive and gram negative bacteria
Mechanism of action:
-inhibits penicilin binding protein/DD Transpeptidase
- stops glycosyltransferase and transpeptidase reactions
- which stops to the crosslinking of D-alanine and D-aspartic acid in bacteria walls
Contraindications:
- allergic to penicillin (anaphylaxis)
Side effects: diarrhoea and nausea
SAFE FOR PREGNANCY
Cefuroxime
Drug class:
2nd generation Cephalosporin Antibiotic
Indication: Treat bacterial infections e.g. bronchitis, sinusitis
Mechanism:
- beta-lactam antibiotic
- binds to PBPs (penicillin - binding proteins) located inside the bacterial cell wall
- inhibits third and last stage of bacterial cell wall synthesis
Benzylpenicilin
Drug class: Antibiotic
Indication: bacterial infections
Mechanism:
- binds to PBPs (penicillin - binding proteins) located inside the bacterial cell wall
- inhibits third and last stage of bacterial cell wall synthesis
Oxytetracycline
Drug class: Tetracycline antibiotic
Indication: infections caused by gram positive and gram negative bacteria
Mechanism:
- inhibits cell growth by inhibiting translation
- binds to 30s ribosome subunit and prevents amino-acyl tRNA from binding to the A site of the ribosome.
Erythromycin
Drug class: macrolide antibiotic
Indication:
- bacteriostatic drug
- against infections
Mechanism: Inhibits protein synthesis by binding to the 23S ribosomal RNA molecule and 50S subunit
Contraindicated: in people with liver disease (hepatotoxicity) because of cytochrome p450.
Gentamycin
Drug class: aminoglycoside antibiotic
Indication: bacterial infections
Mechanism:
- bactericidal
- passes through gram-negative membrane in an oxygen-dependent active transport
Rifampicin
Drug class: Antibiotic
Indication: TB infections
Mechanism: Inhibition of DNA-dependent RNA polymerase leading to suppression of RNA synthesis and cell death
Trimethoprim
Drug class: antifolate antibiotic
Indication:
- used in combination with sulfamethoxazole
- uncomplicated urinary tract infections
Mechanism:
- is a reversible inhibitor of dihydrofolate reductase
which converts DHF (dihydrofolic acid) into THF (tetrahydrofolic acid)
- THF is necessary for the biosynthesis of bacterial nucleic acids
Sulfamethoxazole
Drug class: sulfonamide antibiotic
Indication:
-given in combination with trimethoprim
- treats infections (mainly UTI)
Mechanism:
- Sulfamethoxazole competitively inhibits dihydropteroate synthase, the enzyme responsible for bacterial conversion of PABA to dihydrofolic acid
-inhibits bacterial dihydrofolic acid synthesis due to its similarity to PABA (para-aminobenzoic acid)
- Most bacteria meet their need for folic acid by synthesizing it from PABA,
Vancomycin
Drug class: glycopeptide antibiotic
Indication: used to treat severe but susceptible bacterial infections such as MRSA
Mechanism:
- inhibition of cell wall biosynthesis
- Vancomycin forms hydrogen bonds with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides, preventing the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix
Colistin
Drug class: polymyxin antibiotic
Indications: bacterial infections caused by gram negative bacteria
Mechanism of action: disrupts the bacterial cell membrane
Ciprofloxacin
Drug class: second generation fluoroquinolone
Indication: bacterial infections
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
Fusidic acid
Drug class: topical antibacterial
Indications:
-used to prevent and treat mild to moderate skin infections
Mechanism:
- bacteriostatic antibiotic
- fusidic acid works by interfering with bacterial protein synthesis
- prevents the translocation of the elongation factor G (EF-G) from the ribosome.
- It can also inhibit chloramphenicol acetyltransferase enzymes.
Antiherpes medications
- specific antiviral medications are used to treat herpes. These are called anti-herpes medications.
These antivirals can be used to treat:
- Herpes infections (caused by Herpes Simplex Virus)
- Varicella Zoster Virus (VZV)
- Cytomegalovirus (CMV)
Antiherpes medications can be split into two categories:
- Guanosine analogs
- viral DNA polymerase inhibitors
HSV (herpes simplex virus)
- HSV infects skin and mucosal epithelial cells
- There are two types of HSV: HSV1 and HSV2
HS1: generally causes infections above the waist:
- lips: herpes labialis
-mouth and gums: gingivostomatitis
- rare cases it can spread to the esophagus: esophagitis
- rare case spread to CNS: meningitis or encephalitis
HS2: infections below the waist
- genital organs: herpes genitalis
- HSV can pass from a mother to a baby when the baby passes through the infected maternal vaginal secretions and this can cause severe NEONATAL INFECTIONS.
