Lol... that's cuteI am curious if any has used cocaine daily? As of right now I have been shooting cocaine for about 2 weeks straight. I still eat and sleep but I'm curious is this a drug that my body can handle on a daily basis?
Coke ois not really the same n e more, especially with the impurities these days the prods cut to shit
I still get really good girl. I can do 5 shots out of a 20 bag good enough to give me the train. But I’m also in Florida, closer to the source, and in a port city so that might explain it. I IV so I don’t tolerate cut of any kind on my clean.Yeah absolutely. Some of my friends are pretty into coke and they'll be like "dude I got some FIRE shit this time" and it won't numb my face or throat at all. I'm like, sorry but this isn't coke. Back in 2001-2005 when I was in college we got some pretty good coke, it was cut for sure but it made your throat numb and was that beautiful lovely clean feeling. I've only had really good coke once, I did one tiny ~15mg spoon in each nostril and my entire face went numb and I felt so good I wanted to cry. Then I came down an hour or so later and felt absolutely fine.
Yeah absolutely. Some of my friends are pretty into coke and they'll be like "dude I got some FIRE shit this time" and it won't numb my face or throat at all. I'm like, sorry but this isn't coke..
Seizures may occur, particularly with the more rapid and higher levels achieved when cocaine is injected or smoked as “crack”. In patients with pre-existing enhanced risk of seizures (for example, those with epilepsy or taking other epileptogenic drugs), intranasal cocaine may apparently precipitate fits. When they do occur, seizures may be prolonged and fatal, not only through the secondary consequences of prolonged seizures but also perhaps through the direct effect of the high drug levels.
Hyperpyrexia may develop because of direct effects on the hypothalamus and also the agitation and hyperactivity that these stimulant drugs tend to produce. These may contribute along with muscle vasoconstriction, central rigidity, and seizures to the rhabdomyolysis that sometimes occurs in more sick patients. In addition, cocaine may have a direct toxic effect on skeletal muscle (as it does on cardiac muscle). These problems have been emphasised in patients dying after the use of Ecstasy.
Movement disorders have been reported with these drugs—for example, tics and acute dystonic reactions with cocaine and acute chorea with metamphetamine.
Long term cocaine abuse has been associated with cognitive dysfunction and cerebral atrophy, and with multiple focal perfusion defects on single photon emission computed tomography (SPECT) and positron emission tomography (PET) studies. These effects may all persist despite abstinence. Of course, there are often other confounders in the lifestyles of these individuals which may also be implicated, not just the drug.
About 70% of strokes arising with intranasal and intravenous use are caused by haemorrhage rather than infarction. However, the pattern of stroke may depend upon the preparation used and upon its mode of administration, since infarcts are as likely as haemorrhages when alkaloidal cocaine, “crack”, is smoked. This may be due to a complex interplay of pharmacokinetic and pharmacodynamic factors, as well as the concentration and type of contaminants, and whether there has been coincidental alcohol use (which more commonly accompanies intranasal cocaine use). These factors may all change the half lives of cocaine metabolites, their metabolic pathways, and their effects on the blood vessels. The liver metabolises cocaine with a half life of only about one hour, but its major metabolites last much longer, sometimes days, and they too have vasoconstrictive actions. The pharmacokinetics of cocaine and its metabolites show large inter-individual variation and there is evidence for prolongation of action in chronic cocaine abusers, which may also occur when alcohol is consumed simultaneously. This may explain why most strokes occur in chronic users and/or with alcohol use.
Haemorrhages may be intracerebral (basal ganglia, thalamic, lobar, or brainstem), intraventricular or subarachnoid. They may occur especially in individuals with pre-existing vascular malformations such as aneurysms and arteriovenous malformations (accounting for up to 50% of intracranial haemorrhage with cocaine). Most strokes tend to occur within an hour of use, especially for crack and intravenous cocaine, and most of the others within three hours. The surge in blood pressure is thought to be to blame for acute rupture. Blood pressure may no longer be elevated by the time of presentation, or alternatively, the hypertension may be wrongly attributed at presentation to the haemorrhage itself. Vasospasm has also been postulated to contribute to aneurysm rupture. In injecting addicts, with or without demonstrable infective endocarditis, septic arteritis and/or mycotic aneurysms need consideration as alternative causes of intracranial haemorrhage. Haemorrhagic transformation of infarcts is another cause. The possibility of cerebral vasculitis is often mentioned, but this is usually because of irregularity of arteries seen on angiography (see below). However histological proof is very seldom provided (a handful of cases only), especially in cases involving abuse of cocaine alone. No cases of vasculitis were found in several larger postmortem series of patients dying of intracranial haemorrhages. If vasculitis does occur in pure cocaine abuse, it must be very rare. Cerebral biopsy specimens examine only small vessels but in the few cases that have revealed vasculitis at postmortem, it is limited to these small vessels and spares the larger ones and would not be seen on angiography.
Infarction of brain, cord (usually anterior spinal artery syndromes) or retina is less common than haemorrhage, but may be particularly associated with smoking crack cocaine. There may be preceding transient ischaemic attacks (TIAs) in 10% of crack related infarcts. Patients tend to develop their infarct within a few hours of use, or wake up with a deficit the morning after. Imaging usually shows infarcts involving cortical or deep penetrating arteries. They often occur in individuals without conventional risk factors and through a variety of potential mechanisms, though again proof is seldom possible.
Cocaine and its metabolites do undoubtedly have major effects on cerebral (and other) arteries. The acute vasospasm has been demonstrated in animals, and by magnetic resonance angiography (MRA) and transcranial Doppler in human volunteers, and occurs in large and medium sized arteries, probably mediated by endothelin 1. In patients, angiography may show beading and focal stenosis, and there may also be associated large vessel occlusion. Such abnormalities may arise through vasospasm caused by the drug itself but the possibility of additional subarachnoid haemorrhage needs excluding. Postmortem specimens in a few patients have shown that arteries may sustain damage to the media and elastic lamina, but no abnormality has been detectable in most studies and in some patients no vasculopathy can be demonstrated (other than aneurysms and AVMs in cases with intracranial haemorrhage).
In half the cases of cocaine infarcts, angiography is unremarkable and does not show the above abnormalities. Occasionally intraluminal clot is seen in the internal carotid artery, perhaps possibly because of “stasis” distant to extracranial carotid artery spasm. Artery-to-artery embolism is therefore another possible mechanism for vessel occlusion, in addition to spasm, in situ thrombosis, and embolism from the heart.