Hypersensitivity Reactions: Types, Mechanisms, and Clinical Examples, Exams of Nursing

A comprehensive overview of hypersensitivity reactions, focusing on the four distinct types: type i (ige-mediated), type ii (cytotoxic), type iii (immune complex-mediated), and type iv (cell-mediated). It delves into the mechanisms of each type, including the role of antibodies, immune complexes, and t-lymphocytes. The document also presents clinical examples of each type of hypersensitivity reaction, highlighting their relevance to various diseases and conditions. It further explores the concept of alloimmunity and autoimmunity, emphasizing the immune system's response to foreign tissues and self-antigens, respectively.

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NU
530
Quiz
2
Study
Guide
Chapter 8
Endotoxins are released when the bacteria die/ the are produced by gram-negative bacteria.
Endotoxins released by blood-borne bacteria cause the release of
vasoactive enzymes that increase the permeability of blood vessels.
Bacteria injure cells by producing exotoxins or endotoxins. Exotoxins are
enzymes that
can damage the plasma membranes of host cells or can
inactivate enzymes critical to protein synthesis, and endotoxins activate
the inflammatory response and produce fever.
Gram-negative microbes produce an endotoxin (lipopolysaccharide [LPS]) that
is a structural portion of the cell wall and is released during growth, lysis, or
destruction of the bacteria or during treatment with antibiotics. Therefore,
antibiotics cannot prevent the toxic effects of endotoxin. Bacteria that produce
endotoxins are called pyrogenic bacteria because they activate the
inflammatory process and produce fever.
Septicemia is the proliferation of bacteria in the blood. Endotoxins released by
blood- borne bacteria cause the release of vasoactive enzymes that increase
the permeability of blood vessels. Leakage from vessels causes hypotension
that can result in septic shock.
Bacteremia occurs when bacteria are present in the blood. Gram-negative
sepsis (sepsis
or septicemia) occurs when bacteria are growing in the blood
and release large amounts of endotoxin, when can cause endotoxic shock
with up to 50% mortality. Released
endotoxin, as well as other bacterial
products, reacts with pattern recognition receptors (PRRs) and induces the
overproduction of proinflammatory cytokines, particularly tumor necrosis factor-
alpha (TNF-a), interleukin-1 (IL-1) and interleukin -6 (IL-6) which may
secondarily be immunosuppressive. Endotoxin also is a potent activator of
the
complement and clotting system, leading to a degree of capillary
permeability sufficient
to permit escape of large volumes of plasma into
surrounding tissue, contributing to hypotension and in severe cases,
cardiovascular shock. Activation of the coagulation
cascade leads to the
syndrome of dissemination (or diffuse0 intravascular coagulation.
Virulence: Capacity of a pathogen to cause severe disease (e.g., measles
virus is a low virulence; rabies and Ebola viruses are highly virulent).
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NU 530 Quiz 2 Study Guide

Chapter 8

Endotoxins are released when the bacteria die/ the are produced by gram-negative bacteria.

Endotoxins released by blood-borne bacteria cause the release of vasoactive enzymes that increase the permeability of blood vessels. Bacteria injure cells by producing exotoxins or endotoxins. Exotoxins are enzymes that can damage the plasma membranes of host cells or can inactivate enzymes critical to protein synthesis, and endotoxins activate the inflammatory response and produce fever. Gram-negative microbes produce an endotoxin (lipopolysaccharide [LPS]) that is a structural portion of the cell wall and is released during growth, lysis, or destruction of the bacteria or during treatment with antibiotics. Therefore, antibiotics cannot prevent the toxic effects of endotoxin. Bacteria that produce endotoxins are called pyrogenic bacteria because they activate the inflammatory process and produce fever. Septicemia is the proliferation of bacteria in the blood. Endotoxins released by blood- borne bacteria cause the release of vasoactive enzymes that increase the permeability of blood vessels. Leakage from vessels causes hypotension that can result in septic shock. Bacteremia occurs when bacteria are present in the blood. Gram-negative sepsis (sepsis or septicemia) occurs when bacteria are growing in the blood and release large amounts of endotoxin, when can cause endotoxic shock with up to 50% mortality. Released endotoxin, as well as other bacterial products, reacts with pattern recognition receptors (PRRs) and induces the overproduction of proinflammatory cytokines, particularly tumor necrosis factor- alpha (TNF-a), interleukin-1 (IL-1) and interleukin -6 (IL-6) which may secondarily be immunosuppressive. Endotoxin also is a potent activator of the complement and clotting system, leading to a degree of capillary permeability sufficient to permit escape of large volumes of plasma into surrounding tissue, contributing to hypotension and in severe cases, cardiovascular shock. Activation of the coagulation cascade leads to the syndrome of dissemination (or diffuse0 intravascular coagulation. Virulence : Capacity of a pathogen to cause severe disease (e.g., measles virus is a low virulence; rabies and Ebola viruses are highly virulent). https://www.youtube.com/watch?v= 9 G1OELPrivU

