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Type 1 hypersensitivity: Immediate (hanna)

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Type 1 hypersensitivity: Immediate (hanna)

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The reaction is initiated by the binding of autoantibodies IgG (sometimes IgM) to soluble antigens to form immune complexes, which are deposited in various tissues.

Neutrophils are then recruited, and inflammation is present at the sites where the immune complexes are deposited, causing tissue destruction and inflammatory reactions

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Components of immune system involved (chokka)

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Components of immune system involved (chokka)

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The components of the immune system that are involved are

Antibodies, which form immune complexes with the allergens, also known as antigens

Neutrophils, which are recruited to the site where the immune complexes are deposited, kickstarting the classical signalling pathway and inflammatory reaction through the secretion of cytokines such as CCL2 and IL-1b

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Some symptoms of type III hypersensitivity include:

Purpuras, which are small, non-blanching hemorrhages on the skin

Rheumatoid nodules

A flushed rash on the face

Joint pain and swelling

Rashes

Fever

Kidney damage

Urticaria (also known as hives

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Treatment for type III hypersensitivity largely involves immunosuppression which includes:

Adrenaline, or epinephrine

Systemic glucocorticoids

Antihistamines

Disease-modifying antirheumatic drugs, such as methotrexate, cyclosporine, and cyclophosphamide

Biologic agents, such as TNF-blockers

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Type IV hypersensitivity: Delayed type (danielle)

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Type IV hypersensitivity: Delayed type (danielle)

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Type IV hypersensitivity or delayed-type hypersensitivity(DTH) involves a T-cell-mediated immune response rather than antibody-mediated. It takes around 24-72 hours to developed exposure to the antigen and the reaction could take up to 3 to 4 weeks

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Allergen Exposure: The reaction is initiated by exposure to an allergen, which is a typically harmless substance that triggers an immune response in susceptible individuals. Common allergens include pollen, dust mites, animal dander, insect stings, certain foods (e.g., peanuts, shellfish), and drugs (e.g., penicillin).

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Components of immune system involved (hanna)

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Components of immune system involved (hanna)

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IgE Antibodies: The immune response begins with the production of IgE antibodies specific to the allergen. Upon first exposure, these IgE antibodies are produced and bind to the surface of mast cells and basophils.

Mast Cells and Basophils: These cells have high-affinity receptors for IgE (FcεRI). Upon subsequent exposure to the same allergen, the allergen binds to the IgE on these cells, causing them to degranulate.

Release of Mediators: Degranulation releases various pre-formed mediators like histamine, tryptase, and newly synthesized mediators such as leukotrienes, prostaglandins, and cytokines (e.g., IL-4, IL-5, IL-13).

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Immediate Phase (minutes after exposure): Symptoms result from the release of histamine and other mediators from mast cells and basophils.

Respiratory Tract: Sneezing, nasal congestion, runny nose (rhinitis), itchy eyes, throat irritation (common in hay fever).

Skin: Urticaria (hives), itching, redness, and swelling.

Gastrointestinal Tract: Nausea, vomiting, abdominal pain, diarrhea (common in food allergies).

Systemic: Anaphylaxis, which can include widespread vasodilation, drop in blood pressure (shock), bronchoconstriction (difficulty breathing), and potentially fatal outcomes if not treated promptly.

Late Phase (hours after exposure): Involves recruitment of eosinophils, neutrophils, and other inflammatory cells leading to sustained inflammation and tissue damage. Symptoms may include chronic asthma or atopic dermatitis.

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Hypersensitivity Type I reaction (Immediate or allergic reaction) - pathophysiology

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Acute Management:

Epinephrine (Adrenaline): First-line treatment for anaphylaxis. It works by vasoconstriction, bronchodilation, and increasing cardiac output.

Antihistamines: Such as diphenhydramine or cetirizine, which block histamine receptors and reduce symptoms like itching and hives.

Corticosteroids: Systemic corticosteroids (e.g., prednisone) can reduce inflammation and are used in more severe cases.

Bronchodilators: Such as albuterol for asthma symptoms, to relax bronchial smooth muscles and improve breathing.

Long-term Management:

Avoidance of Known Allergens: Identifying and avoiding triggers can prevent reactions.

Allergen Immunotherapy (Desensitization): Gradual exposure to increasing amounts of the allergen to build tolerance.

