Drug-in-the-drug anesthory: What to know

Anesthorymosis is a rare side effect after the use of certain medications. Drug-in-the-drug edema can be dangerous for patients, especially with respiratory edema.

1. What is drug-in-the-drug anesthorym?

Anesthorization is defined as a sudden swelling of the skin, underal body, under mucous membranes, respiratory tract or gastrointestinal tract. Anesthorymosis does not leave pitting, is usually temporary (lasts only 7 days) and can appear in any position on the body. Drug-in-the-drug anesthorymosis may or may not be caused by allergies. Allergic anesthies are caused by IgE and Histamine. Non-allergic edema is usually caused by increased bradykinin, either heredity or by medications that inhibit yeast transfer. In addition, some groups of drugs, including the NSAIDs, can also cause allergic anesthies and non-allergic anesthies.

Depending on the pathogenic mechanism and the severe extent of edema symptoms, the treatment will vary. According to the anatomy location, swelling of the airway edema is the most worrying edema position due to the effect on the respiratory tract. Respiratory edema is an excessively dilated blood vessel condition, which causes swelling of the masonry and increased secretion in the respiratory tract. Dilated blood vessels, a lot of secretion, undilated airways will cause the person to suffocate, which can lead to respiratory failure, even death.

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Drug-in-the-drug anesthor edema

2. Two forms of drug-in-medicine edema

2.1 Allergic edema

Allergic anesthelosis can be caused by food, insect venom, pollen or medication and is characterized by the person having been exposed to an allergen before. Drugs associated with allergic anesthema include: Antibiotics (most commonly beta-lactam and quinolon groups), neuromuscular inhibitors, and iodine-containing photocterical drugs.

Allergic analley edema causes increased permeability of the vessel city, increased vascular drainage into the tissues. Allergens cause mast cells to focus, releasing inflammatory substances such as histamine. The inflammatory process associated with IgE is classified as a type 1 reaction, which can cause anaphylactic shock.

Allergic anesthies are often accompanied by urticaria. Treatment of allergic anesthies on the skin is mainly taking antihistamines H1, H2 or glucocorticoids.

2.2 Non-allergic analley

Non-allergic anesthose is caused by the following 2 groups of drugs:

Transfer enzyme inhibitors

Transfer enzyme inhibitors are widely used for cardiovascular patients,especially those with hypotension. Anesthorymosis caused by transfer enzyme inhibitors has a incidence of 0.1 – 6%. The risk of anesthage is higher in people with smoking habits, women, color, history of allergies and over 65 years of age. edema caused by the drug inhibits transfer enzymes that often cause symptoms in the lips, peri region and gastrointestinal pattern. This reaction may appear within 1 week to several months or even several years after the start of treatment.

In terms of pathogenesity, yeast inhibitors act on angiotensin-activated enzymes in the subsyneneuine of the kidney and act on other transfer enzymes located on the respiratory tract (typically kininase II – an enzyme responsible for bradykinin decomposition). When kininase is inhibited, bradykinin rises in the blood. Next, bradykinin causes varicose veins. As a result, capillaries dilate, blood is stagnant, increased permeability increases exfoliation, increases mucous secretion and increases airway edema. Finally cause an anesthor edema. This symptom is more likely to occur in people with a deficiency of the enzyme carboxypeptidase-N and congenital aminopeptidase-P (an enzyme with bradykinin decomposition function).

In terms of treatment, anal edema transferred by yeast inhibitors is not associated with histamine, so it does not respond to traditional treatments for IgE-related reactions. Recommendations for contracting this condition include: Stop medications that inhibit transfer yeast and provide appropriate treatment options. Patients should inform their doctor about edema to take other medications. Patients should not quit smoking or switch to other medications on their own as they may be dangerous.

edema transferred by yeast inhibitors has a mechanism similar to heredity, so it is possible to treat it using drugs that treat heredity. It is Icatibant (Firazyr) – antagonistic to receptor bradykinin B2 and ecallantide (Kalbitor) – kallikrein inhibitors in human serum, which can reduce bradykinin over-production.

In addition, patients with angioediosis transferred by yeast inhibitors may switch to the angiotensin receptor blocker group. However, caution should be exercised as patients may still have angioedenia when taking angiotensin receptor blockers. This is caused by a cross reaction rate between the enzyme-converting inhibitor and the receptor blocker angiotensin of about 7-17%.

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Anesthor edema transferred by yeast inhibitors

*Note: During the administration of transfer enzyme inhibitors, patients should not be taken with drugs that make bronchial muscle spasms, sputum drugs, cough inhibitors because they can cover up early symptoms or aggravate complications and side effects of the drug. At the same time, people with a history of asthma should avoid the on-the-go asthma factors during the course of the drug.

Non-steroidal anti-inflammatory group (NSAIDs)

The NSAIDs are the second most common cause after beta-lactam groups that cause hypersensitivity reactions. Aspirin is the most common cause of hypersensitivity. Anesthose and urticaria are the most common side effects of NSAIDs. The effect on the face in edema due to NSAIDs mainly occurs around the eyes. The rate of edema caused by NSAIDs is 0.1 – 0.3%. However, in patients with a history of chronic rhinitis, asthma or urticaria, the rate of anesthetic edema can be up to 20-30%. Regarding treatment, hypersensitivity to an NSAIDs is a desensitization reaction, which if present within 30 minutes or earlier may be associated with IgE. Oral tolerance to Aspirin should be checked to determine whether the patient is allergic to only one NSAIDs or to all NSAIDs. If the patient is tolerant of Aspirin during the examination, it is possible to identify the patient as allergic only to a group of NSAIDs with the same chemical structure and not allergies to all NSAIDs. The treatment will be to avoid taking NSAIDs in that group of chemical structures. More common forms of edema when using NSAIDs may appear within 1 hour of digestion, predictably through increased production of pre-inflammatory leukotrienes associated with COX 1 inhibition. This reaction may appear at the first time of taking the drug. And patients may use COX 2 inhibitors instead. However, there is still a small percentage of patients with cross allergies to COX 2 inhibitors. Patients with cross-sensitivity to NSAIDs may take Acetaminophen because the drug is capable of inhibiting COX by a weak degree.In patients with NSAIDs sensitivity, first treated with low doses of antihistamines with no sedatives and leukotriene receptors for the prevention of anesthetic edema.To determine the patient with drug-ined edema or other causes, a history of medications, known allergies, drug characteristics, the presence of urticaria and the location of anesthetic edema should be evaluated. The treatment of drug-intravenous edema includes the treatment of the cause of an edema and the prevention of recurrence of this condition in the future.

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SEE MORE:

  • Learn about urticaria, anesthor edema
  • Understanding herediosis
  • How does asthma treat to radicalization?

About: John Smith

b1ffdb54307529964874ff53a5c5de33?s=90&r=gI am the author of Share99.net. I had been working in Vinmec International General Hospital for over 10 years. I dedicate my passion on every post in this site.

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