Extra B3 stuff Flashcards
(GNATS - Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin)
What drug class are they?
Aminoglycosides
MOA:
They Inhibit bacterial protein synthesis 30s subunit. Causes mRNA misreading.
● Resistance: Enzymatic modification.
● Side Effects: Nephrotoxicity, ototoxicity
● Clinical Use: Gram-negative bacilli, synergistic with beta-lactams.
MOA:
They Inhibit bacterial protein synthesis 30s subunit. Causes mRNA misreading.
● Resistance: Enzymatic modification.
● Side Effects: Nephrotoxicity, ototoxicity
● Clinical Use: Gram-negative bacilli, synergistic with beta-lactams.
Aminoglycosides
(GNATS - Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin)
MOA:
They Inhibit bacterial protein synthesis 30s subunit. Causes mRNA misreading.
● Resistance: Enzymatic modification.
● Side Effects: Nephrotoxicity, ototoxicity
● Clinical Use: Gram-negative bacilli, synergistic with beta-lactams.
Aminoglycosides
(GNATS - Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin)
Which drugs cause hemolytic anemia in patients with G6PD Deficiency?
Dapsone, Sulfonamides. Antimalarials (primaquine, chloroquine)
● Side Effects: Hemolytic anemia in G6PD deficiency.
Dapsone, Sulfonamides. Antimalarials (primaquine, chloroquine) All cause which side effect?
● Side Effects: Hemolytic anemia in G6PD deficiency.
Primaquine, Chloroquine, Mefloquine, Artensuate
Antimalarials
What is the MOA of Primaquine? (antimalarial)
○ It interferes with the electron transport in the mitochondria of the malaria parasite,
which is crucial for its energy metabolism.
● Side Effects:
1) G6PD deficiency hemolysis
○ It interferes with the electron transport in the mitochondria of the malaria parasite,
which is crucial for its energy metabolism.
● Side Effects:
1) G6PD deficiency hemolysis
Primaquine
What is the MOA of Chloroquine? (antimalarial)
○It inhibits heme polymerization.
Clinical use:
Antimalarial used to treat P. vivax, P. ovale & some strains of P. falciparum
● Side Effects:
1) Retinopathy
● Resistance due to efflux pump
What is the MOA of Mefloquine? (antimalarial)
○ It disrupts heme detoxification within the parasite’s food vacuole.
What is the MOA of Artesunate? (antimalarial)
○ It is rapidly hydrolyzed to dihydroartemisinin, which generates free radicals that damages the proteins and membranes in the malaria parasite.
○ Treats chloroquine-resistant P. falciparum and P. vivax in pregnant females.
○It inhibits heme polymerization.
Clinical use:
Antimalarial used to treat P. vivax, P. ovale & some strains of P. falciparum?
● Side Effects:
1) Retinopathy
● Resistance due to efflux pump
○ Chloroquine
Antimalarial used to treat severe & complicated P. falciparum malaria?
Artesunate
What are the clinical uses of Artesunate?
○ Treats severe and complicated P. falciparum malaria
Rifampin, Isoniazid (INH), Pyrazinamide, Ethambutol, & Streptomycin Are all examples of?
. Anti-TB: First Line Drugs (RIPES)
○ MOA:
Inhibits DNA-dependent RNA polymerase in Mycobacterium tuberculosis, preventing RNA synthesis.
○ Side Effects:
1) Hepatotoxicity
2) orange body fluids (urine, tears, sweat)
3) flu-like symptoms
4) Can also induce cytochrome P-450 enzymes, causing drug-drug interactions
Rifampin
Rifampin
○ MOA:
Inhibits DNA-dependent RNA polymerase in Mycobacterium tuberculosis, preventing RNA synthesis.
○ Side Effects:
1) Hepatotoxicity
2) orange body fluids (urine, tears, sweat)
3) flu-like symptoms
4) Can also induce cytochrome P-450 enzymes, causing drug-drug interactions
○ MOA:
Inhibits the synthesis of mycolic acids, essential components of the mycobacterial cell wall.
○ Side Effects:
1) Hepatotoxicity
2) peripheral neuropathy (preventable with pyridoxine/vit b6)
3) Can also cause drug-induced lupus.
Isoniazid (INH)
Isoniazid (INH)?
○ MOA:
Inhibits the synthesis of mycolic acids, essential components of the mycobacterial cell wall.
○ Side Effects:
1) Hepatotoxicity
2) peripheral neuropathy (preventable with pyridoxine/vit b6)
3) Can also cause drug-induced lupus.
○ MOA:
Disrupt mycobacterial cell membrane metabolism and transport functions.
○ Side Effects:
1) Hepatotoxicity
2) hyperuricemia (can precipitate gout attacks)
3) non-gout polyarthralgia.
