Toxicology Study Guide

The process of identifying the specific type of bacteria causing an infection.

The ability of an antibiotic to stop the growth of a bacteria.

The lowest concentration of an antibiotic needed to inhibit the growth of a bacteria.

The location within the body where the infection is occurring.

Factors related to the patient's health that influence antibiotic choice.

The ability of an antibiotic to reach the infection site, such as crossing the blood-brain barrier for central nervous system infections.

Growing bacteria in a lab to identify them and test their susceptibility to antibiotics.

Advantages of growing bacteria in a lab to guide antibiotic choice.

A variety of Cannabis sativa with low THC content, used for industrial purposes like fabric, insulation, and food products.

Refers to strains of Cannabis sativa with higher concentrations of THC, making it psychoactive and used primarily for medicinal or recreational purposes.

A condition where the diastolic blood pressure (DBP) is elevated above 90 mmHg, indicating narrowing of the arterioles.

A condition where both systolic blood pressure (SBP) and diastolic blood pressure (DBP) are elevated.

Atherosclerosis is a condition where the arterial wall is damaged due to the buildup of white blood cells, calcium, and fat, causing plaque formation in the coronary artery. It leads to structural damage to arteries due to calcium accumulation and increased collagen content.

A condition where the systolic blood pressure (SBP) is elevated above 140 mmHg, indicating increased stiffness of larger arterioles.

Hypertrophy is the thickening of the arterial smooth muscle layer due to high blood pressure, disrupting the endothelial cell layer and leading to the buildup of white blood cells, calcium, and fat in the arteriole wall. It can cause plaque buildup in the coronary artery, leading to structural damage to arteries due to calcium accumulation and increased collagen content.

80% of hypertension cases, with an unknown cause.

Selective beta-1 blockers like metoprolol reduce blood pressure by blocking beta-1 receptors in the heart, decreasing heart rate and contractility, and suppressing the sympathetic nervous system. They also reduce renin release.

Propranolol, a non-selective beta-blocker, reduces blood pressure by obstructing both beta-1 and beta-2 receptors. It lowers blood pressure by decreasing heart rate and contractility, suppressing the sympathetic nervous system, and impacting renin release.

Selective beta-1 blockers like metoprolol mainly affect the heart, causing myocardial depression, decreased exercise tolerance, and possible bradycardia. Their effects on the lungs are minimal due to selective targeting.

Non-selective beta-blockers like propranolol cause myocardial depression, reduced exercise tolerance, and bronchoconstriction due to blocking both beta-1 and beta-2 receptors.

Prazosin, an alpha-1 receptor antagonist, reduces blood pressure by blocking alpha-1 receptors on blood vessels, leading to vasodilation and decreased peripheral resistance. It also reduces venous return by blocking vascular constriction.

A common side effect of alpha-1 receptor antagonists is reflex tachycardia. The body's natural response to low blood pressure is to increase heart rate, leading to faster heartbeats.

Antibiotics are a broad category of substances that inhibit the growth of or kill bacteria. They are used to treat bacterial infections and include commonly known drugs like penicillin and amoxicillin.

Antibacterials are substances that specifically target bacteria, preventing their growth or killing them. While often used interchangeably with antibiotics, antibacterials can also encompass non-medicinal agents like soap and disinfectants.

Infections acquired in healthcare settings. Often associated with higher rates of antibiotic resistance due to extensive antibiotic use in medical environments.

Infections acquired outside of healthcare settings. Typically caused by non-resistant strains but increasingly include resistant bacteria.

Mechanism of bacterial resistance where bacteria evolve to change the target site for antibiotics, reducing the drug's effectiveness.

Mechanism of bacterial resistance where bacteria exchange genes that code for antibiotic resistance.

Bacterial defence mechanism where bacteria pump out antibiotics, preventing them from reaching their target.

A mechanism of bacterial resistance where changes in bacterial cell walls prevent antibiotic entry.

Bacterial defence mechanism where bacteria produce enzymes to degrade antibiotics.

The overuse or misuse of antibiotics can lead to the emergence of resistant bacteria.

The effectiveness of these antibiotics depends on the highest concentration of drug in the blood (Cmax) relative to the MIC of the bacteria. A higher Cmax generally means more effective killing.

The effectiveness of these antibiotics depends on how long the drug concentration stays above the minimum inhibitory concentration (MIC).

A prolonged post-antibiotic effect (PAE) means the bacteria continue to be suppressed even after the antibiotic levels drop below the MIC. This effect is particularly important for antibiotics that only kill bacteria when they are actively growing.

This strategy aims to achieve high peak drug concentrations to maximize killing.

This strategy involves frequent dosing or continuous infusion to maintain consistent drug levels above the MIC.

These antibiotics typically have a longer duration of action, reducing the need for frequent administration. They are also useful for treating severe infections and for patients with impaired kidney or liver function.

Frequent dosing to maintain effective drug concentration, even at lower levels, is crucial for these antibiotics.

The potential risk of toxicity at high peak concentrations is a major disadvantage of these antibiotics.

Treatments used in combination with surgery to destroy remaining cancer cells after the primary tumor has been removed, often involving radiation or pharmacological agents.

Drugs that directly target the process of cell division by interfering with a specific step, leading to cell cycle arrest and death.

A group of cytotoxic agents that form covalent bonds with DNA, causing cross-linking and damage, leading to cell death.

Cyclophosphamide, a drug that requires activation by CYP450 enzymes to become active. It forms covalent bonds with DNA and can be used as an immunosuppressant.

A group of cytotoxic agents that disrupt the assembly of microtubules, crucial for cell division, preventing chromosome separation and leading to cell death.

Vincristine, a drug that prevents microtubule polymerization by binding to β-tubulin, halting mitosis and potentially destabilizing already assembled microtubules.

Treatments that aim to reduce hormone signaling in hormone-responsive cancers, either by inhibiting hormone receptor activation or reducing hormone production.

Tamoxifen, a selective estrogen receptor modulator (SERM) used in estrogen-receptor-positive breast cancer.

Chemotherapeutics that target specific receptors involved in cell growth pathways, often focusing on protein kinases or monoclonal antibodies.

Protein Kinase Inhibitors, a type of molecule targeting agent that inhibits key enzymes involved in cancer growth pathways, often targeting tyrosine kinases involved in growth factor signaling.

Imatinib, a protein kinase inhibitor that targets kinases involved in chronic myeloid leukemia (CML) and gastrointestinal stromal tumors.

Biologics, a type of molecule targeting agent that utilizes monoclonal antibodies to either stimulate the immune system or block tumor growth.

Bevacizumab, a biologic that targets VEGF (vascular endothelial growth factor), a key factor in angiogenesis (formation of new blood vessels).

The phenomenon of cancer cells developing resistance to chemotherapeutic agents, either immediately upon initiation (primary resistance) or during the course of therapy (acquired resistance).

Combination Therapy, a strategy that uses multiple chemotherapeutic agents at lower doses to target different aspects of cancer cell growth, minimizing the likelihood of severe toxicities and maximizing the chance of success.