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Terms in this set (44)

This patient has all the complaints and symptoms of pulmonary tuberculosis (TB). Direct sputum examination by Ziehl-Nielsen stain also helps the diagnosis, but it is still not confirmatory. Sputum needs to be cultured to check what kind of mycobacterium is causing this disease.

It is important to start the treatment as soon as the culture is sent.

The standard treatment for adult respiratory/pulmonary TB includes a complete 6-month regimen comprising of 2 months initial phase with 4 drugs, which include rifampin, isoniazid, pyrazinamide, and ethambutol. This is followed by a 4-month continuation phase consisting of 2 drugs: rifampin and isoniazid. Irrespective of the bacteriological status of the sputum, this is the recommended standard treatment for respiratory tuberculosis (including isolated pleural effusion or mediastinal lymphadenopathy). The 4th drug, ethambutol, may be omitted in patients with a low risk of resistance to isoniazid.

Ethambutol should be started in individuals who are known or suspected to be HIV positive, in those who have had previous treatment, and in immigrants and refugees of any ethnic group who are considered to have a significantly higher risk of resistance to isoniazid and other drugs.

Like most medications, antituberculosis drugs also have some side effects. Since treatment is long-term, it is essential that patients are warned about and checked for side effects. If side effects are not explained well to the patient, it will decrease the compliance. The adverse effect of ethambutol is retrobulbar neuritis.

The important side effects of anti-tubercular drugs are:

INH: Hepatotoxicity, peripheral neuritis, cutaneous hypersensitivity, rarely can cause optic neuritis

RMP: Hepatotoxicity, nephrotoxicity, red discoloration of the body fluids, 'Flu-syndrome,' and thrombocytopenic purpura

PZA: Hepatotoxicity, hyperuricemia

ETH: Retrobulbar neuritis

STM: Nephrotoxicity, ototoxicity
The patient's apnea and pinpoint pupils are consistent with an acute opioid overdose; therefore, treatment with naloxone is indicated. Naloxone is an opioid receptor antagonist with a high affinity for opioid receptors. Naloxone displaces receptor-bound opioids, which leads to a reversal of opioid-induced respiratory depression and coma. Opioid receptors of various subtypes are present throughout the central and peripheral nervous systems. In addition to their analgesic properties, opioids cause respiratory depression via receptors in the medullary respiratory center. Pupillary constriction occurs as a result of opioid receptor activation in the Edinger-Westphal nucleus of the oculomotor nerve. Other side effects of opioids are constipation caused by gastrointestinal smooth muscle relaxation and nausea caused by receptor stimulation in the chemoreceptor trigger center of the 4th ventricle.

Atropine is a muscarinic antagonist. It is used to treat overdoses due to organophosphate-type insecticides that inhibit the acetylcholinesterase enzyme, leading to acute increases in acetylcholine levels. Symptoms of muscarinic activation include salivation, lacrimation, miosis, and bradycardia. Muscarinic activation can also impair diaphragmatic motor function, leading to respiratory distress and ultimately seizure activity. The clinical scenario presented is not consistent with organophosphate exposure, and the heart rate of 80 beats per minute makes the diagnosis unlikely. Therefore, there is no immediate role for atropine administration.

Epinephrine is a direct-acting adrenergic agonist that acts on both alpha and beta-receptors. The principal effect of epinephrine is increased cardiac inotropy and chronotropy, leading to increased cardiac output. Combined vasoconstrictive and vasodilator effects usually lead to a rise in systolic and no change or slight lowering of diastolic blood pressures. Epinephrine is also a powerful bronchodilator due to activation of respiratory beta-2 receptors. Epinephrine is indicated in cases of cardiac arrest as well as anaphylactic shock - neither of which is present in this case.

Flumazenil is a competitive antagonist of the gamma-aminobutyric acid (GABA) receptor and is used in cases of benzodiazepine overdose. Benzodiazepines are used to treat anxiety and have sedative effects that may lead to coma at high doses. Although benzodiazepine overdose is possible in this scenario, it does not explain the pupillary constriction.

Phenobarbital is a barbiturate with sedative-hypnotic and anticonvulsant properties that - like the benzodiazepines - acts by GABA receptor stimulation. Phenobarbital is used to treat status epilecticus. It is also used to minimize brain oxygen consumption under circumstances of compromised regional cerebral perfusion. Based on this case presentation, there is no indication for phenobarbital.
administer bicarb
The patient has taken amitriptyline, which is a tricarboxylic acid antidepressant (TCA); her set of symptoms are consistent with TCA toxicity. The mechanisms of action of TCA are via anticholinergic effects, norepinephrine reuptake blockade, a quinidine effect, a sodium channel blocker, and peripheral alpha blockade. TCA-cardiotoxicity may be demonstrated on an electrocardiogram via sinus tachycardia, QRS complex prolongation > 100 milliseconds, right bundle branch block, ventricular tachycardia, ventricular fibrillation, and QT prolongation.