● Pyrazinamide
● Pyrazinamide
○ MOA:
Disrupt mycobacterial cell membrane metabolism and transport functions.
○ Side Effects:
1) Hepatotoxicity
2) hyperuricemia (can precipitate gout attacks)
3) non-gout polyarthralgia.
○ MOA:
Inhibits arabinosyl transferase, an enzyme involved in the synthesis of the mycobacterial cell wall.
○ Side Effects:
1) Optic neuritis (leading to color blindness and visual field loss)
● Ethambutol
● Ethambutol
○ MOA:
Inhibits arabinosyl transferase, an enzyme involved in the synthesis of the mycobacterial cell wall.
○ Side Effects:
1) Optic neuritis (leading to color blindness and visual field loss)
○ MOA:
An aminoglycoside antibiotic that inhibits protein synthesis by binding to the 30S ribosomal subunit of the mycobacterium.
○ Side Effects:
1) Ototoxicity (both auditory and vestibular)
2) nephrotoxicity
3) allergic reactions
● Streptomycin
Streptomycin?
○ MOA:
An aminoglycoside antibiotic that inhibits protein synthesis by binding to the 30S ribosomal subunit of the mycobacterium.
○ Side Effects:
1) Ototoxicity (both auditory and vestibular)
2) nephrotoxicity
3) allergic reactions
● MOA:
Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV.
● Resistance: Mutation in DNA gyrase, efflux pumps.
● Side Effects: Tendon rupture, QT prolongation.
● Clinical Use: Broad spectrum - respiratory, urinary, GI infections.
Fluoroquinolones
What is the MOA of Fluoroquinolones?
● MOA:
Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV.
● MOA:
Inhibit DNA gyrase (topoisomerase II) and topoisomerase IV.
Fluoroquinolones
How do organisms develop resistance against fluoroquinolones?
● Resistance: Mutation in DNA gyrase, efflux pumps.
What are the adverse effects of Fluoroquinolones?
Side Effects:
1) Tendon rupture
2) QT prolongation.
Side Effects:
1) Tendon rupture
2) QT prolongation.
Fluoroquinolones
What are the clinical uses of Fluoroquinolones?
● Clinical Use: Broad spectrum - respiratory, urinary, GI infections.
● Clinical Use: Broad spectrum - respiratory, urinary, GI infections.
Fluoroquinolones
Aminoglycosides and Tetracyclines
Protein Synthesis Inhibitors: 30S inhibitors
“Buy AT 30, SELL at 50”
Streptogramin, Erythromycin, Lincosamides, and Linezolid
Protein Synthesis Inhibitors: 50S inhibitors
“Buy AT 30, SELL at 50”
■ MOA: Bind to 30S. Interferes with initiation complex of protein synthesis.
■ Note: These are bactericidal and are primarily effective against aerobic Gram-negative bacteria.
Aminoglycosides (e.g., Gentamicin, Streptomycin):
■ MOA:
They bind to the 30S ribosomal subunit and prevent the attachment of aminoacyl-tRNA to the mRNA-ribosome complex.
■ Mechanism of Resistance:
1) Efflux pumps (actively pumping the drug out of the
bacterial cell)
2) Ribosomal protection (altering the ribosomal binding site to reduce drug binding).
■ Note: These are generally bacteriostatic and have a broad spectrum of activity, including against some Gram-positive and Gram-negative bacteria, as well as atypical organisms.
○ Tetracyclines (e.g., Doxycycline, Tetracycline):
What is the MOA of Tetracyclines?
■ MOA:
They bind to the 30S ribosomal subunit and prevent the attachment of aminoacyl-tRNA to the mRNA-ribosome complex.
■ MOA:
They bind to the 30S ribosomal subunit and prevent the attachment of aminoacyl-tRNA to the mRNA-ribosome complex.
Tetracyclines
What is the MOA of Aminoglycosides?
■ MOA: Bind to 30S. Interferes with initiation complex of protein synthesis.
■ MOA: Bind to 30S. Interferes with initiation complex of protein synthesis.
Aminoglycosides
■ MOA:
They bind to the 50S subunit, but they do so in a sequential manner. One component inhibits the early phase of protein synthesis, while the other inhibits the late phase. Together, they produce a
synergistic bactericidal effect.
■ Note: Used mainly for resistant Gram-positive infections.
○ Streptogramins (e.g., Quinupristin/Dalfopristin)
■ MOA:
These drugs bind to the 50S ribosomal subunit and block the translocation step of protein synthesis.
○ Erythromycin (and other Macrolides):
What is the MOA of Erythromycin (and other Macrolides)?
