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Kultur Dokumente
Rationale (10%)
Mechanism of action: Binds with mu receptor and inhibits the reuptake of norepinephrine and serotonin, which may account for tramadols analgesic effect.
Adverse/Side Be aware that Effects: tramadol Sweating,dizziness, shouldnt be muzziness, given to vomiting, dry patients with a mouth. In rare history of cases, influence on anaphylactoid CVS regulation, reactions to esp after IV codeine or administration, other opioids headache, retching, vomiting, constipation, GI Assess patient irritation, skin for evidence reactions. In very of dependence rare cases, motor or abuse. weakness, blurred vision, appetite changes, micturition disorders, psychic side effects eg mood, perception, & activity changes, Avoid giving tramadol to allergic reactions & patient with anaphylaxis. acute Cerebral abdominal convulsions esp on conditions. co-medication w/ neuroleptics, increase in BP,
Urge patient to follow prescribed dose limits and dosing intervals to prevent respiratory depression and seizures. Instruct patient prescribed extendedrelease form to swallow tablet whole and not to chew, crush, or split tablet. Caution patient not to stop tramadol abruptly. Intstruct patient to avoid hazardous
Because it may mask evidence and disrupt assessment of the abdomen. (Jones&Bartlett,2011; p.254)
bradycardia. Drug Interactions: Avoid concurrent administration of MAOIs. Comedication w/ other centrallyacting depressants including alcohol may potentiate CNS effects. Carbamazepine may reduce analgesic effect Expect to taper tramadol rather than stopping it abruptly. To avoid such acute withdrawal symptoms as anxiety, diarrhea, insomnia, nausea, pain, panic attacks, paresthesias, piloerection, rigors, sweating, tremor, and upper respiratory symptoms. ( www.mims.com) For evidence of suicidal thinking or behavior. (Edmunds,2009;p.796)
activities until drugs CNS effects are known. Advise patient to avoid alcohol while taking tramadol. Tell patient to notify prescriber immediately if he develops any sudden onset, unusual, persisitent, or severe adverse reaction
Generic Name/ Brand Name Classification Generic Name: metronidazole Brand Name:
Dose, Strength & Formulation Ordered: 500mg IV drip q 8hr Timing: Every 8 hours
Classification: Antibiotic
Duration: 7days
Indication/ Mechanism of Drug Action Indications: To treat systemic anaerobic infections caused by Bacteroidesflagilis, amebiasis, trichomoniasis, bacterial vaginosis, acne in patients with rosacea and to prevent perioperative bowel infections. Mechanism of action: Undergoes intracellular chemical reduction during anaerobic metabolism. After metronidazole is reduced, it damages DNAs helical structure and breaks its strands which inhibits bacterial nucleic acid synthesis and causes cell death. (Jones and Bartlett,2011:p.667)
Adverse/ Side Effects Drug Interaction CNS: aseptic meningitis,ataxia, confusion, dizziness, encephalopathy, fever, headache, incoordination, insomnia, irritability, light headedness, peripheral neuropathy, seizures. EENT: dry mouth, lacrimation, metallic taste, nasl congestion, optic neuropathy, pharyngitis. GI: abdominal cramps or pain, anorexia, diarrhea, nausea, pancreatitis, vomiting GU: dark urine, urinary frequency, vuluitis HEME:
Nursing Responsibilities
Rationale
Client Teaching
1.Caution patient to avoid alcohol during therapy and for at least 3days afterward 2.Give I.V. drug slowly infusion over 1hr.(Jones & Bartlett,2011:p.667)
1.Alcohol may alter the effect of the medication .(Jones & Bartlett,2011:p.667 2 .To facilitate the effect of the medication and prevent adverse reactions to occur .(Jones & Bartlett,2011:p.667)
2..Advise patient to avoid hazardous activities until drugs CNS effects are known and to 3.Dont give by 3.To prevent such report any direct I.V. infusion adverse reaction in abnormal during CNS and to neurologic signs metronidazole discontinue the or symptoms infusion. primary I.V. such as infusion. .(Jones & weakness, Bartlett,2011:p.667) numbness, seizures or 4.Urge patient to 4.To minimize vision changes. take metronidazole adverse GI at evenly spaced reactions. 3..Urge patient intervals day and ( Jones&Bartlett, to complete the with food.(Jones & 2011; p. 668) entire course of Bartlett,2011:p.667) therapy. 5. Caution patient 5.This drug may 4.If patient
leucopenia MS: back pain, dysarthria SKIN: burning sensation dry skin.
Indication/ Mechanism of Drug Action Indications: -To control hypertension Mechanism of action:
Adverse/ Side Effects Drug Interaction CNS: fever CV: Chest pain, hypotension, palpitations, , tachycardia, EENT: loss of taste GU: Dysuria, impotence, nephritic syndrome, nocturia, oliguria, urinary frequency RESP: Cough SKIN: Photosensitivity, pruritus Other: Angioedema,
Nursing Responsibilities
Rationale
Client Teaching
1.Closely monitor patients blood pressure, especially when therapy starts 2. Give Captopril 1 hour before meals
Its beneficial effects in hypertension and heart failure appear to result primarily from suppression of the renin-angiotensinaldosterone system. However, there is no consistent correlation between renin levels and
1. Instruct patient to avoid sunlight or wear sunscreen in direct sunlight because photosensitivity can occur. 2. Warn patient to not to stop drug abruptly. 3. Urge patient to use salt substitutes that contain potassium and to consult prescriber before increasing potassium intake to avoid increasing risk of hyperkalemia.
3. Captopril should be stored at room temperature, 15 to 30 C (59 to 86 F) and away from too much heat and moisture. 4. Monitor renal function tests for signs of Nephrotic sundrome, such as proteinuria and increased BUN
3. Extremes of temperature beyond Captoprils desired temperature could possibly alter the drugs potency.
(Jones&Bartlett2011;p.85)
4. This signs indicates that the paient is experiencing the drugs adverse effects which should be stopped and
hypercalcemia, response to the hyponatremia, drug. Renin, an enzyme synthesized by the kidneys, is released into the circulation where it acts on a plasma globulin substrate to produce angiotensin I, a relatively inactive decapeptide. Angiotensin I is then converted by angiotensin converting enzyme (ACE) to angiotensin II, a potent endogenous vasoconstrictor substance. Angiotensin II also stimulates aldosterone secretion from the adrenal cortex, thereby contributing to sodium and fluid retention.
evaluated immediately .
(Jones&Bartlett2011;p.85)
5. Check and monitor the patient manifestations are such as chest pain, swelling of the face, eyes, lips, tongue, arms, or legs,difficulty breathing or swallowing, rash, fainting,
Captopril prevents the conversion of angiotensin I to angiotensin II by inhibition of ACE, a peptidyldipeptide carboxy hydrolase. This inhibition has been demonstrated in both healthy human subjects and in animals by showing that the elevation of blood pressure caused by exogenously administered angiotensin I was attenuated or abolished by captopril. In animal studies, captopril did not alter the pressor responses to a number of other agents, including angiotensin II and norepinephrine, indicating
specificity of action
(Jones and Bartlett,2011:p.667)