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Antihistamines, epinephrine and steroids in the setting of hereditary angioedema have an unpredictable effect. The most important is direct visualization of the tube passing between the vocal cords, also: no air during gastric auscultation, bilateral breath sounds, reservoir bag compliance, bag movement, condensation, carbon dioxide in exhaled gas. The long term survival of emergent airways is 45-55%, induction can cause cardiac arrest. Gum elastic bougie can help obtain an airway, as well more muscle relaxants and narcotics as this likely decreases complications; an experienced attending decreases complications. If a patient receives a bolus of succinylcholine for intubation and has not moved in two hours. It is a depolarizing paralytic and is rapidly degraded [within minutes] by pseudocholinesterase which is present in the synapse and the serum. If the patient is deficient in this enzyme, succinylcholine will last for quite some time. If there is a rapid drop in blood pressure and jump in heart rate, then think tension pneumothorax. Mucous plugging of the endotracheal tube could produce similar results, so suction should always be tried. It is essentially ubiquitous and you can expect it in a good portion of all patients. Etomidate - one dose can be associated with adrenal suppression for 48 hours or longer in trauma patients. There was no difference between ketamine and etomidate in terms of intubation outcome/hypotension. There is some experimental evidence that injured lung may be more resistant to oxygen-induced injury. While each failed to demonstrate enhanced survival, all showed a trend in that direction. Normally the airway opening pressure rises linearly during constant flow, volumecontrolled ventilation because respiratory system mechanical properties [compliance and resistance] do not vary much over the tidal range. If the pressure-time display is concave [scooped] upward, compliance is falling as lung is being over-distended. The problem with this information is that it is unknown if this worsens outcome or if modifying it improves outcome. The only way the deflation curve can provide meaningful information is if the ventilator tube is intermittently occluded to allow the Paw to equilibrate with the alveolar pressure. Therefore, the difference between the two curves does not say anything about the hysteresis properties of the lungs [under dynamic conditions]. As below, the mode of ventilation refers to the types of breaths that the ventilator allows. During use of pressurepreset modes, the patient also has greater control over inspiratory flow rate which may improve comfort. Several features of pressure - preset modes have raised concern that lung protection cannot be assured. Moreover, unless the patient is fully passive, the trans-pulmonary pressure cannot be controlled or known using pressure-preset modes. A final limitation is that pressure-preset modes do not allow ready determination of the respiratory system mechanical properties. Is it the reduction in the plateau pressure or tidal volume that benefits the lung Remember that tidal volume best reflects trans-pulmonary pressure whereas plateau pressure does not. People who play windinstruments generate more than 100 cmH2O in their airways when playing the instrument, but this does not cause lung injury, because their trans-pulmonary pressure [i. Consider a patient with a respiratory system compliance of 20 mL/cm H2O and a resistance of 10 cm/1000mL/s.

Which of the following supraspinal structures is implicated in pain-modulating descending pathways Indicate the neurons, which are located in the locus ceruleus or the lateral tegmental area of the reticular formation: a) Dopaminergic b) Serotoninergic c) Nonadrenergic d) Gabaergic 47 013. Tick narcotic analgesic, which is a phenylpiperidine derivative: a) Codeine b) Dezocine c) Fentanyl d) Buprenorphine 015. Indicate the narcotic analgesic, which is a natural agonist: a) Meperidine b) Fentanyl c) Morphine d) Naloxone 017. Select the narcotic analgesic, which is an antagonist or partial mu receptor agonist: a) Fentanyl b) Pentazocine c) Codeine d) Methadone 018. The principal central nervous system effect of the opioid analgesics with affinity for a mu receptor is: a) Analgesia b) Respiratory depression c) Euphoria d) All of the above 020. Which of the following opioid analgesics can produce dysphoria, anxiety and hallucinations Indicate the opioid analgesic, which has 80 times analgesic potency and respiratory depressant properties of morphine, and is more effective than morphine in maintaining hemodynamic stability Which of the following opioid analgesics is used in combination with droperidol in neuroleptanalgesia Fentanyl can produce significant respiratory depression by: a) Inhibiting brain stem respiratory mechanisms b) Suppression of the cough reflex leading to airway obstruction c) Development of truncal rigidity d) Both a and c 024. Most strong mu receptor agonists cause: a) Hypertension b) Increasing the pulmonary arterial pressure and myocardial work c) Cerebral vasodilatation, causing an increase in intracranial pressure d) All of the above 48 025. Which of the following opioid analgesics can produce an increase in the pulmonary arterial pressure and myocardial work Therapeutic doses of the opioid analgesics: a) Decrease body temperature b) Increase body temperature c) Decrease body heat loss d) Do not affect body temperature 028. Indicate the opioid analgesic, which is used for relieving the acute, severe pain of renal colic: a) Morphine b) Naloxone c) Methadone d) Meperidine 030. Which of the following opioid analgesics is used in the treatment of acute pulmonary edema The relief produced by intravenous morphine in dyspnea from pulmonary edema is associated with reduced: a) Perception of shortness of breath b) Patient anxiety c) Cardiac preload (reduced venous tone) and afterload (decreased peripheral resistance) d) All of the above 032. Rhinorrhea, lacrimation, chills, gooseflesh, hyperventilation, hyperthermia, mydriasis, muscular aches, vomiting, diarrhea, anxiety, and hostility are effects of: a) Tolerance b) Opioid