Reflex After Effects Crack
Cornea. Cocaine abuse (whether via smoking or snorting) may lead to a condition called crack cornea, a well-reported syndrome of chronic corneal toxicity ranging in severity from mild punctate keratitis to severe bilateral infectious ulcers.80,81 Although the mechanism is unknown, it has several known contributors. Snorted cocaine, absorbed through the nasal mucosa, produces bilateral keratitis (worse on the side most frequently used for snorting) secondary to corneal nerve devitalization.75 Smoked cocaine makes direct contact with the cornea and acts like most topical anesthetics, softening the cornea and indirectly reducing the blink reflex.80,81 Aerosolized adulterants such as talc, sugar, flour, starch or procaine may cause surface damage as well.82
Reflex after effects crack
Retinal vasculature. Ocular vascular sequelae from any mode of intake may result from chronic cocaine use secondary to its sympathetic effects created by increased norepinephrine and resulting vasospasm, hypertension and atherosclerosis. Reported retinal vascular complications include central retinal artery occlusion, cilioretinal artery occlusion, intraretinal bleeding and CRVO.75 Additionally, cutting agents such as talcum powder (magnesium silicate) can deposit in retinal arterioles after chronic intravenous administration producing embolic sequellae.75,78 These particles appear as fine, refractile yellow-white crystals in the inner retinal layers and have been found in patients who inject other illicit substances such as heroin and methylphenidate.88,89
Binocular system. While exo posture and pupillary miosis are associated with opioid dependence, opioid withdrawal is associated with eso posture and pupillary mydriasis.99-101 A comitant acute eso deviation may develop and last for months after detoxification.99,100 This finding does not involve cranial nerve VI pathology and is not correlated with a hyperopic shift.99,100 There is no accepted mechanism for this; however, some theories assert that overactive accommodative convergence is the driving force (spasm of the near reflex).99 This seems to suggest that both opioid use and withdrawal creates a disequilibrium within the accommodative triad of miosis, convergence and accommodation, likely due to the disruption of normal mu opioid receptor activity in the midbrain.99,100
Elevation of the pain threshold during methamphetamine use may decrease the blink reflex and predispose to exposure keratopathy.110 Diluent additives such as lidocaine may further weaken the epithelium and lead to ulceration.110 Nasal inhalation brings methamphetamine into both spatial and circulatory proximity to the eye and may increase the risk of keratitis.110 Compounding the issue, mental effects of the drug such as increased awareness, heightened concentration and irritability result in excessive and harmful rubbing and scratching of the eyelids and ocular surface if symptoms develop.110
Cocaine can be snorted, swallowed, injected, or smoked. Its pharmacodynamics involves multiple complex mechanisms, although its half-life is short at about 1 hour. This drug binds and blocks monoamine (dopamine, norepinephrine, and serotonin) reuptake transporters with equal affinity. Monoamines accumulate in the synaptic cleft resulting in enhanced and prolonged sympathetic effects. The principal actions of cocaine on the cardiovascular system are from alpha- and beta-1-adrenoceptor stimulation resulting in increased heart rate, systemic arterial pressure, and myocardial contractility, which are major determinants of myocardial oxygen demand. Cocaine and its metabolites may cause arterial vasoconstriction hours after use. Epicardial coronary arteries are especially vulnerable to these effects, leading to decreased myocardial oxygen supply. Cocaine-induced platelet activation and thrombus formation are another deleterious effects caused by alpha-adrenergic- and adenosine diphosphate-mediated increase in platelet aggregation. Plasminogen activator inhibitor is also increased following cocaine use, thereby promoting thrombosis. Similar to local anesthetics such as lidocaine, cocaine blocks sodium channels and interferes with action potential propagation. This Vaughn-Williams class IC effect increases the risk of conduction disturbance and tachyarrhythmias. Adding to its complex toxicity, cocaine targets muscarinic acetylcholine, N-methyl-D-aspartate (NMDA), sigma, and kappa-opioid receptors.
Across the spectrum of acute and chronic effects, nearly every organ system can be affected. Trauma is often associated with cocaine use. Even the absence of cocaine, after a cocaine binge, may precipitate an ED visit due to withdrawal symptoms.