■ MOA:
These drugs bind to the 50S ribosomal subunit and block the translocation step of protein synthesis.
■ MOA:
It binds to the 50S ribosomal subunit and prevents the formation of the 70S initiation complex.
■ Note: Mainly used for Gram-positive bacteria, including resistant strains such as MRSA and VRE.
○ Linezolid
What is the MOA of Streptogramins (e.g., Quinupristin/Dalfopristin)
■ MOA:
They bind to the 50S subunit, but they do so in a sequential manner. One component inhibits the early phase of protein synthesis (Quinupristin), while the other inhibits the late phase (Dalfopristin). Together, they produce a synergistic bactericidal effect.
What is the MOA of Linezolid?
■ MOA:
It binds to the 50S ribosomal subunit and prevents the formation of the 70S initiation complex.
■ MOA:
It binds to the 50S ribosomal subunit and inhibits peptide bond formation
○ Lincosamides (e.g., Clindamycin):
○ Lincosamides (e.g., Clindamycin):
■ MOA:
It binds to the 50S ribosomal subunit and inhibits peptide bond formation
● Drug: Doxycycline, Amoxicillin and Cefuroxime (in pregnancy). Are all examples of drugs to treat what?
Lyme Disease
Pregnancy: Amoxicillin and cefuroxime preferred due to teratogenic potential of doxycycline (bone abnormalities).
MOA: 2 DRUGS
1) Inhibits neuraminidase
2) Amantadine blocks viral uncoating.
● Resistance: Mutations in neuraminidase and targets M2 protein, respectively
● Clinical Use:
Influenza treatment and prophylaxis. (A for A) ________ for JUST Influenza A, & _____ for both
- Oseltamivir
- Amantadine
Which drugs are used to treat influenza viruses?
Amantidine for influenza A
Oseltamivir for Influenza A & B
Which Lyme disease treatment drugs are preferred & why?
Amoxicillin & Ceftriaxone (& other cephalosporins) because Doxycycline is a teratogen (bone abnormalities)
Antiherpes Drugs
● MOA:
Inhibit viral DNA polymerase.
● Resistance: Thymidine kinase mutations
● Clinical Use: Herpes simplex & Varicella-zoster
Acyclovir
● Classes: NRTIs, NNRTIs, Protease Inhibitors, Integrase Inhibitors. Are all examples of drugs that treat»>
HIV
What are the drugs of choice for treating CMV?
Ganciclovir & Valganciclovir (prodrug of ganciclovir)
What is the drug of choice for treating HSV & VZV?
Acyclovir
What are the drugs of choice when treating HBV?
IFN-a & Lamivudine
What is the drug of choice of treating influenza A & or B?
Oseltamivir
Atazanavir, Darunavir, Indinavir, Ritonavir are all examples of which class of drugs that treat which condition?
Protease inhibitors that inhibit HIV protein cleavage to treat HIV
Tenofovir, Emtricitabine, Lamivudine, Abacavir, & Zidovudine are all examples of which class of drugs that treat which condition?
NRTI’s that act as a nucleoside & nucleotide RT inhibitor to inhibit HIV DNA synthesis by terminating DNA chain elongation
Efavirenz & Nevirapine are all examples of which class of drugs that treat which condition?
NNRTI’s that act as allosteric RT inhibitors to inhibit HIV DNA synthesis by terminating DNA chain elongation
Dolutegravir & Raltegravir are all examples of which class of drugs that treat which condition?
Integrase inhibitors that inhibit HIV DNA integration into the hosts genome
Enfuvirtide is an example of which class of drugs that treat which condition?
Fusion inhibitor which prevents HIV fusion with a target cell membrane by binding to gp41
Maraviroc is an example of which class of drugs that treat which condition?
CCR5 antagonist tht inhibits HIV entry by blocking the HIV gp120allosteric interactions with CCR5
Zidovudine is associated with which side effect?
Myelosuppression/bone marrow suppression
Abacavir is associated with which side effect?
Fever & rash (allergic reaction)
Didanosine is associated with which side effect?
Pancreatitis
Stavudine is associated with which side effect?
Lipodystrophy
Lamivudine is associated with which side effect?
Least toxic form of Hep B
Tenofovir is associated with which side effect?
Gi upset
Azole, Amphotericin B, Caspofungin
Antifungal:
What is the MOA of Azoles?
● MOA:
inhibit ergosterol synthesis
What is the MOA of Amphotericin B
● MOA:
B binds ergosterol;
What is the MOA of Caspofungin?
● MOA:
Caspofungin inhibits cell wall synthesis.
What are the side effects of Azoles?
Hepatotoxicity
What are the side effects of Amphotericin B?
nephrotoxicity and thrombophlebitis at injection
site
What are the drugs of choice for treating Chlamydia?
