Abdominal pain concentrate

Cardiac glycosides have a small ratio of toxic to therapeutic concentration. Possible adverse effects are nausea, vomiting, abdominal pain, diarrhoea, fatigue, headache, drowsiness, colour vision disturbances, sinus bradycardia, premature ventricular complexes, AV-block, bigeminy, atrial tachycardia with AV-Block, ventricular fibrillation. There are several mechanisms relevant for their toxic action (Table 2). 

Amylase enters the blood largely via the lymphatics. An increase in hydrostatic pressure in the pancreatic ducts leads to a fairly prompt rise in the amylase concentration of the blood. Neither an increase in volume flow of pancreatic juice nor stimulation of pancreatic enzyme production will cause an increase in senm enzyme concentration. Elevation of intraductal pressure is the important determinant. Stimulation of flow in the face of obstruction can, however, augment the entry of amylase into the blood, as can disruption of acinar cells and ducts. A functional pancreas must be present for the serum amylase to rise. Serum amylase determination is indicated in acute pancreatitis in patients with acute abdominal pain where the clinical findings are not typical of other diseases such as appendicitis, cholecystitis, peptic ulcer, vascular disease or intestinal obstruction. In acute pancreatitis, the serum amylase starts to rise within a few hours simultaneously with the onset of symptoms and remains elevated for 2 to 3 days after which it returns to normal. The peak level is reached within 24 hours. Absence of increase in serum amylase in first 24 hours after the onset of symptoms is evidence against a diagnosis of acute pancreatitis (76). 

Nephrolithiasis/ urolithiasis/ crystalluria IDV Onset Any time after initiation of therapy, especially if 4- fluid intake Symptoms Flank pain and/or abdominal pain, dysuria, frequency pyuria, hematuria, crystallauria rarely, Tserum creatinine and acute renal failure 1. History of nephrolithiasis 2. Fhtients unable to maintain adequate fluid intake 3. High peak IDV concentration 4. tDuration of exposure Drink at least 1.5-2 L of non-caffeinated fluid per day Tfluid intake at first sign of darkened urine monitor urinalysis and serum creatinine every 3-6 months Increased hydration pain control may consider switching to alternative agent stent placement may be required... 

Levinsky et al. (1970) reported on three men exposed to an unknown concentration of arsine for an estimated, 2, 3, and 15 min. Signs and symptoms of exposure (malaise, headache, abdominal pain, chills, nausea, vomiting, oliguria/ anuria, hematuria, bronze skin color) developed within 1-2 h. All three individuals required extensive medical intervention to save their lives. Clinical findings were indicative of massive hemolysis and repeated blood exchange transfusions were necessary for the survival of these individuals. 

Acute intermittent porphyria is a dominantly inherited partial deficiency of porphobilinogen deaminase, and causes axonal polyneuropathy. Acute intermittent porphyria is caused by partial deficiency of porphobilinogen deaminase, an enzyme required for heme biosynthesis. Patients may present with acute abdominal pain, rapidly progressive sensorimotor axonal polyneuropathy or psychosis, and have elevated concentrations of the heme precursor 8-amino-levulinic acid in their urine. Symptoms may be precipitated by treatment with barbiturates or other drugs and are suppressed by treatment with hematin [59]. 

Symptoms of exposure Ingestion may cause acidosis and blindness. Symptoms of poisoning include nausea, abdominal pain, headache, blurred vision, shortness of breath, and dizziness (Patnaik, 1992). An irritation concentration of 22.875 g/m in air was reported by Ruth (1986). 

There are no reports of adverse effects in humans. By analogy to NaOH, the effects from dust or mist could be expected to vary from mild irritation of the upper respiratory tract to pneumonitis, depending on the severity of the exposure. The greatest industrial hazard is rapid tissue destruction of the eyes on contact with the solid or a concentrated solution. If cesium hydroxide is not removed from the skin, it is anticipated that burns will occur after a period of time. Ingestion would be expected to cause corrosion of the lips, mouth, tongue, and pharynx, as well as abdominal pain. 

In humans, systemic effects are anorexia, nausea, edema of the face and hands, and abdominal pain. In a survey of 34 workers exposed to concentrations of up to 2.2mg/m complaints were a burning sensation of the face and hands, nausea, and a persistent (uncharacterized) body odor. One had chloracne, and five had an eczematous rash on the legs and the hands. Although hepatic function tests were normal, the mean blood level of chlorodiphenyl in the exposed group was approximately 400 ppb, whereas none was detected in the control group. ... 

Workers exposed to an airborne fluoride concentration of 5mg/m complained of eye and respiratory tract irritation and nausea. The lethal oral dose of sodium fluoride for humans has been estimated to be 32-65 mg F/kg of body weight. Effects from ingestion are diffuse abdominal pain, diarrhea, and vomiting excessive salivation, thirst, and perspiration painful spasms of the limbs and sometimes albuminuria." Gastrointestinal effects produced after the acute ingestion of toxic amounts of fluoride likely arise from the corrosive action of hydrofluoric acid, which is produced within the acidic environment of the stomach. Cardiac arrest after accidental exposure to high levels of fluoride has been attributed to the development of hypocalcemia and/or hyperkalemia. ... 

Yellow phosphorus burns spontaneously in air, and the vapor released is irritating to the respiratory tract. The early signs of systemic intoxication by phosphorus are abdominal pain, jaundice, and a garlic odor of the breath prolonged intake may cause anemia, as well as cachexia and necrosis of bone, involving typically the maxilla and mandible (phossy jaw). In chronic phosphorus intoxication, lowered potassium blood levels or increased chloride concentrations along with leukopenia have also been reported. ... 

A worker exposed to an undetermined concentration of a mixture of sulfuryl fluoride and 1% chloropicrin for 4 hours developed nausea, vomiting, abdominal pain, and pruritis ... 

Gl Gl symptoms are the most common reactions to miglitol. The incidence of diarrhea and abdominal pain tend to diminish considerably with continued treatment. Renal function impairment Plasma concentrations of miglitol in renally impaired volunteers were proportionally increased relative to the degree of renal dysfunction. Long-term clinical trials in diabetic patients with significant renal dysfunction (serum creatinine more than 2 mg/dL) have not been conducted. Treatment of these patients with miglitol is not recommended. 

Adverse reactions that occurred in 3% or more of patients include the following abnormal gait, abdominal pain, accidental injury, amblyopia, asthenia, ataxia, confusion, cough increased, depression, diarrhea, difficulty with concentration/attention, difficulty with memory, dizziness, ecchymosis, emotional lability, flu syndrome, hostility, infection, insomnia, myalgia, nausea, nervousness, paresthesia, pain (unspecified), pharyngitis, rash, somnolence, speech disorder, tremor, urinary tract infection, vomiting. 

Adverse reactions occurring in 3% or more of patients include Abdominal pain insomnia dream abnormality anxiety disturbed concentration dizziness nervousness application site reaction rash pruritus nausea dry mouth constipation diarrhea anorexia myalgia arthralgia rhinitis increased cough pharyngitis taste perversion. 

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