overdosage c) Drug interactions between opioid analgesics and sedative-hypnotics d) Abstinence syndrome 033. The diagnostic triad of opioid overdosage is: a) Mydriasis, coma and hyperventilation b) Coma, depressed respiration and miosis c) Mydriasis, chills and abdominal cramps d) Miosis, tremor and vomiting 034. Which of the following opioid agents is used in the treatment of acute opioid overdose Indicate the pure opioid antagonist, which has a half-life of 10 hours: a) Naloxone b) Naltrexone c) Tramadol d) Pentazocine 036. In contrast to morphine, methadone: a) Causes tolerance and physical dependence more slowly b) Is more effective orally c) Withdrawal is less severe, although more prolonged 49 d) All of the above 037. Indicate a partial mu receptor agonist, which has 20-60 times analgesic potency of morphine, and a longer duration of action: a) Pentazocine b) Buprenorphine c) Nalbuphine d) Naltrexone 039. Which of the following opioid analgesics is a strong kappa receptor agonist and a mu receptor antagonist Non-narcotic analgesics are mainly effective against pain associated with: a) Inflammation or tissue damage b) Trauma c) Myocardial infarction d) Surgery 002. Non-narcotic agents cause: a) Respiratory depression b) Antipyretic effect c) Euphoria d) Physical dependence 003. Select the non-narcotic drug, which is a paraaminophenol derivative: a) Analgin b) Aspirin c) Baclophen d) Paracetamol 005. Tick pirazolone derivative: a) Methylsalicylate b) Analgin c) Paracetamol d) Ketoralac 007. Most of non-narcotic analgetics have: a) Anti-inflammatory effect b) Analgesic effect c) Antipyretic effect d) All of the above 009. Indicate the non-narcotic analgesic, which lacks an anti-inflammatory effect: a) Naloxone b) Paracetamol c) Metamizole d) Aspirin 010. Characteristic findinds of salicylism include: a) Headache, mental confusion and drowsiness b) Tinnitus and difficulty in hearing c) Hyperthermia, sweating, thirst, hyperventilation, vomiting and diarrhea d) All of the above 014. Analgin usefulness is limited by: a) Agranulocytosis b) Erosions and gastric bleeding c) Methemoglobinemia d) Hearing impairment 015. Methemoglobinemia is possible adverse effect of: a) Aspirin b) Paracetamol c) Analgin d) Ketorolac 016.

These fears are largely based upon seizures associated with overdoses, which have little predictive value when levels are within therapeutic range (27,28). Patients with primary generalized epilepsy may have a greater propensity for seizure exacerbation secondary to antidepressants; depression in such patients appears to respond well to low doses of these agents (15). The medications with substantial risk are few; however, it is prudent to avoid bupropion, maprotiline, clomipramine, and amoxapine because of their potential for exacerbating seizures (29). The immediate-release preparation presents a particular concern, with a seizure incidence of 0. The epileptogenicity of clomipramine varies by dose, with seizures in up to 3% of patients taking 250 mg/day. Women tend to be more responsive than men, however, and sexual dysfunction and weight gain are common adverse reactions. Kanner and associates used sertraline to treat depression in 100 patients with epilepsy. Depressive symptoms improved in the majority of subjects, with seizures definitely worsening in only one patient (16). Starting with the lowest dose is recommended, with a gradual dose increase at 1- to 2-week intervals. If a more rapid increase is necessary due to severe symptoms, closer observation is required. Also of concern are the potential for cardiac conduction abnormalities and the greater tendency to induce mania. The anticholinergic effects may exacerbate memory dysfunction in patients with Alzheimer disease as well. Finally, these medications have been shown to increase the risk of seizures in the general population in up to 0. This class of medications is contraindicated in children with epilepsy due to the seizure risk. Imipramine and amitriptyline at dosages 200 mg/day, however, do not generally provoke seizures in adults. They are not often prescribed due to their side effect profile, however, which includes hypertensive crises due to interactions with tyraminecontaining foods. Although useful for atypical features of depression, these are third-line agents and should be prescribed only by psychiatrists. Dosages as high as 225 mg/day have been demonstrated to be safe in depressed patients with epilepsy. The goal of treatment for depression is symptom remission; those with any residual symptoms have a greater likelihood for relapse. If a patient has three or more episodes of depression, residual symptoms, suicidality, psychosis, or an otherwise severe episode, long-term prophylaxis is indicated. Children tend to have high relapse rates, with continuation of symptoms into adulthood (30). Psychotherapy can help patients cope with limitations imposed by epilepsy and may result in significant improvements in rating scales of depression and anxiety, as well as seizure frequency (31). A medication from a different class than that used in Stages 1 or 2 should be administered. Chapter 93: Psychiatric Comorbidity of Epilepsy 1041 When transitioning between drugs, an overlap and taper strategy should be used to avoid withdrawal symptoms. Patients with seizures are also at greater risk of completing suicide compared to controls: 2. The prevalence of suicide in epilepsy increases with comorbid psychiatric diagnoses, including depression, psychosis, anxiety, personality disorders, and bipolar disorder (33). Ictal and postictal depression, mania, postictal psychosis, and command hallucinations present particular risks. In 90% to 95% of patients who commit suicide, prior psychiatric diagnoses were present (33). Other risk factors include psychosocial stressors, poor physical health, young age in men (25 to 49 years), early age of seizure onset (18 years, particularly during adolescence), presence of brain lesions, inadequate follow-up or treatment of seizures, access to firearms or other methods of self-harm, and interictal behavioral disorders. Furthermore, cognitive impairment carries a 10 to 25 times greater risk than normal cognition.