(Mucopurulent discharge, pleomorphic gram-negative, intracellular)
Azithromycin or Doxycycline
What are the drugs of choice for treating Gonorrhea?
○ Yellow-green discharge, gram-negative intracellular diplococci
Ceftriaxone + Azithromycin or Doxycycline.
What are the drugs of choice for treating Syphilis?
○ Painless chancre, gram-negative spiral-shaped bacteria
Penicillin G.
What are the drugs of choice for treating Trichomoniasis?
○ Foul-smelling, yellow -green purulent discharge, trophozoites w/multiple flagella
Metronidazole or Tinidazole.
What are the drugs of choice for treating Herpes?
○ Pain, pruiritis, rash
Antivirals like Acyclovir, Valacyclovir.
What are the drugs of choice for treating Candida Vaginosis?
○ Milky, curdy white discharge, yeast infection
Fluconazole, clotrimazole
What are the drugs of choice for treating Bacterial Vaginosis (Gardnerella)?
○ Grayish milky discharge, whiff test: fishy odour, clue cells, pleomorphic gram negative
rods.
Metronidazole
Albendazole, Praziquantel, Pyrantel Pamoate are examples of which type of medication
Anthelminthics
○ MOA:
It inhibits microtubule synthesis in helminths, impairing glucose uptake and depleting glycogen stores in the worm, which eventually leads to its death.
○ Clinical Uses:
* Broad spectrum of activity against intestinal and tissue parasites:
1) hookworms
2) pinworms
3) roundworms
4) tapeworms (e.g., Taenia solium),
- cystic hydatid disease caused by Echinococcus granulosus.
● Albendazole:
What is the MOA of Albendazole?
○ MOA:
It inhibits microtubule synthesis in helminths, impairing glucose uptake and depleting glycogen stores in the worm, which eventually leads to its death.
○ MOA:
It increases the permeability of cell membranes in worms to calcium ions, causing severe muscular contractions, paralysis, and death of the parasite.
○ Clinical Uses:
1) schistosomes (blood flukes)
2) flukes (like liver and lung flukes)
● Praziquantel
What is the drug of choice for schistosomiasis and many other trematode infections.
● Praziquantel
What is the MOA of Praziquantel?
○ MOA:
It increases the permeability of cell membranes in worms to calcium ions, causing severe muscular contractions, paralysis, and death of the parasite.
○ MOA:
A depolarizing neuromuscular blocking agent that paralyses a helminth (it’s expelled in poop)
○ Clinical Uses:
1) Intestinal nematodes Pinworms (Enterobius
vermicularis)
Roundworms (Ascaris lumbricoides)
Hookworms
(Necator americanus and
Ancylostoma duodenale).
● Pyrantel Pamoate
Which Anthelminthic is preferred in preggos with a Scotch tape test +?
pyrantel pamoate
What is the MOA of pyrantel pamoate?
○ MOA:
It acts as a depolarizing neuromuscular blocking agent, causing spastic paralysis of the helminth. The paralyzed worms are then expelled from the gastrointestinal tract by peristalsis.
● MOA: 2 Drugs
Alkylating agents, cross-link DNA; marked effect on B cells than T cells
● Side Effects:
1) Hemorrhagic cystitis
2) myelosuppression
3) early menopause.
Clinical uses:
1) Bone marrow transplantation
2) Autoimmune disorders.
● Management: MESNA to prevent hemorrhagic cystitis, hydration.
- Ifosfamide & Cyclophosphamide
Ifosfamide & Cyclophosphamide, Which one is the least leukemogenic (causing acute myelogenous leukemia)?
Cyclophosphamide
What is the MOA of Ifosfamide & Cyclophosphamide?
Alkylating agents, cross-link DNA; marked effect on B cells than T cells
● MOA: Inhibit microtubule formation. Blocking M phase.
● Side Effects:
1) Peripheral neuropathy
2) myelosuppression.
● Management: Dose adjustment, supportive care.
- Vincristine & Cell Cycle Specific Agents
What is the MOA of Vincristine & Cell Cycle Specific Agents?
● MOA: Inhibit microtubule formation. Blocking M phase.
● MOA:
Inhibits interleukin-1 and interleukin-2 receptor → inhibits T-cell activation.
● Side Effects:
1) Nephrotoxicity
2) hypertension.
● Clinical Use: Prevent transplant rejection, autoimmune disorders.
- Cyclosporine
What is the MOA of Cyclosporine?
● MOA:
Inhibits interleukin-1 and interleukin-2 receptor → inhibits T-cell activation.
MOA:
It Inhibits cytosine monophosphate dehydrogenase, and inhibits T-cell lymphocyte proliferation.