Monoclonal Antibodies: Omalizumab (anti-IgE) can be used in severe asthma or chronic urticaria to reduce IgE levels and prevent mast cell degranulation.

Education and Emergency Plan: Educating patients and caregivers on recognizing symptoms and using emergency medications like auto-injectable epinephrine (e.g., EpiPen).

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Earn 1 Contact Hour - Free of Charge

The goal of this CE activity is to provide nurses and nurse practitioners with knowledge and skills to recognize and manage acute hypersensitivity reactions (HSRs) occurring as a result of medication administration. After reading this article, you will be able to:

Recognize early signs and symptoms of acute HSRs

Describe evidence-based nursing and medical management of HSRs

Discuss prevention of HSRs

An acute hypersensitivity reaction is a rare but serious complication of exposure to foods, natural-rubber latex, medications, and other antigens. Patient allergies are not always clearly defined in the medical record, and severe reactions may not be anticipated. Nurses and nurse practitioners must recognize HSR risk factors, read early signs and symptoms, and intervene to protect the patient from further harm.
Authors: Brenda Shelton, MSN, RN, CCRN, AOCN; and Jane C. Shivnan, MScN, RN, AOCN

What are Hypersensitivity Reactions?

A hypersensitivity reaction (HSR) is an exaggerated immune response to an antigen which results in local tissue injury and may include life-threatening systemic effects. The most extreme form of HSR is anaphylaxis or anaphylactoid reactions, a life-threatening emergency. Common antigens eliciting HSRs include foods such as peanuts and shellfish, environmental antigens such as natural rubber latex, venoms such as those from bee stings and fire ants, and medications such as antibiotics, monoclonal anti-bodies and chemotherapy. Although acute HSRs generally occur within minutes of antigen exposure, there is a wide spectrum of HSR presentations-including biphasic and delayed reactions-that may occur hours to days after antigen exposure. The type of reaction is determined by the primary immunologic mechanism as outlined in Table 1, although it is important to be aware that HSRs in clinical practice often involve multiple immune pathways and may be difficult to categorize.

For the purposes of this CE activity, we will limit our discussion to acute HSRs resulting from exposure to medications and biologic agents. Most of these are categorized as Type I or anaphylactic HSRs. Type I reactions manifest almost immediately upon anti-gen exposure. The primary mediator of Type I reaction is immunoglobulin E (IgE). Anaphylactoid or pseudo-anaphylactic reactions produce identical symptoms, but are not charac-terized by progressive symptoms with each exposure or the presence of IgE antibody. All HSRs are complex immune responses of mast cell degranulation activating histamine release, complement system, prostaglandins, and inflammatory leuko-trienes. The effects of these immune response mediators are responsible for most of the symptoms seen in HSRs, whether they are cutaneous reaction char-ac-terized by itching and hives (histamine) or bronchospasm and vasospasm (leukotrienes and prostaglandins).

Table 1: Immunology of HSR's

I

Anaphylactic: Immediate immunoglobin E-mediated reaction

Fever, nausea, vomiting, flushing, back pain, angioedema, rash, dyspnea, bronchospasm, feelings of impending doom, circulatory collapse

II

Cytotoxic: Antigen-antibody complexes activate inflammatory pathways

Hemolysis

III

Serum Sickness: Immune complexes form and deposit in various tissues

Vasculitis, nephritis, arthritis

IV

Delayed Cytotoxic: Activated T cells destroy targeted cells

Graft rejection, contact dermatitis, granuloma formation, Graft-Versus-Host Disease

When are acute HSRs likely to occur?
Acute HSRs are rare, with 1-15% of Americans considered at risk if exposed to known allergens. ¹ Of those who experience anaphylaxis, approximately 1% will die as a result. ¹ In hospitalized patients, anaphylactic reactions account for about 6% of reported adverse drug reactions. ² HSRs are more likely to occur with intravenous administration. Complex, protein-based molecules are more likely to elicit the immune-mediated response of an acute HSR, which accounts for the increased incidence of acute HSRs with infusions of biological agents such as antisera or monoclonal antibodies. These agents are often administered in ambulatory settings to patients with diseases such as Crohn's disease, multiple sclerosis, auto-immune disorders, and cancers. Some smaller molecules, like the penicillins, bind to circulating serum proteins, resulting in increased size and antigenic potential in susceptible individuals. Some diluents used in medication admixture contribute to the risk for HSR. ³ Cremophor, for example, is a diluent for paclitaxel, cyclosporin, and tenoposide.