Attenuated vaccines: alive, but less infectious. Live attenuated vaccines are created by weakening infectious organisms that can still replicate and induce protective immune responses without causing disease in the host. Vaccination with the live but attenuated organism generates an immune response that protects the vaccinated person against severe disease or even infection. Available since the 1950s, live attenuated vaccines (LAV)

and literally attack normal body tissues. This type of reaction is known as an autoimmune response. Both hypersensitivity and autoimmune responses can damage cells, tissues, or organs and have serious consequences.

Hypersensitivity is an immune response misdirected against the host’s own tissues ( autoimmunity) or directed against beneficial foreign tissues, such as transfusions or transplants (alloimmunity); or it can be exaggerated responses against environmental antigens (allergy). NEED TO figure this out and break it down more Allergy means a hypersensitivity to environmental antigens. Immunity is the protective response to antigens. The four distinct types of hypersensitivity reactions:

- Type 1 IgE allergic reactions o Type I (IgE-mediated) reactions occur after antigen reacts with IgE on mast cells, leading to mast cell degranulation and the release of histamine and other inflammatory substances. o Allergens are antigens that cause allergic responses, usually a type I hypersensitivity response. Some reactions are confined to the areas exposed to the antigen, such as the mucous membranes of the nose and eyes, causing symptoms of rhinorrhea, sneezing, and itchy, red, and watery eyes. Other reactions may involve all blood vessels and bronchiolar smooth muscle, causing widespread vasodi-lation, decreased cardiac output, and severe bronchoconstric-tion; this condition is known as **anaphylaxis.

  • Type II tissue-specific reactions
  • Type III immune complex reactions** Type III (immune complex–mediated) Immune complex disease can be a systemic reaction, such as serum sickness (e.g., Raynaud phenomenon), or localized, such as the Arthus reaction

• TYPE I: RAPID HYPERSENSITIVITY REACTIONS

Type I (rapid) hypersensitivity, sometimes called atopic allergy, is the most common type of hypersensitivity. This type results from increased production of the immunoglobulin E (IgE) antibody class. An acute inflammatory reaction occurs when IgE responds to an otherwise harmless antigen (e.g., pollen) and causes the release of histamine and other vasoactive amines from basophils, eosinophils and mast cells. ******Clinical examples of type I reactions include systemic anaphylaxis, allergic asthma, and atopic (genetic tendency) allergies such as hay fever, allergic rhinitis, and allergies to specific allergens such as latex, bee venom, peanuts, iodine, shellfish, drugs, and thousands of other environmental antigens. TYPE II: CYTOTOXIC REACTIONS OVERVIEW In a type II (cytotoxic) reaction, the body makes special au-toantibodies directed against self-cells or tissues that have some form of foreign protein attached to them Clinical examples of type II reactions include Coombs'-positive hemolytic anemias, thrombocy-topenic purpura, hemolytic transfusion reactions (when an individual receives the wrong blood type during a transfu- sion), hemolytic disease of the newborn, Goodpasture's syndrome, and drug-induced hemolytic anemia