Crack is lipid soluble and therefore rapidly absorbed in the pulmonary capillaries. The term crack describes the crackling sound heard when cocaine freebase is smoked. Crack may be smoked in a pipe bowl containing 50-100 mg or in a cigarette with as much as 300 mg. Smoking crack bypasses the vasoconstriction that results when cocaine is snorted; therefore, the effects are similar to taking cocaine intravenously. Crack smokers may aggressively inhale against a small pipe and then perform a Valsalva maneuver before exhaling against pursed lips or forcefully blow the drug into a partner's mouth. These techniques are reputed to enhance the euphoria of cocaine.
Combining cocaine and heroin into a "speedball" causes frequent complications, as evidenced by the high-profile cases of actors John Belushi, River Phoenix, and Chris Farley in the 1980s and 1990s. Speedballing accounts for 12-15% of cocaine-related episodes in patients presenting to EDs in the United States. In speedballing, heroin is injected or snorted, followed immediately by smoking of cocaine. Cocaine is harder to purchase during the summer months than at other times, thus heroin users may speedball with crack in the summer. The effects of heroin last longer than do those of crack, and it modulates symptoms secondary to withdrawal from crack. In both cases, the second drug is used to supplement, rather than substitute, the primary drug.
Various agents can heighten the effects of cocaine and contribute to complications. Organophosphates may be taken to inhibit pseudocholinesterase, prolonging the effects of cocaine. However, because it produces organophosphate toxicity, the risk of fatality is increased. Cholinesterase inhibitors, such as carbamates, have a similar effect. Another practice involves coabusing crack cocaine and phenytoin to enhance the intoxication. In this practice, unbound phenytoin causes persons with hypoalbuminemia to become symptomatic at lowered drug levels; if death occurs, it usually is the result of respiratory and subsequent circulatory collapse.
Cocaine causes a direct negative inotropic effect on cardiac muscle, resulting in transient toxic cardiomyopathy. In one small series, 8 of 10 subjects who used cocaine long term had chest pain without MI but left ventricular ejection fractions less than 50%. In a case report, Jouriles describes a 35-year-old woman with hypotension, seizures, and hypoxemia who had an ejection fraction of 10% after smoking crack cocaine. 
The principal effect of cocaine, like ethanol, on mortality may be its association with homicide, suicide, and motor vehicle collisions.  In a study of 14,843 persons who were fatally injured in New York City over 3 years, fatal injury after cocaine use exceeded all deaths associated with other causes in persons aged 15-24 years. Although approximately one third of deaths associated with cocaine use were the result of its direct pharmacologic effects, two thirds were the result of traumatic injuries.
There's something about the sound of a crack in your back as you stretch that can feel just so darn satisfying. In fact there are entire social media feeds devoted to this "ahh" feeling: video after video of people instinctively groaning in pleasure as their back loudly pops.
Ferreira says cracking joints may trigger a release of "feel-good" chemicals, like endorphins, which help relieve pain. Then there is the power of the mind. There is research suggesting that a placebo effect may be involved, with people enjoying the feeling and the sound despite clinical effects of spinal treatment often being the same with or without a "pop".
There's something about the sound of a crack in your back as you stretch that can feel just so darn satisfying. In fact there are entire social media feeds devoted to this \\\"ahh\\\" feeling: video after video of people instinctively groaning in pleasure as their back loudly pops.
Ferreira says cracking joints may trigger a release of \\\"feel-good\\\" chemicals, like endorphins, which help relieve pain. Then there is the power of the mind. There is suggesting that a placebo effect may be involved, with people enjoying the feeling and the sound despite clinical effects of spinal treatment often being the same with or without a \\\"pop\\\".
I had a very difficult pregnancy with my daughter that led me to no choice but to deliver via CS. Along with it is a dose of Epidural Anesthesia which was both originally not in my birth plan. I had a really, really hard time recovering after the effect of the anesthesia was wearing down. It started when I was still in the recovery room. I experienced all the routine side effects of the anesthesia like vomiting, chills, you name it. But what caused me to prolong my stay in the recovery room was the blood in my urine bag. I stayed in the recovery room for almost eight hours because of it. Then when I got to my room, it took me 2 days before I could fully mobilize my entire body. It did give a relief during my delivery but it also took its toll after the effects are gone.
Conclusion: Corneal complications of crack cocaine smoking are caused by a number of synergistic factors, including direct toxicity of crack cocaine vapours to surface cells, impairment of neurogenic support to corneal epithelial integrity, desiccation of the eye surface due to diminished blinking reflex, low level chemical burns and mechanical denudement of surface cells through eye rubbing. 350c69d7ab