Table 2: Definition of Anaphylaxis
(National Institute of Allergy and Infectious Disease/ Food Allergy and Anaphylaxis Network)

Diagnostic Criteria for Anaphylaxis Symptom onset within minutes to hours of exposure to antigen including symptoms involving the skin or mucosal tissue with any one of the following: hives, pruritis, airway edema, with respiratory difficulty or hypotension.ORAny two of the following within minutes to hours of antigen exposure:

Skin or mucosa involvement

Respiratory distress

Hypotension, or

Gastrointestinal symptomsORHypotension within minutes to hours after antigen exposure

Source: Sampson HA, Munoz-Furlong A, Campbell RL, et al. Second symposium on the definition and management of anaphylaxis: summary report-Second National Institute of Allergy and Infectious Disease/ Food Allergy and Anaphylaxis Network symposium, J Allergy Clin Immunol, 2006; 117(2): 391-397.

Oncology nurses are particularly likely to witness HSRs from antimicrobials, biological and chemotherapeutic agents. All chemotherapy has the potential to cause an HSR. Chemotherapeutic agents with the highest reported incidence of HSRs include L-asparaginase (10-35%), taxanes (2-5%), platinum compounds (10-27%), etoposide and teniposide (6-40%), and procabazine. ⁴ Platinum compound HSRs are considered IgE-mediated, occurring after seven to nine doses have been safely administered. On the other hand, nearly 95% of reactions to taxanes and L-asparaginase occur during the first or second infusion.

Monoclonal antibodies used in medi-cine, neurology, cardiology and oncology can cause severe infusion reactions induced by cytokine release. Although these are not Type I acute HSRs, their implications for assessment and management are similar. The incidence of reactions with monoclonal antibodies varies: rituximab (up to 75%), trastuzumab (up to 40%), cetuximab (19%), infliximab (1-6%), bevacizumab (1%), natalizumab (1%), and abiciximab (0.6%).

Severe HSRs may also be triggered by medications used to manage general medical-surgical conditions. As many as seven individuals in a thousand may experience angioedema upon exposure to ACE inhibitors. ² Other medications known to cause significant HSRs include anesthetics, anticonvulsants, antiarrhythmics, aspirin, radiocontrast media, and sedative-hypnotics. Antibiotics such as penicillins, beta lactams, sulfonamides, and trimethoprim sulfamethoxazole also commonly trigger HSRs of variable severity.
What are the signs and symptoms of acute HSRs?
Some of the signs and symptoms of acute HSRs overlap with milder infusion reactions. Patients may experience fevers, chills, rigors, flushing, and diaphoresis (sweating) as temperature regulation is disrupted by circulating cytokines. Histamine release from mast cell degranulation may cause pruritis (itching) and rashes, including hives. Arthralgias (joint pain) and myalgias (muscle pain) may occur. The patient may complain of a headache, dizziness, abdominal pain, or nausea.

Serious systemic effects include dyspnea, bronchospasm, cyanosis, tachycardia, and hypotension or hypertension. Abdominal or lower back pain may indicate visceral smooth muscle contraction. The patient may also experience a sense of impending doom, may lose consciousness, and may suffer a circulatory collapse. A uniquely life-threatening event in an acute anaphylactic HSR is angioedema, a rapid swelling of tongue and throat tissues that can obstruct the patient's airway. Life-threatening HSRs are more likely to occur with intravenous administration, which places the antigen into the blood-stream, particularly with more rapid infusion rates.
Nurses should be alert to possible symptoms during and immediately after administration of the at-risk agent. Initial subtle symptoms may progress to life-threatening complications within minutes. Anaphylaxis diagnostic criteria are described in Table 2. Clinical suspicion is augmented with diagnostic tests to validate HSRs, so that future antigen exposure can be controlled. Allergen-specific IgE levels are available for some drug allergens, but can be complemented with nonspecific tests of immunologic activity such as eosinophilia, serum total tryptase, or flow-cytometry basophil activation assays on CD63 and CD203c.
How should acute HSRs be managed?
Stop, Call, Assess, Prepare.

If you suspect your patient is experiencing early symptoms of an acute HSR, donÕt hesitate to implement your emergency interventions. STOP the infusion but maintain IV access. CALL the provider. ASSESS your patient further: collect vital signs, use a pulse oximeter to obtain oxygen saturation, listen to breath sounds, and check for symptom progression. Finally, PREPARE for emergency treatment, including the potential need to administer IV fluids, oxygen, and resuscitative medications.

