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Cocaine hypertension with

The association of cocaine abuse with progressive chronic renal failure has received increased attention in recent years [156-158]. Ward and co-workers have reported on the possibility of a progressive nephropathy with features of hypertension, azotemia... [Pg.606]

II. Indications. Labetalol may be used to treat hypertension and tachycardia associated with stimulant dmg overdose (eg, cocaine or amphetamines). Note Hypertension with bradycardia suggests excessive alpha-mediated vasoconstric-... [Pg.459]

Serious adverse effects of epinephrine potentially occur when it is given in an excessive dose, or too rapidly, for example, as an intravenous bolus or a rapid intravenous infusion. These include ventricular dysrhythmias, angina, myocardial infarction, pulmonary edema, sudden sharp increase in blood pressure, and cerebral hemorrhage. The risk of epinephrine adverse effects is also potentially increased in patients with hypertension or ischemic heart disease, and in those using (3-blockers (due to unopposed epinephrine action on vascular Ui-adrenergic receptors), monoamine oxidase inhibitors, tricyclic antidepressants, or cocaine. Even in these patients, there is no absolute contraindication for the use of epinephrine in the treatment of anaphylaxis [1,5,6]. [Pg.213]

CH, a 42-year-old man, comes into the emergency department after his sister discovered him seizing at home. He has a history of hypertension, diabetes, epilepsy, and rheumatoid arthritis. His medications include hydrochlorothiazide, gly-buride, phenytoin, and aspirin. He smokes one pack per day, drinks heavily on the weekends, and has a history of cocaine use. Upon further discussion with his sister, you discover that he stopped taking his phenytoin 4 days ago due to failure to obtain a refill from his doctor. He is currently unarousable since his last seizure 10 minutes ago. [Pg.462]

Cocaine differs from the other local anesthetics with respect to its cardiovascular effects. Cocaine s blockade of norepinephrine reuptake results in vasoconstriction and hypertension, as well as cardiac arrhythmias. The vasoconstriction produced by cocaine can lead to local ischemia and, in chronic abusers who use the nasal route, ulceration of the mucous membrane and damage to the nasal septum have been reported. The vasoconstrictor properties of cocaine can be used clinically to decrease bleeding from mucosal damage or surgical trauma in the nasopharyneal region. [Pg.570]

At higher doses, cocaine can produce undesirable effects, including tremor, emotional lability, restlessness, irritability, paranoia, panic, and repetitive stereotyped behavior. At even higher doses, it can induce intense anxiety, paranoia, and hallucinations, along with hypertension, tachycardia, ventricular irritability, hyperthermia, and respiratory depression. In overdose, cocaine can cause acute heart failure, stroke, and seizures. Acute intoxication with cocaine produces these various clinical effects, depending on the dose these effects are mediated by inhibition of the dopamine transporter and in turn by the effects of excessive dopamine activity in dopamine synapses, as well as by norepinephrine and serotonin in their respective synapses. [Pg.505]

Four substances have been described as having pressor effects, which are probably amines or aminelike. Urosympathin, described by Holtz, Credner, and Kronberg (34), is a substance found in normal urine in amounts per day, giving a pressor response equal to 2 to 3 mg. of hydroxytyramine or 100 to 150 micrograms of epinephrine or arterenol. In cases of essential hypertension the amount is said to be increased three- to fourfold. Because its action was intensified by cocaine and lessened by ergotoxin and yohimbine, they believed that it represented a mixture of hydroxytyramine, epinephrine, and arterenol. The material was recovered by lead acetate precipitation of urine with subsequent acid hydrolysis. [Pg.12]

An unidentified substance, named nephrin, was described by Enger (19). Nephrin is a pressor material having a prolonged action, obtained from extracts of renal cortex, but not present in any other tissues. It was also found in urine and in blood and was said to have been present in increased amounts both in hypertensive dogs and in patients with hypertension, eclampsia, nephritis, and other hypertensive conditions. Its action was not intensified by cocaine nor affected by ergotoxin and it did not act upon the guinea pig uterine muscle. As it was dialyzable, it probably was not renin. If this work is substantiated, nephrin represents yet another renal pressor substance probably of nonprotein nature. Its relation to hypertension has not been substantiated. [Pg.16]

The hazards of cocaine specific for pregnant women include premature rupture of placental membranes, spontaneous abortion, abnormal labor, and several general medical risks (e.g., hypertension). Their babies typically have growth retardation with consequent lowered birthweight. Cocaine use is also related to sudden infant death syndrome, characterized by abnormal respiratory control, particularly during sleep. [Pg.41]

