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Diarrhea acute

Pantothenic acid toxicity has not been reported in humans. Massive doses (10 g/d) in humans have produced mild intestinal distress and diarrhea. Acute toxicity was observed in case of mice and rats by using calcium pantothenate at fairly large doses (92). [Pg.63]

Indications Lower respiratory infection Bone and joint infection Skin and skin structure infection Urinary tract infection Infectious diarrhea Acute sinusitis Prostatitis Typhoid fever Complicated intra-abdominal infection Gonorrhea... [Pg.48]

Gastrointestinal Anthrax. Gastrointestinal (GI) anthrax is contracted by germination of ingested spores in the upper or lower GI tract. The GI forms of the disease are generally an upper GI form and a lower GI form. In the upper GI form, oral or esophageal ulcers develop with associated edema, lymphadenopathy, and sepsis. In the lower GI form, partial necrosis of the GI tract can occur with symptoms including bloody diarrhea, acute abdomen, ascites, or sepsis. [Pg.406]

Gastrotoxicity due to mefenamic acid is marked. Other than the common adverse effects (nausea, anorexia, vomiting, pain, diarrhea), acute peptic ulcer, intestinal hemorrhage, hematemesis, abdominal distension, and profuse steatorrhea (SEDA-2, 97) have been reported. Mefenamic acid, unhke other NSAIDs, can provoke enteritis and cohtis in patients with no known predisposing factors (8). It accelerates bowel transit in healthy volunteers (SEDA-16,112). [Pg.2230]

Sodium borate decomposes into borate and peroxide and is less toxic than potassium bromate. From 3 to 6g and from 15 to 30 g boric acid is potentially fatal to children and adults, respectively. Cutaneous manifestations include desquamating, erythematous rash commonly over palms, soles, buttocks, and scrotum. The lesion may progress to exfoliation. Central nervous system (CNS) effects range from irritability, restlessness, and headache to coma and convulsions in severe cases. Gastrointestinal symptoms include anorexia, nausea, vomiting, and diarrhea. Acute renal tubular necrosis may lead to renal failure in moderate to severe cases. [Pg.671]

This is pathogenic flagellate which usually inhabits the duodenum and upper jejunum but may also be found in the gall bladder. The parasite occurs both in the trophozoite and encysted forms. The infection is acquired by consuming food or drink contaminated with cysts and, therefore, it is more prevalent in children than the adults. The clinical manifestations of the disease may include epigastric pain, nausea, flatulence and diarrhea. Acute giardiasis may be associated with steatorrhea and weight loss [49]. [Pg.26]

FIGURE 36-1. Recommendations for treating acute diarrhea. Foiiow these steps (1) Perform a compiete history and physicai examination. (2) is the diarrhea acute or chronic if chronic diarrhea, go to Fig. 36-2. (3) if acute diarrhea, check for fever and/or systemic signs and symptoms (i.e., toxic patient), if systemic illness (fever, anorexia, or volume depletion), check for an infectious source. If positive for infectious diarrhea, use appropriate antibiotic/anthelmintic drug and symptomatic therapy. If negative for infectious cause, use only symptomatic treatment. (4) If no systemic findings, then use symptomatic therapy based on severity of volume depletion, oral or parenteral fluid/electrolytes, an-tidiarrheal agents (see Table 36-4), and diet. [Pg.680]

Diarrhea acute (cramping, flushing, vomiting, diaphoresis within 1 hour of completion related to cholinergic effects) and delayed (>12 hours after administration usually after the second or third dose) may be severe moderately high emetogenic potential myelosuppression neutropenia alopecia fatigue increased liver function tests pulmonary toxicity diffuse infiltrates, fever, dyspnea... [Pg.2303]

Hypotension, hyperkalemia, cough, rash, taste disturbances, headache, dizziness, fatigue, nausea, vomiting, diarrhea, acute renal failure, neutropenia, proteinuria, and angioedema... [Pg.1130]

Acute intoxication with DHBs occurs mainly by the oral route symptoms are close to those induced by phenol poisoning including nausea, vomiting, diarrhea, tachypnea, pulmonary edema, and CNS excitation with possibiUty of seizures followed by CNS depression. Convulsions are more frequent with catechol as well as hypotension due to peripheral vasoconstriction. Hypotension and hepatitis seem more frequent with hydroquinone and resorcinol. Methemoglobinemia and hepatic injury may be noted within a few days after intoxication by DHBs. [Pg.494]