The most likely acute HSR medica-tion orders for adults include epinephrine (0.3-0.5 ml of a 1:1000 solution as intramuscular or subcutaneous injection, repeated every five to fifteen minutes), albuterol (two puffs from a multi-dose inhaler), a rapid-acting corticosteroid such as hydrocortisone 100 mg, and an antihistamine such as diphenhydramine 50 mg. For pediatric patients, epinephrine at 0.01 mg/kg is repeated every five minutes as necessary. IV fluids, vasopressors such as norepinephrine, and histamine 1 receptor blocker such as ranitidine may also be ordered. Oxygen therapy is appropriate for most patients, but is only effective if bronchospasm is effectively controlled.

Your organization may have developed a protocol for managing severe anaphy-lactic hypersensitivity reactions. These treatment algorithms are generally based on expert opinion and consensus; there is limited published evidence due to the rarity of HSRs and the urgency of management. ² Some controversial components of therapy include the best route for epinephrine administration and preferred vasopressor agents. Intravenous epinephrine administration is associated with extreme tachycardia and myocardial ischemia. Intramuscular and subcutaneous administration may be equivalent if there is not excess edema or obesity. Dopamine is associated with enhanced tachycardia, but higher efficacy of norepinephrine has not been established. The administration of histamine 2 receptor blockers such as ranitidine (50 mg IV) is a common practice, but is not based upon clinical evidence of efficacy.

If your patient is experiencing angio-edema, be aware that an emergency crychothryrotomy or tracheostomy may be needed. Availability of emergency surgical airway supplies and expert clini-cians is recommended when admin-istering agents with high risk for HSRs.

An acute HSR is a frightening experience. After the initial event, supportive care and close monitoring will be needed for several hours to ensure that symptoms do not recur. Immediate-acting medications treating the reaction may dissipate before the agent that triggered it does, and residual antigens can cause a recurrence of symptoms 4Ð6 hours after the initial event. ⁵ The patient and family members will need explanations of treatments and reassurance that close monitoring and proactive strategies can prevent harm. For some patients who experience mild HSRs, it may be appropriate to consider readministration of the agent in spite of the reaction. This should only be attempted under carefully controlled and monitored conditions, with premedications and a slower infusion rate. Published desensitization protocols exist for some medications and may be useful in these situations.

An acute HSR is also an adverse drug reaction (ADR) and should be reported according to your organizationÕs policies. The World Health Organization defines an ADR as "any response to a drug which is noxious and unintended, and which occurs at doses normally used in humans for prophylaxis, diagnosis, or therapy of disease, or for the modification of physiological function." ⁶ Enhanced reporting of ADRs will assist in defining true incidences of drug reactions.
Can acute HSRs be prevented?
Recognizing high-risk patients and situations is an essential first step in reducing HSR morbidity and mortality. Clinical variables known to increase risk for HSRs include personal history of drug allergy, multiple allergy syndrome, presence of Epstein-Barr or HIV infection, or concurrent asthma. For high-risk medications, premedications with antihistamines and corticosteroids are widely used. Skin testing may be performed before administration of medications with high incidence of HSRs. Desensitization protocols may also be useful in preventing IgE-mediated HSRs. Most involve administering a greatly diluted amount of the antigenic agent (usually a dose in micrograms, rather than milligrams) and then gradually increasing the dose every 15 to 30 minutes to induce tolerance. ² The patient must be closely monitored by experienced healthcare personnel, as reactions are still possible.
Key Points
In summary, hypersensitivity reactions to food, medications and biological agents are uncommon but potentially serious reactions that require astute nursing assessment and critical thinking skills.Paramount to this proactive approach is recognition of allergenic risk factors and significant signs or symptoms before they become life-threatening. Readily available emergency supplies and medications can minimize the adverse outcomes of severe HSRs.
Earn free contact hours at: www.ijhn.jhmi.edu
This activity is free to read here, but you also have an opportunity to earn contact hours for free! All you have to do is go to www.ijhn.jhmi.edu, register for this activity, and pass the short posttest. When you register for this activity, you will instantly become a member of the IJHN community and will see this activity listed on your homepage. Simply click the link on your homepage to electronically access the activity, posttest, course evaluation, and upon passing the posttest, a downloadable certificate. This 1-contact-hour educational activity (which includes 0.2 of pharmacology hours) is provided by the Institute for Johns Hopkins Nursing. Contact hours will be awarded until March 30th, 2013.To receive contact hours, visit www.ijhn.jhmi.edu and register for this activity online by clicking here or call 443-287-4745 to request materials in the mail.