HSV presentation
- small painful fluid filled blisters -ooze and ulcerate. Heal after a few weeks
- HSV also infects the nearby sensory neurons, which aren’t destroyed, but instead, they become a permanent home for the herpes virus. This is referred to as the latent phase of the infection and is typically asymptomatic.
- From time to time the herpes virus uses sensory neurons to produce copies of itself and these are released and infect epithelial cells.
Varicella Zoster Virus
- Varicella Zoster Virus causes a primary infection called varicella or chickenpox
- Chickenpox: a rash on the scalp, face, and trunk that contains macules, papules, vesicles, and scabs at the same time.
- From the neurons in the skin, VZV travels retrogradely to the nerve ganglia, where it remains dormant. Later on, if the immune system weakens, due to aging, stress, or immunosuppressive therapy, the virus can be reactivated.
- It can then travel back up through the sensory nerves, anterogradely to the skin and cause an infection in the innervated dermatome - that’s called herpes zoster or shingles.
Cytomegalovirus (CMV)
- CMV causes mononucleosis aka ‘mono’
Mono:
- sore throat
- lymphadenopathy
- fever
- malaise
- headache
symptoms resolve over a few weeks
- Now, in immunocompromised individuals, CMV can cause more severe infections including pneumonia, esophagitis, and retinitis which can lead to vision loss.
- CMV can also pass from a mother to a baby via the placenta causing a potentially life-threatening congenital infection.
Aciclovir (Acyclovir)
-Once they’re inside an infected cell acyclovir is phosphorylated to a monophosphate form by a viral enzyme, which is called viral kinase.
-acyclovir is converted to the acyclovir monophosphate by the viral thymidine kinase,
-Next, the monophosphate form is phosphorylated twice to the active triphosphate form by cellular enzymes.
-This triphosphate form acts as a guanosine analog which means that it’s similar in structure with the normal guanosine nucleotide.
-When this analog is inserted into the replicating viral DNA, it causes the growing DNA chain to terminate and DNA synthesis is halted.
Aciclovir
Drug class: Guanosine analog
Indication:
- used to treat herpes simplex, varicella zoster, herpes zoster.
- topical cream: indicated to treat recurrent herpes labialis (patients who are 12 yrs and older).
-tablets
- used to treat mild mucocutaneous lesions
- genital lesions
- herpes prophylaxis in immunocomprimised individuals.
Mechanism:
- Acyclovir becomes acyclovir monophosphate due to the action of viral thymidine kinase.
- Acyclovir triphosphate has higher affinity for viral DNA polymerase than cellular DNA polymerase and incorporates into the DNA where the missing 2’ and 3’ carbons causes DNA chain termination.
Side effects:
Malaria
- plasmodium gets into the bloodstream - it infects liver cells and red blood cells - which causes a variety of symptoms and sometimes even leads to death.
- medications: antimalarials
How malaria is spread:
- in mosquito gut - sporozoite
- sporozoites travel to liver and invade hepatocytes
- Schizogony (asexual reproduction) in hepatocytes.
- Merozoites released into blood
ERYTHROCYTIC PHASE:
- merozoites invade RBCs
- inside RBC- Plasmodium feeds on hemoglobin via a process called endocytosis. Plasma membrane around hemoglobin - called a food vacuole - where hemoglobin can be broken down
- Plasmodium uses the GLOBIN PROTEINS to fuel their growth, but the heme is toxic to them, so they are converted into insoluble HEMOZOIN CRYSTALS
- As the parasite feeds, it undergoes mitosis and differentiates into lots of merozoites, which then burst out of the red blood cell and enter back into circulation.
GAMETOGENIC PHASE:
- they divide and give rise to gametocytes, which are little sausage -shaped sexual forms that can be either male or female
- These gametocytes remain inside of a red blood cell, and can get sucked up by another female mosquito that bites the same malaria carrier.
- SPOROGONY (sexual reproduction): The gametocytes can then fuse together inside the mosquito to form a zygote.