Cardiovascular effects include tachycardia, hypertension, and increased cardiac irritability large intravenous doses can cause cardiac failure. Cardiac dysrhythmias have been ascribed to a direct toxic effect of cocaine and a secondary sensitization of ventricular tissue to catecholamines (17), along with slowed cardiac conduction secondary to local anesthetic effects. Myocardial infarction has increased as a complication of cocaine abuse (7,8). Dilated cardiomyopathies, with subsequent recurrent myocardial infarction, have been associated with long-term use of cocaine, raising the possibility of chronic effects on the heart (18). Many victims have evidence of pre-existing fixed coronary artery disease precipitated by cocaine (SEDA-9, 35) (19-21). However, myocardial infarction has been noted even in young intranasal users with no evidence of coronary disease (22), defined by autopsy or angiography (23,24). If applied to mucous membranes, cocaine causes local vasoconstriction, and, with chronic use, necrosis. [Pg.490]

Tachycardia and vasoconstriction from cocaine can exacerbate coronary insufficiency, complicated by dysrhythmias and hypertensive and vascular hemorrhage (1). Sudden deaths have been reported in patients with angina (40). Chronic dosing includes cardiomyopathy and cardiomegaly other chronic conditions include endocarditis and thrombophlebitis. Crack smoking has led to pneumopericardium (41). [Pg.490]

A 52-year-old woman with a history of hypertension for 15 years developed acute left flank pain, nausea, and vomiting. On a previous similar occasion 2 weeks before she had had a trace of proteinuria and microscopic hematuria. A contrast-enhanced CT scan of the abdomen had not shown stones, hydronephrosis, or morphological abnormalities. She had had no rash. Her urine contained cocaine. Creatine kinase and lactate dehydrogenase activities were raised and there... [Pg.494]

Dissection of the aorta has been reported during cocaine use (82,83). The authors of these two reports noted that all six cases of this rare complication reported in the past 5 years were in men with pre-existing essential hypertension. In a review of emergency visits to a hospital during a 20-year period, 14 of 38 cases of acute aortic dissection involved cocaine use 6 were of type A and 8 of type B (84). Crack cocaine had been smoked in 13 cases and powder cocaine had been snorted in one case. The mean time of onset of chest pain was 12 hours after cocaine use. The chronicity of cocaine use was not known in most of the cases. The cocaine users were typically younger than the non-cocaine users. Chronic untreated hypertension and cigarette smoking were often present. [Pg.494]

Absorption of cocaine from the nasal mucosa in eight patients using cotton pledglets soaked in 4 ml of 4% cocaine and applied for 10 or 20 minutes resulted in an absorption rate four times higher than expected, but was not associated with any cardiovascular disturbance however, one of four patients who received 4 ml of 10% cocaine for 20 minutes developed intraoperative hypertension and another transient ventricular tachycardia (99). The authors advised against topical use of 10% cocaine. [Pg.496]

A 44-year-old man with hepatitis C and cirrhosis, esophageal varices, and poorly controlled hypertension, who was also a chronic alcoholic and crack cocaine abuser, had his varices injected at endoscopy and... [Pg.502]

Cocaine can cause acute renal insufficiency (SEDA-21,19) (SEDA-24, 38). Acute renal insufficiency, with malignant hypertension, apparently precipitated by... [Pg.508]

Chronic cocaine use can exacerbate pre-existing hypertension, when renal blood vessels narrow secondary to cocaine-induced intimal fibrosis. Acute renal insufficiency with concomitant rhabdomyolysis after cocaine use has been reported (207,208), but it can also occur, albeit rarely, in the absence of rhabdomyolysis (209). [Pg.508]

Hypertensive crisis with headache, intracranial bleeding, and death may result from combining MAO inhibitors with sympathomimetic drugs (e.g., amphetamines, methylphenidate, cocaine, dopamine, epinephrine, norepinephrine, and related compounds methyidopa,... [Pg.231]


See other pages where Cocaine hypertension with is mentioned: [Pg.718]    [Pg.606]    [Pg.150]    [Pg.394]    [Pg.240]    [Pg.257]    [Pg.163]    [Pg.532]    [Pg.535]    [Pg.55]    [Pg.1250]    [Pg.179]    [Pg.732]    [Pg.1399]    [Pg.164]    [Pg.171]    [Pg.493]    [Pg.494]    [Pg.502]    [Pg.503]    [Pg.508]    [Pg.512]    [Pg.524]    [Pg.524]    [Pg.578]    [Pg.607]    [Pg.109]   
See also in sourсe #XX -- [ Pg.186 ]




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Hypertension with

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