Toxic Effects on Cardiovascular System and Visual/Skin Responses Quiz

Cardiac Function and Cardiotoxicity

• Left-sided heart failure results in pulmonary edema, while right-sided heart failure leads to pooling of blood in the extremities, mainly the lower legs.
• Cardiomyopathies encompass any disease state that alters myocardial function and may result from exposure to toxins causing high blood pressure, leading to cardiac hypertrophy.
• Cardiac function is dependent on tight regulation of ion channel activity and homeostasis, any disruption of which may induce a cardiotoxic reaction, resulting in disturbances in heart rhythm.
• Cardiotoxicity can be caused by inhibition of Na+, K+-ATPase, resulting in increased intracellular Na+ and elevated Ca2+, leading to inotropic actions.
• Cardiotoxicity can also be caused by channel blockade, which can lead to reduction of conduction velocity, prolonged QRS duration, and negative inotropic effects.
• Xenobiotic-induced constriction of the coronary vasculature can result in ischemia, and ischemia-reperfusion injury may lead to the production of toxic oxygen radicals, causing tissue damage.
• Organellar dysfunction due to exposure to certain toxins can disturb the regulation of intracellular Ca2+ and compromise ATP production, leading to cardiotoxicity.
• Ethanol metabolites from chronic consumption can lead to lipid peroxidation of cardiac myocytes, resulting in reduced conductivity, arrhythmias, and disturbances in actin and myosin association.
• Cardiac glycosides like digoxin, used to treat heart failure, can lead to arrhythmias and reduced resting membrane potential due to Ca2+ overload.
• Tricyclic antidepressants may have direct cardiotoxic actions on cardiac myocytes and Purkinje fibers, depressing inward Na+ and Ca2+ and outward K+ currents.
• General anesthetics may decrease cardiac output and contractility, resulting in arrhythmias, through actions like blocking Ca2+ channels.
• Vascular endothelial cells play a crucial role in the regulation of vascular tone and angiogenesis, and blood vessel injury is positively correlated with vascular diseases like atherosclerosis, which leads to vessel wall changes and plaque formation, potentially causing ischemia, hypertension, and infarction.

Vascular Toxicity and Toxic Responses of the Visual System and Skin

• Atherosclerosis involves vessel wall changes with focal intimal thickenings and plaque formation, leading to ischemia and hypertension
• Major hypotheses for atherosclerosis formation include chemical injury triggering recruitment of platelets and smooth muscle cell migration
• Disturbances of vascular structure and function can result from hypotension, hypertension, and thrombosis caused by toxicant exposure
• Mechanisms of vascular toxicity include alterations in membrane structure and function, redox stress, and vessel-specific bioactivation of protoxicants
• Common vasculotoxic agents include nicotine, cocaine, heavy metals, and 1,3-butadiene, each with specific effects on the cardiovascular system
• All toxicants absorbed into the circulatory system contact vascular cells before reaching other body sites
• Chemically induced disturbances in cardiac function may consist of effects on heart rate, contractility, conductivity, and excitability
• Exposure to toxic chemicals, vapors, or therapeutic drugs can result in structural and functional alterations in the eye and visual system
• Ocular absorption and distribution following topical exposure can affect the cornea, conjunctiva, and eyelids
• Tear film, with both hydrophobic and hydrophilic properties, is the first site of action for toxic chemicals and systemic drugs
• Toxic responses of the visual system and skin can result from environmental and occupational exposure to various toxins
• Direct exposure to chemicals, gases, and particles can affect all parts of the eye, leading to structural and functional alterations