References
¹Neugut AJ, Ghatak AT, Miller RL. (2001). Anaphylaxis in the United States: An investigation into its epidemiology. Arch Intern Med, 161(1): 15-21.
²Kanji S & Chant C. (2010). Allergic and hypersensitivity reactions in the intensive care unit. Crit Care Med, 38(6), S162-S168.
³Gobel BH. (2005). Chemotherapy-induced hypersensitivity reactions. Onc Nurs Forum, 32(5), 1027-1035.
⁴Syrigou E, Makrilia N, Koti I, et. al. (2009). Hypersensitivity reactions to antineoplastic agents: an overview. Anti-Cancer Drugs, 20, 1-6.
⁵Viale PH. (2009). Management of hypersensitivity reactions: A nursing perspective. Onc Nurs Forum, 23(2),
⁶Safety of Medicines: A Guide to Detecting and Reporting Adverse Drug Reactions. Geneva, Switzerland, World Health Organiza-tion, 2002. Available at: http://whqlibdoc.who.int/hq/2002/WHO_EDM_QSM_2002.2.pdf. Accessed January 26, 2010
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Acute Hypersensitivity Reactions: What Nurses Need to Know - Johns Hopkins School of Nursing

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Earn 1 Contact Hour - Free of Charge The goal of this CE activity is to provide nurses and nurse practitioners with knowledge and skills to recognize and manage acute hypersensitivity reactions (HSRs) occurring as a result of medication administration. After reading this article, you will be able to: Recognize early signs and symptoms of [...]

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Type II hypersensitivity: Cytotoxic (aikin)

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Type II hypersensitivity: Cytotoxic (aikin)

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Antigens in DTH are small molecules referred to as hapten where they penetrate the skin and bind to proteins. This causes it to form complexes that are recognized as foreign:

Antigens that are environmental:

Urushiol in poison Ivy--> Urushiol binds to proteins in the skin and alters the protein, making the immune system recognize these changed proteins as foreign, this causes a reduced number of proteins to be needed for immune complexes, other plant resins including poison oak and poison sumac which similarly initiates this reaction

Autoantigens:

self-antigens that are mistakenly targeted by the immune system leading to autoimmune diseases. In DTH T cells recognize these autoantigens as foreign resulting in chronic inflammation and tissue damage. --> e.g, would be beta cell antigens, which are targeted by T cells in the pancreas, causing a deficiency in insulin

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Antibodies: Type II hypersensitivity is mediated by antibodies, such as IgG and IgM, directed against antigens on host cells, which causes cell and tissue destruction by complement activation (classical pathway) or antibody dependent cell-mediated cytotoxicity. For example, Antibody-Dependent Cell Cytotoxicity (ADCC) via IgG with NK cells, or phagocytes. Type II hypersensitivity is a type of immune response in which the immune system attacks the body's own cells or tissues.

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Components of immune system involved (danielle)

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Components of immune system involved (danielle)

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1. T cells :

--> CD4+ T helper cells such as Th1 and Th17

--> they can recognize the antigen presented by APCs which are antigen-presenting cells and secrete cytokines such as interferon-gamma(IFN-γ) & IL-17.

--> The sensitized Th1 cells release cytokines that activate the macrophages (phagocytes) leading to an inflammatory response where they undergo phagocytosis

--> Th1 cells take several days to become fully active where the Th1 effector cell recognizes the processed antigens and releases cytokines that act on the vascular endothelium

2. CD8+ cytotoxic T cells (Tc cells)

--> These cells kill infected cells, presenting the antigen via MHC class I molecules directly and thus mediating direct cellular damage.

3. APCs - anitgen-presenting cells

--> dendritic cells capture the antigens and present them to T cells to initiate the immune response and migrate to lymph nodes to interact with the T cells or naive T cells which will then present a portion of the protein using MHC class 2 receptors to allow naive T helper cells to recognize and bind to after binding of APC to the naive T helper cell

--> certain cytokines are released from the naive T helper cell to differentiate into a type 1 T helper cell releasing interferon-gamma(IFN-γ) which is a cytokine, a mediator.

