The potentially fatal acute hypersensitivity reaction known as anaphylaxis is a frequent emergency. It can be characterized as a fast-developing, multi-system, widespread allergic response. Anaphylaxis frequently results in death if untreated because it quickly progresses to pulmonary collapse.
Anaphylactic reactions have traditionally been classified as IgE-based responses, whereas anaphylactoid responses have been classified as IgE-independent occurrences.
Recently, anaphylaxis has been diagnosed using all of these names together. Regardless of the cause, each reaction results in the same stage of the disease and therapy; hence this unified language is today the de facto standard.
Epidemiology
Though the frequency is rising, it is projected that the global population has a higher incidence of between 1% and 3%. Although reactions can happen to people of any age, younger people and developed nations tend to notice them the most.
Anaphylaxis, unfortunately, is frequently incorrectly or never identified. Increased mortality and morbidity are the results of delayed or missed diagnosis.
Anatomy
Pathophysiology
After re-exposure to a particular antigen, basophils and mast cells degranulate, releasing a variety of chemical facilitators, which causes anaphylaxis, which is typically a type 1 IgE-mediated hypersensitivity response.
The fast release of inflammatory mediators that have been stored is caused by IgE linkage and the resulting aggregation of strong affinity receptors. Tryptase, histamine, proteoglycans, and carboxypeptidase A are a few of these inflammatory mediators.
Platelet-activating factors, leukotrienes, and prostaglandins are formed from arachidonic acid by the stimulation of lipoxygenases, phospholipase A, & cyclooxygenases. TNF-alpha, both as a formed & delayed reactant, then mediates the inflammatory reaction.
The following describes the precise physiology of these inflammatory mediators:
With simultaneous constriction of the cardiac or respiratory arteries, prostaglandin D works as a bronchoconstrictor.
Vascular permeability, bronchoconstriction, and airway remodeling are all increased by leukotrienes.
Additionally, the platelet-activating factor constricts the airways and raises capillary permeability.
In the course of the stress reaction leukocytosis, TNF-alpha stimulates neutrophils & boosts the production of chemokines.
Histamine causes tissues to be under-perfused by increasing capillary permeability & vasodilation.
Etiology
Exposure to specific drugs, certain meals, and insect bites are examples of common instigating factors. Hyper-acute reactions can result from immunotherapy infusions intended to improve overall allergy reactions.
Latex allergy is becoming more common, and like with other hypersensitivity, there is a danger of anaphylaxis.
Idiopathic anaphylactic is the name given to reactions in which the causative agent is not always known. Alpha-1,3-galactose-induced anaphylaxis is characterized by an IgE antibody reaction.
0.1 mg/ml solution
Administer 0.1 mg via intravenous route within 5 minutes at a pace of 1 to 4 mcg/minute to decrease the need for frequent injection dose
1 mg/ml solution
Administer an undiluted drug of 0.3 to 0.5 mg via intramuscular or subcutaneous injection into the front and outer part of the thigh.
Repeat the process every 5 to 10 minutes as required.
prefilled autoinjector or syringe
Administer 0.3 mg intramuscularly or subcutaneously into the front and outer part of the thigh and repeat for 5 to 15 minutes, as necessary.
<30 kg weight:
Administer 0.01 mg/kg of the medication via intramuscular or subcutaneous injection into the front and outer area of the thigh and maximum dose not more than 0.3 mg per vial.
Repeat the dosage every 5 to 10 minutes as required.
≥30 kg weight
Administer 0.3 to 0.5 mg of via intramuscular or subcutaneous injection in the anterolateral region of the thigh and maximum dose not more than 0.5 mg per vial
Repeat the process every 5 to 10 minutes as required.
Future Trends
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References
https://www.ncbi.nlm.nih.gov/books/NBK482124/
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The potentially fatal acute hypersensitivity reaction known as anaphylaxis is a frequent emergency. It can be characterized as a fast-developing, multi-system, widespread allergic response. Anaphylaxis frequently results in death if untreated because it quickly progresses to pulmonary collapse.
Anaphylactic reactions have traditionally been classified as IgE-based responses, whereas anaphylactoid responses have been classified as IgE-independent occurrences.
Recently, anaphylaxis has been diagnosed using all of these names together. Regardless of the cause, each reaction results in the same stage of the disease and therapy; hence this unified language is today the de facto standard.
Though the frequency is rising, it is projected that the global population has a higher incidence of between 1% and 3%. Although reactions can happen to people of any age, younger people and developed nations tend to notice them the most.
Anaphylaxis, unfortunately, is frequently incorrectly or never identified. Increased mortality and morbidity are the results of delayed or missed diagnosis.
After re-exposure to a particular antigen, basophils and mast cells degranulate, releasing a variety of chemical facilitators, which causes anaphylaxis, which is typically a type 1 IgE-mediated hypersensitivity response.
The fast release of inflammatory mediators that have been stored is caused by IgE linkage and the resulting aggregation of strong affinity receptors. Tryptase, histamine, proteoglycans, and carboxypeptidase A are a few of these inflammatory mediators.