Clinical use:
1) Renal disease post SLE
2) Vasculitis
Mycophenolate Mofetil
What is the MOA of Mycophenolate Mofetil?
MOA:
It Inhibits cytosine monophosphate dehydrogenase, and inhibits T-cell lymphocyte proliferation.
● MOA:
Monoclonal antibody against CD20 on B cells.
● Side Effects:
1) Infusion reactions
2) immunosuppression
● Clinical Use:
1) Non-Hodgkin lymphoma
2) Rheumatoid arthritis.
- Rituximab
What is the MOA of Rituximab?
● MOA:
Monoclonal antibody against CD20 on B cells.
● MOA:
Inhibits ribonucleotide reductase halting the cell cycle in S phase.
● Side Effects: Myelosuppression
● Clinical Use:
1) Chronic myelogenous leukemia
2) Sickle cell anemia
- Hydroxyurea
What is the MOA of Hydroxyurea?
● MOA:
Inhibits ribonucleotide reductase halting the cell cycle in S phase.
● MOA:
They inhibit specific tyrosine kinase activity of protein product of bcr-abl oncogene (chronic
myelogenous leukemia) → philadelphia chromosome translocation.
● Side Effects/toxicity:
1) Diarrhea
2) rash
3) myelosuppression
● Clinical Use: Targeted cancer therapy.
- Tyrosine Kinase Inhibitors (Imatinib, Dasatinib, Nilotinib)
● MOA:
Purine analogue, inhibits DNA synthesis, antimetabolite
● Side Effects:
1) Myelosuppression
2) hepatotoxicity
● Clinical Use:
1) Leukemias
2) autoimmune conditions
6-Mercaptopurine (6-MP)
What can lead to severe 6-MP toxicity?
When 6-Mercaptopurine is given with Allopurinol, it inhibits xanthine oxidase resulting in increased levels of 6-MP and its active metabolites in the body.
This can lead to severe toxicity, including myelosuppression (bone marrow suppression), which can manifest as:
1) neutropenia
2) thrombocytopenia
3) anemia
- Cancer Chemotherapy Toxicity and Management
Cisplastin, Methotrexate can both cause which form of toxicity?
● Renal Toxicity: Cisplastin, Methotrexate
○ Give Amifostine for Cisplatin (Platinum analogs)
- Cancer Chemotherapy Toxicity and Management
Bleomycin, Busulfan, & Procarbazine can all cause which form of toxicity?
● Pulmonary Toxicity: Bleomycin, Busulfan, Procarbazine
- Cancer Chemotherapy Toxicity and Management
Doxorubicin, Daunorubicin can both cause which form of toxicity?
● Cardiac Toxicity: Doxorubicin, Daunorubicin
- Cancer Chemotherapy Toxicity and Management
Vincristine, Cisplatin can both cause which form of toxicity?
● Neurologic Toxicity: Vincristine, Cisplatin
- Cancer Chemotherapy Toxicity and Management
Cyclophosphamide, Methotrexate can both cause which form of toxicity?
● Immunosuppressive Toxicity: Cyclophosphamide, Methotrexate
○ Give Leucovorin for methotrexate toxicity
○ Give Mesna for cyclophosphamide toxicity
● Drugs: Tamoxifen, Trastuzumab are clinically used for
- Breast Cancer Treatment
● MOA:
A selective Estrogen Receptor Modulator (SERM) → estrogen antagonist, preventing estrogen from binding to its receptor, thereby inhibiting the growth of estrogen-dependent breast cancer cells.
● Side Effects: Menopausal symptoms
● Clinical Use:
○ Tamoxifen is primarily used in the treatment of hormone receptor-positive breast cancer
Tamoxifen
What is the MOA of Tamoxifen?
● MOA:
A selective Estrogen Receptor Modulator (SERM) → estrogen antagonist, preventing estrogen from binding to its receptor, thereby inhibiting the growth of estrogen-dependent breast cancer cells.
● MOA:
A monoclonal antibody that targets the HER2/neu receptor, a protein overexpressed in some forms of breast cancer.
● Side Effects: cardiotoxicity
● Clinical Use:
treating HER2-positive breast cancer (more aggressive form)
Trastuzumab
What is the MOA of Trastuzumab?
● MOA:
A monoclonal antibody that targets the HER2/neu receptor, a protein overexpressed in some forms of breast cancer.
● If breast cancer patient are resistant to Tamoxifen, give them ____________:
aromatase inhibitors
( Anastrozole, Letrozole, and Exemestane)
3 Drugs
● MOA:
These drugs inhibit aromatase, an enzyme that converts androgens to estrogens in
postmenopausal women, thereby reducing estrogen levels.