- zygote - ookinete - oocyst ruptures in mosquito gut releases thousands of sporozoites
Malaria
- Fever in bursts due to TNF a and other inflammatory cytokines being released.
RBC destroyed:
- hemolytic pneumonia
- fatigue
- headaches
- jaundice
- splenomegaly
Quinine
These medications work by entering the plasmodium and accumulating in their food vacuoles.
Here, they bind to heme and prevent it from being converted into hemozoin.
Since heme is toxic to the Plasmodium, this eventually leads to their death
Quinine
Drug class: Alkaloid
Indication:
- used to treat uncomplicated plasmodium falciparum malaria (MALARIA)
Mechanism:
- drugs interfere with the parasite’s ability to break down and digest hemoglobin
- heme toxic to plasmodium - dies
Artemisinin derivatives
-These medications build up in the food vacuoles of the Plasmodium, where they bind to the iron found in heme and create free radicals that damage parasite proteins.
-They are especially useful since they are effective against all Plasmodium species, including the strains that are resistant to chloroquine and other quinoline derivatives.
-Their effectiveness is so high that they are considered the first choice for chloroquine resistant malaria.
Aremether aka Artemisinin
Drug class: antimalarial agent
Indication:
- used in combination with lumefantrine
- treat acute uncomplicated malaria
caused by Plasmodium falciparum.
Mechanism of action:
- interaction with ferriprotoporphyrin IX or ferrous ions in the acidic parasite food vacuole, which results in the generation of cytotoxic radical species
Side effects:
Chloroquine
Drug bank: antimalarial drug
Indication:
- Infections with P.vivax, P. malariae, P. ovale and P.falciparum.
Mechanism of action:
-inhibits the action of heme polymerase in malarial trophozites, preventing the conversion of heme to hemazoin.
- Plasmodium species continue to accumulate toxic heme, killing the parasite.
Amprenavir
Drug class: protease inhibitor
Indication: treat HIV -1 (Virus Type -1 )
Mechanism:
- inhibits the HIV viral proteinase enzyme
- which prevents cleavage of the gag-pol polyprotein
- results in noninfectious immature viral particles
Reverse transcriptase inhibitors
- Reverse transcriptase inhibitors are an important part of HAART.
- HAART combination of medications used in the treatment of AIDS.
- AIDS is caused by a RNA containing retrovirus - HIV.
- retro - refers to it needing to use an enzyme called reverse transcriptase to transcribe a piece of “proviral” DNA from its RNA
- transcriptase inhibitors go and inhibit this enzyme, and prevent HIV replication.
- Based on their structure, they can be classified into nucleoside reverse transcriptase inhibitors, or NRTIs; and non-nucleoside reverse transcriptase inhibitors, or NNRTIs.
NRTI
- NRTIs resemble nucleosides, which are tiny molecules which when attached to a phosphate group give rise to nucleotides, which are building blocks of nucleic acids like DNA and RNA.
- HIV is a single-stranded, positive-sense, enveloped RNA retrovirus that targets cells in the immune system that have a molecule called CD4 on their membrane.
- HIV attaches to the CD4 molecule via a protein called gp120 found on its envelope.
- NRTIs part of HAART. So typically you use two NRTIS and another antiretroviral which acts by a different mechanism.
-NRTI are also used alone in post-exposure prophylaxis, for example, in individuals who’ve recently been exposed to HIV infected blood in the past 72 hours.
-They can also be used in children born to HIV infected mothers who are at the risk of developing the disease.
HIV attack
- HIV contains nucleocapsid which is a capsule containing single stranded RNA, REVERSE TRANSCRIPTASE and INTERGRASE (enzymes)
- HIV binds releases reverse transcriptase into host cell
- RT uses the single stranded viral RNA as a template, and uses the nucleotides present in the cytoplasm of the CD4+ cell to transcribe a complementary double-stranded “proviral” DNA,
Proviral just means that it’s ready to be integrated into the host’s DNA. So it enters the T-helper cell’s nucleus and pops itself into the cell’s DNA, ready to be transcribed into new viruses, - immune cd4 cell activated start transcribing and translating proteins needed for the immune response.
- Over time, more and more immune cells are infected, and the immune system begins to fail which is called immunodeficiency, and this increases the risk of infections and tumors that a healthy immune system would usually be able to fend off.
- These complications are referred to as AIDS