Treatment of Manic—Depressive Illness. Siace the 1960s, lithium carbonate [10377-37-4] and other lithium salts have represented the standard treatment of mild-to-moderate manic-depressive disorders (175). It is effective ia about 60—80% of all acute manic episodes within one to three weeks of adrninistration. Lithium ions can reduce the frequency of manic or depressive episodes ia bipolar patients providing a mood-stabilising effect. Patients ate maintained on low, stabilising doses of lithium salts indefinitely as a prophylaxis. However, the therapeutic iadex is low, thus requiring monitoring of semm concentration. Adverse effects iaclude tremor, diarrhea, problems with eyes (adaptation to darkness), hypothyroidism, and cardiac problems (bradycardia—tachycardia syndrome). [Pg.233]

Other agents are also used for the treatment of manic-depressive disorders based on preliminary clinical results (177). The antiepileptic carbamazepine [298-46-4] has been reported in some clinical studies to be therapeutically beneficial in mild-to-moderate manic depression. Carbamazepine treatment is used especially in bipolar patients intolerant to lithium or nonresponders. A majority of Hthium-resistant, rapidly cycling manic-depressive patients were reported in one study to improve on carbamazepine (178). Carbamazepine blocks noradrenaline reuptake and inhibits noradrenaline exocytosis. The main adverse events are those found commonly with antiepileptics, ie, vigilance problems, nystagmus, ataxia, and anemia, in addition to nausea, diarrhea, or constipation. Carbamazepine can be used in combination with lithium. Several clinical studies report that the calcium channel blocker verapamil [52-53-9] registered for angina pectoris and supraventricular arrhythmias, may also be effective in the treatment of acute mania. Its use as a mood stabilizer may be unrelated to its calcium-blocking properties. Verapamil also decreases the activity of several neurotransmitters. Severe manic depression is often treated with antipsychotics or benzodiazepine anxiolytics. [Pg.233]

Toxicity. Sugar alcohols are classified as relatively harmless. Acute oral toxicity values in mice for mannitol and sorbitol (5) are given in Table 4. The acute oral LD q value for xyUtol in mice is 25.7 g/kg (205). Ingestion of 10 g/d of either mannitol or sorbitol by a normal human subject for one month resulted in no untoward effects (206). XyUtol given to healthy humans for 21 d in increasing doses up to 75 g/d produced no adverse effects (207). The limiting dose of xyUtol for production of diarrhea in humans is 20—30 g (4), but tolerance usually develops on continued adrninistration (207). [Pg.53]

Chinese Liver Fluke. The adult worm of the Chinese Hver fluke Clonorchis sinensis) can grow to be 2 cm long. Worms infect the bihary tree where they cause local inflammation, diarrhea, and hepatomegaly in the acute infection. Progressive biUary obstmction and cirrhosis can occur in the more advanced disease state. The presence of 20—200 worms is common, but they may number over 20,000. Infection is the consequence of eating raw fish that contain viable parasites. Untreated worms can Hve for up to 30 years. Treatment is with pra2iquantil (1). [Pg.244]

Gastroenteritis Gastroenteritis is an acute inflammation of the lining of the stomach and intestines. Symptoms include anorexia, nausea, diarrhea, abdominal pain and weakness. Gastroenteritis has many causes, such as bacteria (food poisoning), viruses, parasites, consumption of irritating food or drink, as well as stress. Treatment for the condition depends on the underlying cause. [Pg.531]

Health Hazards Information - Recommended Personal Protective Equipment Dust mask goggles or face shield protective gloves Symptoms Following Exposure inhalation of dust causes irritation of nose and throat. Ingestion may cause vomiting, salty taste, abdominal pain, diarrhea, convulsions, collapse, thirst, disturbed color vision, and acute toxic nephritis. Contact with eyes causes irritation. [Pg.341]

Escherichia coli Enteropathogenic E. coli infection acute diarrhea... [Pg.516]

Unless ordered otherwise, the nurse should save all stools that are passed after the drug is given. It is important to visually inspect each stool for passage of the helminth. If stool specimens are to be saved for laboratory examination, the nurse follows hospital procedure for saving the stool and transporting it to the laboratory. If the patient is acutely ill or has a massive infection, it is important to monitor vital signs every 4 hours and measure and record fluid intake and output. The nurse observes the patient for adverse drug reactions, as well as severe episodes of diarrhea. It is important to notify the primary health care provider if these occur. [Pg.140]

If the patient is acutely ill or has vomiting and diarrhea, the nurse measures the fluid intake and output and observes the patient closely for signs of dehydration. If dehydration is apparent, the nurse notifies the primary health care provider. If the patient is or becomes dehydrated, oral or IV fluid and electrolyte replacement may be necessary. The nurse takes vital signs every 4 hours or as ordered by the primary health care provider. [Pg.147]


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See also in sourсe #XX -- [ Pg.311 , Pg.312 , Pg.314 ]

See also in sourсe #XX -- [ Pg.258 , Pg.259 ]

See also in sourсe #XX -- [ Pg.258 , Pg.259 ]

See also in sourсe #XX -- [ Pg.684 ]




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