- Type IV cell-mediated reactions Type IV ( cell-mediated) reactions are caused by specifically sensitized T – lymphocytes cells, which either kill target cells directly or release lymphokines that activate other cells, such as macrophages. Anemia Lymphoede ma SLE Antigen s Cell mediated Unlike with a type I hypersensitivity reaction, which occurs immediately, a type IV response typically occurs hours to days after exposure. Other clinical examples of type IV hypersensitivity reactions include contact dermatitis, poison ivy skin rashes, a local response to insect stings, allograft (tissue transplant) rejections, and granulomatous diseases in which the antigen is unknown (e.g., sarcoidosis).

Types of Immunity and associated labs, IgE, Cell-mediated The most common infections in individuals with defects of cell-mediated immune response are fungal and viral, whereas infections in individuals with defects of the humoral immune response or complement function are primarily bacterial. Most type I reactions are allergic. They are mediated by IgE. Most occur against environmental antigens and do contribute to some autoimmune diseases. The most Potent mediator of IgE is Histamine. Histamine contracts bronchial smooth muscle, and this causes bronchoconstriction. There is also increased vascular permeability, edema, and vasodilation.

98% have detectable antibodies against nuclear antigens causing severe kidney inflammation.

Reactions in the brain, heart, spleen, lungs, gastrointestinal tract, peritoneum, and skin. Some of the

symptoms, such as destruction of red blood cells (anemia), lymphocytes (lymphopenia) and

other cells, may be type II hypersensitivity reactions.

Symptoms include: arthralgias or arthritis (90 %) , vasculitis and rash (70-80%) renal disease (40-

50%). Hematologic abnormalities (50%) – anemia most common complication and

cardiovascular disease (30-50%).

11 Common Clinical Findings: Type II hypersensitivity in

green 1. Facial rash confined to the cheeks (malar rash)

2. Discoid rash (raised patches, scaling)

3. Photosensitivity (Development of skin rash as a result of exospore to sunlight)

4. Oral or nasopharyngeal ulcers

5. Nonerosive arthritis of at least two peripheral joints

6. Serositis (inflammation of membranes of lungs [pleurisy] or heart [pericarditis])

7. Renal disorders (persistent proteinuria of >0.5g/day or >3 on dipstick or cellular casts)

8. Neurologic disorders (seizures or psychosis in the absence of known causes)

9. Hematologic disorders, (hemolytic anemia, leukopenia, lymphopenia, or thrombocytopenia)

  1. Immunologic disorders (anti-double-stranded DNA ([sDNA] anti- Smith [Sm] antigen, false-positive serologic test for syphilis or antiphospholipid antibodies [Anticardiolipin antibody or lupus anticoagulant])
  2. Presence of antinuclear antibody (ANA) Laboratory diagnosis – positive ANA screening test: 98% of SLE test positive The presence of autoantibodies is a diagnostic criteria for SLE. Diagnostic criterion for SLE would include positive LE NO CURE HIV AIDS is an acquired dysfunction of the immune system caused by a retrovirus (HIV) that infects and destroys CD4+ lymphocytes (T-helper cells). Depletion of CD4+ cells – effect the immune system. HIV infection begins when a virion binds to CD Human immunodeficiency virus (HIV) infection and AIDS are associated with cardiac abnormalities, including myocarditis, endocarditis, pericarditis, and cardiomyopathy.

Stage 1: Acute HIV Infection

Within 2 to 4 weeks after infection with HIV, about two-thirds of people

will have a flu-like illness. This is the body’s natural response to HIV

infection.

Flu-like symptoms can include:

  • Fever
  • Chills
  • Rash
  • Night sweats
  • Muscle aches
  • Sore throat
  • Fatigue
  • Swollen lymph nodes
  • Mouth ulcers Stage 2: Clinical Latency
  • In this stage, the virus still multiplies, but at very low levels.

People in this stage may not feel sick or have any symptoms.

This stage is also called chronic HIV infection.

