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The optic nerve is especially susceptible to damage by formic acid, and visual disturbances occur in 29 – 72% of cases (10). These visual disturbances range from initial blurriness, to photophobia, altered visual fields and, if left untreated, eventual blindness (9). Although methanol and ethylene glycol both produce CNS depression, isopropanol generates the most profound degree (1).

One of the most sensitive pathways to the acute and chronic effects of alcohol abuse is the hypothalamo-pituitary-adrenal (HPA) axis (FIGURE 3). Responsiveness of the HPA axis to psychological and physical stressors can be heightened or blunted depending on duration of alcohol abuse (97). Alcohol-mediated disruption in HPA function has been implicated in the pathophysiology of pseudo-Cushing’s syndrome (19), addiction (48), dependence (48), and relapse of recovering alcoholics (3). Alcohol produces dose-, frequency-, and duration-specific effects on arginine vasopressin (AVP), leading to alterations in water balance and mean arterial blood pressure homeostasis (115). Our studies have shown that acute alcohol intoxication augments paraventricular nucleus nitric oxide inhibitory tone and suppresses the hypovolemia- but not hyperosmolarity-induced AVP release (127).

Who is more prone to the risks

Alcoholic liver disease is one of the primary causes of chronic liver disease. Acute alcohol intoxication can cause alcoholic hepatitis and acute on chronic liver failure. This is usually in patients who are chronic alcohol abusers or patients already affected by alcoholic cirrhosis.

Chronic alcohol abuse increases risk for cardiovascular and pulmonary disease. Alcohol-induced myocardial dysfunction results from oxidative stress, cardiomyocyte mitochondrial and sarcoplasmic reticulum damage, altered calcium dynamics, and cardiac fibrosis. Alcohol-mediated hypertension results from potentiation of the RAAS reflected in elevated circulating angiotensin II levels, cardiac angiotensin converting enzyme, and angiotensin type 1 (AT1) receptor expression.

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It’s not necessary to have all the above symptoms before seeking medical help. A person with alcohol poisoning who has passed out or can’t wake up could die. If you think that someone has alcohol poisoning, get medical attention right away. Jellinek viewed alcoholism as a chronic relapsing condition that needed to be treated by health professionals and developed a theory on the progression of alcoholism through various stages. Consuming too much alcohol can inhibit the breakdown of fats in the liver, causing fat accumulation. Alcohol-related liver disease actually encompasses three different liver conditions.

stages of alcohol poisoning

Oxidative stress resulting from either an excess production of ROS or a reduction in reducing antioxidant equivalents has been consistently demonstrated to be an overall mechanism of tissue injury resulting from chronic alcohol abuse (25, 40). Although acute alcohol intoxication has been consistently seen to reduce inflammation in response to infectious challenges, chronic alcohol consumption favors a pro-inflammatory milieu that plays an important role in tissue injury (114). The average rate at which alcohol is eliminated from the body is ∼7 g/h, which translates to ∼1 drink/h. Alcohol undergoes first pass gastric metabolism by the enzyme alcohol dehydrogenase (ADH).

Death

Alcohol decreases GSH, which leaves pulmonary cells susceptible to oxidative stress injury (50). As mentioned above, alcohol activates the RAAS, which promotes superoxide production by NADPH-oxidases in the lung (90). Chronic alcohol also interferes with the production of pulmonary surfactant by disrupting the composition of dipalmitoyl-lecithin stages of alcohol poisoning (50). As a result, susceptible alveolar type II cells are lost to oxidative stress-induced apoptosis and necrosis, which reduces barrier function and increases alveolar-capillary permeability. A low level of alcohol intoxication causes mild symptoms, while severe intoxication, or alcohol poisoning, can be life threatening.

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