● Clinical use:
1) hormone receptor-positive breast cancer that is resistant to tamoxifen
(especially in postmenopausal women)
Aromatase inhibitors
● Drugs: Anastrozole, Letrozole, and Exemestane.
What is the MOA of Aromatase inhibitors (Anastrozole, Letrozole, and Exemestane)?
● MOA:
These drugs inhibit aromatase, an enzyme that converts androgens to estrogens in
postmenopausal women, thereby reducing estrogen levels.
MOA
It targets μ-opioid receptors in the myenteric plexus of the large intestine & acts as an agonist to reduce intestinal motility and increase the absorption of fluid and electrolytes. (antidiarrheal)
Clinical use:
1) Acute and Chronic diarrhea (It does not
readily cross the blood-brain barrier, so it has a lower risk of central opioid effects)
● Loperamide
What is the MOA Loperamide?
It targets μ-opioid receptors in the myenteric plexus of the large intestine & acts as an agonist to reduce intestinal motility and increase the absorption of fluid and electrolytes. (antidiarrheal)
What are Naloxone and Naltrexone?
They are opioid antagonists
Side effects: Withdrawal
MOA:
It is a synthetic disaccharide that is not absorbed in the gut & metabolized by Gi flora into acid that draws water into the bowel (osmotic effect).(Laxative)
○ Key Point:
1) Constipation
2) Hepatic encephalopathy
(reduces ammonia absorption)
Lactulose
What is the MOA of lactulose?
MOA:
It is a synthetic disaccharide that is not absorbed in the gut & metabolized by Gi flora into acid that draws water into the bowel (osmotic effect).(Laxative)
MOA:
It blocks the D2 receptors in the chemoreceptor trigger zone and enhances the response to acetylcholine in the upper GI tract.
This promotes gastric emptying (prokinetic effect) and reducing nausea and vomiting (antiemetic effect).
○ Clinical use:
1) Diabetic gastroparesis
2) antiemetic
Metoclopramide
What is a major side effect concerning Metoclopramide blocking D2 receptors?
extrapyramidal symptoms
What is the MOA of Metoclopramide?
MOA:
It blocks the D2 receptors in the chemoreceptor trigger zone and enhances the response to acetylcholine in the upper GI tract.
○ MOA: These irreversibly bind to and inactivate the H+/K+ ATPase (proton pump) in gastric parietal cells to reduce gastric acid secretion.
Clinical use:
1) GERD
2) Peptic ulcers
3) Zollinger-Ellison syndrome
● Proton Pump Inhibitors (PPIs): omeprazole
○ Key Point: PPIs need an acidic environment to be activated, so they are usually taken before ______
meals
What is the MOA of PPI’s?
○ MOA: These irreversibly bind to and inactivate the H+/K+ ATPase (proton pump) in gastric parietal cells to reduce gastric acid secretion.
○ MOA: A PGE1 analogue that increases the production and secretion of gastric mucus and bicarbonate, to helps protect the gastric mucosa.
It also inhibits gastric acid secretion.
○ Clinical uses:
1) NSAID-induced peptic ulcers
● Misoprostol
What is the MOA of Misoprostol
○ MOA: A PGE1 analogue that increases the production and secretion of gastric mucus and bicarbonate, to helps protect the gastric mucosa.
It also inhibits gastric acid secretion.
○ MOA:
It blocks 5-HT3 receptors, particularly in the chemoreceptor trigger zone and the GIT to controls nausea and vomiting.
○ Clinical use:
1) chemotherapy-induced and postoperative nausea and vomiting.
● Ondansetron
What is the MOA of Ondansetron?
○ MOA:
It blocks 5-HT3 receptors, particularly in the chemoreceptor trigger zone and the GIT to controls nausea and vomiting.
Morphine (Opioid)
● Target: μ (mu), κ (kappa), and δ (delta) opioid receptors.
● MOA:
Primarily acts as an agonist at the μ-opioid receptors, leading to analgesia, sedation, euphoria, and respiratory depression & slowed Gi motility.
● Key Point: Widely used for pain relief but has a high potential for dependence and tolerance.
Morphine (Opioid)
● Targets: Dopamine, norepinephrine, and serotonin reuptake transporters.
● MOA:
It inhibits the reuptake of these neurotransmitters, leading to their increased concentration at the synapse and causing euphoria, increased alertness, and vasoconstriction.
● Key Point: High abuse potential; acute overdose can lead to cardiac arrhythmias and
myocardial infarction.
Cocaine:
acute overdose of this drug can lead to cardiac arrhythmias and myocardial infarction
Cocaine
● MOA: Interferes with cellular respiration by inhibiting pyruvate dehydrogenase and
disrupting ATP production.