Platelet-activating factors, leukotrienes, and prostaglandins are formed from arachidonic acid by the stimulation of lipoxygenases, phospholipase A, & cyclooxygenases. TNF-alpha, both as a formed & delayed reactant, then mediates the inflammatory reaction.
The following describes the precise physiology of these inflammatory mediators:
With simultaneous constriction of the cardiac or respiratory arteries, prostaglandin D works as a bronchoconstrictor.
Vascular permeability, bronchoconstriction, and airway remodeling are all increased by leukotrienes.
Additionally, the platelet-activating factor constricts the airways and raises capillary permeability.
In the course of the stress reaction leukocytosis, TNF-alpha stimulates neutrophils & boosts the production of chemokines.
Histamine causes tissues to be under-perfused by increasing capillary permeability & vasodilation.
Exposure to specific drugs, certain meals, and insect bites are examples of common instigating factors. Hyper-acute reactions can result from immunotherapy infusions intended to improve overall allergy reactions.
Latex allergy is becoming more common, and like with other hypersensitivity, there is a danger of anaphylaxis.
Idiopathic anaphylactic is the name given to reactions in which the causative agent is not always known. Alpha-1,3-galactose-induced anaphylaxis is characterized by an IgE antibody reaction.
0.1 mg/ml solution
Administer 0.1 mg via intravenous route within 5 minutes at a pace of 1 to 4 mcg/minute to decrease the need for frequent injection dose
1 mg/ml solution
Administer an undiluted drug of 0.3 to 0.5 mg via intramuscular or subcutaneous injection into the front and outer part of the thigh.
Repeat the process every 5 to 10 minutes as required.
prefilled autoinjector or syringe
Administer 0.3 mg intramuscularly or subcutaneously into the front and outer part of the thigh and repeat for 5 to 15 minutes, as necessary.
<30 kg weight:
Administer 0.01 mg/kg of the medication via intramuscular or subcutaneous injection into the front and outer area of the thigh and maximum dose not more than 0.3 mg per vial.
Repeat the dosage every 5 to 10 minutes as required.
≥30 kg weight
Administer 0.3 to 0.5 mg of via intramuscular or subcutaneous injection in the anterolateral region of the thigh and maximum dose not more than 0.5 mg per vial
Repeat the process every 5 to 10 minutes as required.
https://www.ncbi.nlm.nih.gov/books/NBK482124/
medtigo
Anaphylaxis
Updated :
December 6, 2022
The potentially fatal acute hypersensitivity reaction known as anaphylaxis is a frequent emergency. It can be characterized as a fast-developing, multi-system, widespread allergic response. Anaphylaxis frequently results in death if untreated because it quickly progresses to pulmonary collapse.
Anaphylactic reactions have traditionally been classified as IgE-based responses, whereas anaphylactoid responses have been classified as IgE-independent occurrences.
Recently, anaphylaxis has been diagnosed using all of these names together. Regardless of the cause, each reaction results in the same stage of the disease and therapy; hence this unified language is today the de facto standard.
Though the frequency is rising, it is projected that the global population has a higher incidence of between 1% and 3%. Although reactions can happen to people of any age, younger people and developed nations tend to notice them the most.
Anaphylaxis, unfortunately, is frequently incorrectly or never identified. Increased mortality and morbidity are the results of delayed or missed diagnosis.
After re-exposure to a particular antigen, basophils and mast cells degranulate, releasing a variety of chemical facilitators, which causes anaphylaxis, which is typically a type 1 IgE-mediated hypersensitivity response.
The fast release of inflammatory mediators that have been stored is caused by IgE linkage and the resulting aggregation of strong affinity receptors. Tryptase, histamine, proteoglycans, and carboxypeptidase A are a few of these inflammatory mediators.
Platelet-activating factors, leukotrienes, and prostaglandins are formed from arachidonic acid by the stimulation of lipoxygenases, phospholipase A, & cyclooxygenases. TNF-alpha, both as a formed & delayed reactant, then mediates the inflammatory reaction.
The following describes the precise physiology of these inflammatory mediators:
With simultaneous constriction of the cardiac or respiratory arteries, prostaglandin D works as a bronchoconstrictor.
Vascular permeability, bronchoconstriction, and airway remodeling are all increased by leukotrienes.
Additionally, the platelet-activating factor constricts the airways and raises capillary permeability.
In the course of the stress reaction leukocytosis, TNF-alpha stimulates neutrophils & boosts the production of chemokines.
Histamine causes tissues to be under-perfused by increasing capillary permeability & vasodilation.
Exposure to specific drugs, certain meals, and insect bites are examples of common instigating factors. Hyper-acute reactions can result from immunotherapy infusions intended to improve overall allergy reactions.
Latex allergy is becoming more common, and like with other hypersensitivity, there is a danger of anaphylaxis.
Idiopathic anaphylactic is the name given to reactions in which the causative agent is not always known. Alpha-1,3-galactose-induced anaphylaxis is characterized by an IgE antibody reaction.
https://www.ncbi.nlm.nih.gov/books/NBK482124/
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