Lactate accumulation reduces contractility and eventually necroses cardiomyocytes, releasing their troponin storage into the bloodstream. Serum troponin elevation is a characteristic biomarker of MI.Depending on the severity of ischemia, MIs are categorized as NSTEMI or STEMI. NSTEMI stands for Non-ST Elevation Myocardial Infarction, referencing the lack of ST-segment elevation in ECG traces. This is because in NSTEMI, only part of the myocardial wall is infarcted, which does not diagnostically present with ST-elevation. NSTEMI becomes STEMI when the entire myocardial wall is infarcted. Diagnostically, STEMI displays prolonged ST-segment elevation in ECG traces, and is thus named ST-Elevation Myocardial Infarction. Minutes after STEMI, fatal cardiac arrest could occur. STEMI is life-threatening if immediate reperfusion therapy is not initiated. Gangrene
Gangrene, specifically dry gangrene, is caused by an atherosclerotic or thromboembolic arterial occlusion. Gangrene is a complication of prolonged PAD, leading to shriveling, blackening, and infarction of peripheral tissue, commonly in the extremities. In severe cases, amputation of the affected limb is required. Ischemic Stroke
Ischemic stroke is a thrombotic, or rarely, thromboembolic or atherosclerotic complication of arteries supplying the brain. Occlusion of brain arteries leads to rapid ischemic death of neurons, both at the infarct core and ischemic penumbra. Similar to cardiomyocytes, neurons require constant perfusion for proper function. Any interruption of blood supply causes neurons to switch to anaerobic metabolism, exhausting intracellular ATP levels. ATP depletion causes an influx of calcium cations into neurons and efflux of excess glutamate, triggering the apoptosis and necroptosis of neurons.Neuronal necrosis precipitates irreversible brain damage.
Reactive airways dysfunction syndrome
While the acronyms are similar, reactive airway disease (RAD) and reactive airways dysfunction syndrome (RADS) are not the same.Reactive airways dysfunction syndrome was first identified by Stuart M. Brooks and colleagues in 1985 as an asthma-like syndrome developing after a single exposure to high levels of an irritating vapor, fume, or smoke. It can manifest in adults with exposure to high levels of chlorine, ammonia, acetic acid, or sulphur dioxide, creating symptoms like asthma. These symptoms can vary from mild to fatal and can even create long-term airway damage, depending on the amount of exposure and the concentration of chlorine. Patients that have been diagnosed with RADS will likely have methacholine airway hyperreactivity, yet other tests that also measure pulmonary functions may appear normal. Some experts classify RADS as occupational asthma. Those with exposure to highly irritating substances should receive treatment to mitigate harmful effects. Treatment for RADS is similar to treatment for other disorders that result from acute inhalation. Preexisting allergies can be a risk factor for developing RADS.The main difference between RAD and RADS is that RADS can occur after just one exposure to the inhalants and without any prior sensitization. In addition, although the symptoms of RADS are very similar to those of asthma, they may be resolved. While some physicians argue that RADS is also not a real clinical syndrome, it is more commonly recognized in legitimate associations than RAD. These associations include the American Thoracic Society and the American College of Chest Physicians.