● Key Point: Symptoms include garlic breath, vomiting, diarrhea, QT prolongation, and hyperkeratosis.
Arsenic (As) poisoning treat with chelators & removal from the contaminant
● MOA:
It inhibits various enzymes involved in heme synthesis and interferes with calcium metabolism.
Lead
Abdominal pain, anemia, and neurologic symptoms
(e.g., encephalopathy, peripheral neuropathy).
Lead poisoning (plumbism)
Treat with a lead chelator:
Calcium disodium ethylenediaminetetraacetic acid (EDTA)
● MOA:
It inhibits COX enzymes in the CNS, reducing pain and fever.
Acetaminophen (Paracetamol):
● Overdose leads to hepatic necrosis
Acetaminophen toxicity
treat with N-acetylcysteine as an antidote to
replenish glutathione.
● Target: Muscarinic acetylcholine receptors
● MOA:
It acts as a competitive antagonist at muscarinic receptors, to reduce parasympathetic activity (anticholinergic effects).
● Key Point: Used to treat bradycardia and as an antidote for organophosphate poisoning.
Atropine
Hyperthermia, dry/flushed skin, tachycardia, constipation, dry eyes & dilated pupils
Atropine poisoning treat with physostigmine
● MOA:
Inhibits acetylcholinesterase, leading to an accumulation of acetylcholine at
synapses and overstimulation of cholinergic receptors.
● Presents with DUMBBELSS symptoms
(Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, Salivation)
Organophosphate Poisoning treat with atropine & pralidoxime
● MOA:
Binds to cytochrome c oxidase in mitochondria, inhibiting cellular respiration.
● Key Point: Presents with altered mental status, seizures, and lactic acidosis
Cyanide Toxicity it is treated with
hydroxocobalamin or sodium thiosulfate.
● MOA:
Metabolized to toxic metabolites causing metabolic acidosis and renal failure.
● Key Point: Early symptoms include inebriation, vomiting, and respiratory depression; late
symptoms include renal failure and calcium oxalate crystal deposition.
Ethylene Glycol Poisoning:
Treat with
1) Sodium bicarbonate to correct the metabolic acidosis
2) Fomepizole or ethanol to inhibit the metabolism of ethylene glycol to its more toxic metabolites
● Target: Nicotinic acetylcholine receptors
● MOA:
It acts as a (alpha 4 beta 2) partial agonist at these receptors, reducing craving and withdrawal symptoms.
● Key Point: Useful for smoking cessation but can cause mood changes and vivid dreams.
Smoking Cessation Medication – Varenicline
● MOA:
Disulfiram inhibits aldehyde dehydrogenase, leading to the accumulation of acetaldehyde when ethanol is consumed.
● Key Point: Causes unpleasant symptoms like flushing, headache, nausea, and palpitations,
deterring alcohol consumption
Disulfiram Reaction (Enzyme: Aldehyde Dehydrogenase):
Antibiotic resistance to penicillin occurs via
1) Beta-lactamase & ESBL
2) Mutated PBP
3) Mutated porin proteins
Antibiotic resistance to vancomycin occurs via
1) Mutated peptidoglycan cell wall
2) Impaired influx/increased efflux
Antibiotic resistance to Quinolones occurs via
1) Mutated DNA gyrase
2) Impaired influx/increased efflux
Antibiotic resistance to Aminoglycosides occurs via
1) Aminoglycoside-modifying enzymes
2) Mutated ribosomal subunit protein
3) Mutated porin protein
Antibiotic resistance to TCAs occurs via
1) Impaired influx/increased efflux
2) Inactivated enzyme
Antibiotic resistance to Rifamycins occurs via
1) Mutated RNA polymerase
What is the MOA of Amifostine?
What does it treat?
MOA:
It is a free radical scavenger (protects against them)
Treats:
Nephrotoxicity
(induced by platinum)
What is the MOA of Dexrazoxane?
What does it treat?
MOA:
It’s an iron chelator
Treats:
Cardiotoxicity
(induced from anthracyclines)
What is the MOA of Leucovorin acid (folinic acid)?
What does it treat?
MOA:
A tetrahydrofolate precursor
Treats:
Myelosuppression (from methotrexate & it enhances the effect of 5-FU
What is the MOA of Mesna?
What does it treat?
MOA:
A sulfhydryl compound that binds acrolein (toxic metabolite of cyclophosphamide/ifosfamide)
Treats:
Hemorrhagic cystitis from cyclophosphamide/ifosfamide
What is the MOA of Rasburicase?
What does it treat?
MOA:
A recombinant uricase that catalyzes metabolism of uric acid to allantoin
Treats:
Tumor lysis syndrome
What is the MOA of Ondansetron & Granisetron?