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Type IV Hypersensitivity (Described Concisely) (1)

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Components of immune system involved (aikin)

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Components of immune system involved (aikin)

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Antibodies IgG and IgM: IgG and IgM are the main mediators of type 2 hypersensitivity. They are produced by B cells and specifically bind to antigens present on the surface of cells or extracellular matrix.

Antigens: In type 2 hypersensitivity, the antigens that antibodies target are typically specific molecules or markers found on the cell surface or within the extracellular matrix. This can include Rh antigen, acetylcholine receptors, drug molecules and autoantigens.

Phagocytes: Cells such as macrophages and neutrophils can identify and engulf antibody-coated cells or cellular debris through the process of phagocytosis.

Natural Killer (NK) Cells: NK cells release perforin and granzymes to kill a target cell. Perforin creates an opening in the target cell so the NK cell can insert granzymes. The granzyme kills the cell.

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1. Contact Dermatitis

Redness and itchy rash

Swelling

Blisters and Hives

2. Inflammation of Granulomatous

cluster of macrophages that form granulomas causing infections that are chronic such as tuberculosis --> causing erythema due to tissue damage and inflammation, and sarcoidosis --> when leukocytes like T cells and macrophages, etc., infiltrate a site of antigen exposure and cause a delayed form of inflammatory tissue damage

Further leading to persistent cough, weight loss, and even fever

3. Autoimmune reactions

such as organ dysfunction --> including joint pain and swelling in rheumatoid arthritis and multiple sclerosis which causes neurological symptoms

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Autoimmune Hemolytic Anemia:

Fatigue

Pallor

Shortness of breath

Jaundice

Immune Thrombocytopenic Purpura (ITP):

Easy bruising

Petechiae (small red or purple spots on the skin)

Excessive bleeding from minor cuts

Frequent nosebleeds or gum bleeding

Anaphylactic shock

Watery Eyes

Itching

Redness

Swelling

Nausea and Vomiting: Feeling queasy and the act of forcefully expelling stomach contents.

Diarrhea: Frequent, loose, or watery bowel movements.

Constipation: Difficulty passing stools or infrequent bowel movements.

Abdominal Pain: Discomfort or pain in the stomach or abdominal area, which can be sharp, crampy, or dull.

Indigestion (Dyspepsia): Discomfort or pain in the upper abdomen, often associated with bloating, fullness, and nausea.

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Topical corticosteroids --> to reduce inflammation and alleviate symptoms for contact dermatitis

Systemic corticosteroids --> more severe reactions and is taken orally to reduce internal inflammation of body

Immunosuppressive drugs--> example TNF inhibitors which can be used in diseases such as rheumatoid arthritis and psoriasis

Antibiotics or Antimicrobial drugs --> for example antitubercular drugs to reduce the spread of tuberculosis and kill the causative agent Mycobacterium tuberculosis

Desensitization therapies --> to increase T cells (Tregs) to suppress the allergic responses. It is also to increase the allergen-specific IgG antibodies (such as IgG4 Ab) which can block allergens from binding to IgE on mast cells and basophils preventing allergic reaction

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Type III hypersensitivity: Immune Complex (chokka)

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Type III hypersensitivity: Immune Complex (chokka)

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Type III hypersensitivity involves the formation of immune complexes composed of antigen-antibody complexes. The reaction time is approximately 3-10 hours after initial exposure.

The immune complexes formed can accumulate in different types of tissues and trigger an inflammatory response, causing damage to the tissue/s involved. Active complements and immune cells will be recruited as well, which leads to tissue inflammation and injury.

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Immunosuppressants (e.g. corticosteroids or azathioprine)

systemic glucocorticoids

cyclophosphamide and cyclosporin agents

intravenous immunoglobulin infusions

plasmapheresis (remove some plasma from the blood, exchanging for a healthier one)

Avoid taking these drugs (common causes of Type II Hypersensitivity)

penicillin

methyldopa

thiazides

cephalosporins

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Republic poly immunology lesson 12 scorm package

https://ditki.com/course/pathology/glossary/term/hypersensitivity-type-iv

https://dermnetnz.org/topics/allergies-explained

https://youtu.be/kQFmrQfBW5k?si=EvnI6Dqa-p3l_XbX