Sodium bicarbonate is the drug of choice for the treatment of ventricular dysrhythmias and/or hypotension, secondary to tricarboxylic acid antidepressant (TCA) poisoning. Hyperventilation and hypertonic saline (e.g. lactated Ringer's) may also be useful, but clinical and experimental experience with these modalities is less extensive than with sodium bicarbonate. In patients with severe toxicity, bicarbonate needs to be given in order to achieve a serum pH of 7.50 to 7.55. Intermittent boluses of sodium bicarbonate are preferred to a constant infusion.

Procainamide is not recommended due to similarity in action of TCAs as Class 1A antiarrhythmics. Sodium bicarbonate works by alkalinization of blood, thereby promoting protein binding of drugs; this results in less of the toxic drug in circulation. It improves conduction through sodium channels, and treats acidosis that results from seizure activity.

After treatment with sodium bicarbonate, peripheral maneuvers to improve the TCA-induced hypotension include placing the patient in the Trendelenburg position, administering intravenous fluids, administering pressor agents (e.g., norepinephrine) for the treatment of alpha-blockade-induced hypotension, and administering dopamine (intermediate dosing stimulates beta-receptors, allowing increases in cardiac output; higher dosing stimulates alpha-blockade).

TCA-associated seizures should be aggressively treated in order to avoid cardiotoxicity resulting from acidosis. Benzodiazepines, phenobarbital, and intubation are the mainstay of treatment. In general, phenytoin is not efficacious with toxic seizures. There is debate as to whether there are any cardiovascular effects with phenytoinbeing a type 1B antiarrhythmic agent that counteracts the type 1A effect of TCA.

Physostigmine in a hemodynamically-unstable patient is not the first-line drug; it may even be contraindicated. It should be considered if there are severe life-threatening anticholinergic effects.

Hemodialysis and hemoperfusion are not effective in TCA poisoning because small amounts of free TCA are present in the serum (mostly bound to serum proteins); they are not recommended.
4 hours
n an acute ingestion, the peak concentration may not be achieved until 4 hoursafter ingestion. Absorption may be affected by coingestants that affect gastric motility. Concretions of multiple tablets ingested at the same time may form bezoars in the stomach and alter absorption, or provide a continuing source of supply. A single acetaminophen level drawn at least 4 hours after ingestion is sufficient to determine patient management. If time of ingestion is unknown, an immediate level and at least 2 additional levels drawn 4 hours apart may be useful. Clinical toxicity may not be evident soon after overdose, and the risk of morbidity increases when the initiation of therapy is delayed.

At therapeutic doses, peak concentration is generally achieved after 1 hour, with half-life of 2 to 4 hours. The toxic dose of acetaminophen is approximately 150 mg/kg or 7 grams in adults. Children may tolerate doses up to 200 mg/kg. Acetaminophen is rapidly absorbed from the stomach and small intestine and metabolized by conjugation in the liver to nontoxic agents. These water-soluble conjugates are then eliminated in the urine. Ninety percent are metabolized to either metabolites of sulfate (primarily in children) or glucuronide (primarily in adults). Approximately 4% is metabolized by the cytochrome p450 system to an active metabolite, NAPQI (n-acetyl-p-benzoquinoneimine). Normally, NAPQI is conjugated with glutathione resulting in detoxification and excreted as mercapturic acid and cysteine conjugates. In acute ingestion, glutathione is depleted, so NAPQI covalently binds to vital proteins and the lipid bilayer of hepatocyte membranes. The result is hepatocellular death and centrilobular liver necrosis. Other organs may be affected.

The acetaminophen level should be plotted on the Rumack-Matthew nomogram, a semi-logarithmic plot of the acetaminophen level over time (4-24 hours post ingestion) based on adult data. Approximately 60% of patients with levels above the line will develop serum transaminases >1000 IU/L. A second line 25% below the first line was added. Levels between the first and second line are considered possibly toxic and take into account such factors as lab error and error in time of ingestion. There is no clinical evidence suggesting that patients in this range need to be treated. Levels below the second line are low risk. The nomogram is not valid for ingestions less than 4 hours, chronic ingestions, or for patients who have ingested toxic doses of extended release preparations. Because the absorption of extended release preparations is delayed, a measurement at 4 hours will not accurately reflect absorption. The nomogram is also not valid for patients with chronic alcohol consumption.