What does it treat?
MOA:
A 5-HT3 receptor antagonist
Treats:
Acute nausea & vomiting (1-2hr post chemo or post op)
What is the MOA of Prochlorperazine & Metoclopramide?
What does it treat?
MOA:
D1 receptor antagonist
Treats:
Acute nausea & vomiting (1-2hr post chemo or post op)
What is the MOA of Aprepitant & Fosaprepitant?
What does it treat?
MOA:
An NK1 receptor antagonist
Treats:
Delayed nausea & vomiting (>24hrs after chemo)
What is the MOA of Filgrastim & Sargramostim?
What does it treat?
MOA:
A recombinant G(M)-CSF
Treats:
Neutropenia
What is the MOA of Epoetin alfa
What does it treat?
MOA:
Recombinant erythropoietin
Treats:
Anemia
Drugs to treat alcohol abuse?
1) Disulfiram
2) Naltrexone (Reduce Craving Opioid Receptor Antagonist)
3) Acamprosate
4) BZDs
1) Disulfiram
2) Naltrexone (Reduce Craving Opioid Receptor Antagonist)
3) Acamprosate
4) BZDs
Can all be used in therapy against ______abuse
Alcohol abuse
Nicotine addition can be treated with which drugs?
1) Varenicline
2) Bupropion
3) Clonidine
1) Varenicline
2) Bupropion
3) Clonidine
Can all be used in therapy against ______addiction
Nicotine
Opioid addiction maintenance can be treated with which drugs?
Opioid intoxication on the other hand can be treated with?
Opioid Maintenance:
1) Methadaone
2) Buprenorphine
3) Clonidine
4) Naltrexone
Opiod Intoxication: Naloxone
________Maintenance:
1) Methadaone
2) Buprenorphine
3) Clonidine
4) Naltrexone
________Intoxication: Naloxone
Opioid
Which drugs can treat BZD abuse?
Flumazenil ( Overdose)
Flumazenil ( Overdose) can treat _____
BZD OD
Which metabolite causes a Disulfiram like reaction in alcohol abuse?
Aldehyde dehydrogenase
Causing elevated formic acid:
1) Respiratory failure
2) Severe anion gap metabolic acidosis
3) Ocular damage
Cocaine vs Amphetamines
MOA
Cocaine MOA:
Blocks DA, NE, & 5-HT reuptake in the CNS to cause local anesthesia because of Na blockade
Amphetamine MOA:
Blocks NE & DA reuptake & it releases amines from a mobile pool to act as weak MAO inhibitors
Cocaine vs Amphetamines
Effects
Cocaine
1) Increased NE causing sympathomimetic effects
(high HR, Contractility, BP, Mydriasis, CNS excitation)
2) Increased DA (psychotic episodes, paranoia, hallucinations, & dyskinesias)
3) Increased 5-HT (behavioral changes/decreased appetite)
Amphetamines
1) Increased NE causing sympathomimetic effects
(high HR, Contractility, BP, Mydriasis, CNS excitation)
2) Increased DA (psychotic episodes, paranoia, hallucinations, & dyskinesias)
Cocaine vs Amphetamines
Toxicity
Cocaine
1) Excess NE (arrythmias, generalized ischemia + MI, strokes, & acute renal/hepatic failure)
2) Excess DA (major psychosis)
3) Excess 5HT (Serotonin syndrome)
Amphetamines
1) Excess NE (arrythmias, generalized ischemia + MI, strokes, & acute renal/hepatic failure)
2) Excess DA (major psychosis)
Cocaine vs Amphetamines
Withdrawal
Cocaine & Amphetamines
Cravings
Severe depression
Anhedonia
Anxiety
Benzodiazepines vs Barbiturates & Ethanol
MOA
BZD
Potentiates GABA interaction with GABA(A) receptors involving BZ1 & BZ2 binding sites
Barbiturates & Ethanol
Prolongs GABA, a GABA mimetic at high doses on GABA(A) receptors
Benzodiazepines vs Barbiturates & Ethanol
Effects
BZD
Light-to-moderate CNS depression
Barbiturates & Ethanol
CNS depression
Benzodiazepines vs Barbiturates & Ethanol
Toxicity
BZD
1) Sedation
2) Anterograde amnesia
(reverse with fluazenil)
Barbiturates & ethanol
1) Severe CNS depression
2) Respiratory depression
3) Death
Benzodiazepines vs Barbiturates & Ethanol
Withdrawal
Benzodiazepines
1) Rebound insomnia
2) Rebound anxiety
Barbiturates & ethanol
1) Agitation
2) Anxiety
3) Hyperreflexia
4) Life threatening seizures
5) Hallucinations
6) Delirium tremens