  • Without HIV treatment, people can stay in this stage for 10 or 15

years, but some move through this stage faster.

Stage 3: AIDS

If you have HIV and you are not on HIV treatment, eventually the virus will

weaken your body’s immune system and you will progress to AIDS

( acquired immunodeficiency syndrome). This is the late stage of HIV

infection. The major immunologic finding in AIDS is the striking decrease in the

number of CD4+T cells.

Symptoms of AIDS can include:

  • Rapid weight loss = Cachexia includes anorexia, early satiety,

weight loss, anemia, asthenia, taste alterations, and altered

metabolism.

  • Recurring fever or profuse night sweats
  • Extreme and unexplained tiredness
  • Prolonged swelling of the lymph glands in the armpits, groin, or neck
  • Diarrhea that lasts for more than a week
  • Sores of the mouth, anus, or genitals
  • Pneumonia
  • Red, brown, pink, or purplish blotches on or under the skin or inside the mouth, nose, or eyelids
  • Memory loss, depression, and other neurologic disorders

Melanoma – can that is formed in the skin pigment cell Ultraviolet radiation from sunlight causes basal cell and squamous cell carcinomas and increases the risk for malignant melanoma Adenocarcinoma – small intestine The disease may develop in

Tumors that arise from or form ductal or glandular structures Granular tissue adenocarcinoma uncommon Sex men than in women. Age most often found in people in their 60s and 70s. Race/ethnicity African Americans are affected more often by these cancers than people of other races/ethnicities. Smoking and alcohol use Diet diets high in red meat and salted or smoked foods Celiac disease Colon cancer Crohn's disease Inherited syndromes Familial adenomatous polyposis (FAP) In this condition, many (often hundreds) of polyps develop in the colon and rectum. Cystic fibrosis (CF) many different places, but it is most prevalent in the following cancer types: Lung cancer: Non- small cell lung cancer accounts for 80 percent of lung cancers, and adenocarcinoma is the most common type. Prostate cancer: Cancer that forms in the prostate gland is typically an adenocarcinoma, which accounts for 99 percent of all prostate cancers. Pancreatic cancer: Exocrine pancreatic cancer tumors are called adenocarcinomas. They form in the pancreas ducts. Esophageal cancer: Cancer that forms in the glandular cells of the esophagus is known as adenocarcinoma. This is the most common type of esophageal cancer. Colorectal cancer: Cancer that develops in the intestinal gland cells that line the inside of the colon and/or rectum is an adenocarcinoma. It makes up 95 percent of colon and rectal cancers. squamous cell – Ultraviolet light Tobacco smoking is responsible for small cell and squamous cell carcinoma of the lungs. It also causes damage to blood vessels and a number of other diseases. It causes 4- million deaths a year worldwide. It is responsible for 30% of cancer deaths. Neoplasm – abnormal and excessive growth, called neoplasia, of tissue. The growth of a neoplasm is uncoordinated with that of the normal surrounding tissue, and it persists growing abnormally, even if the original trigger is removed. This abnormal growth usually (but not always) forms a mass. The terms benign and malignant correlate to the course of the neoplasm.

Leukemia is a cancer of blood- forming cells. Smoking, xrays, radiation, benzene, genetics Most common in Children Human papillomavirus (HPV) has been linked to cervical, anogenital, and penile cancers. Most common Sexually transmitted disease Direct skin contact Causes warts that may lead to cancer Cervical Cancer Human papillomavirus type 16 & 18

Know the different types of cervical cancer and how they are likely to be acquired -There are

over 100 subtypes of HPV, and the virus is found in 99.7% of women with cervical cancer. HPV-

16 accounts for 50-60% of cervical cancer cases, followed by HPV-18 (10-12%) and HPV-31 and

HPV-45 (4-5% each). HPV-16 is directly mutagenic by inducing the viral genes E6 and E7.

Persistence of infection with high-risk HPV is a prerequisite for the development of cervical

intraepithelial neoplasia.

Hepatitis B and hepatitis C have been linked to the development of liver cancer, usually due to

chronic inflammation.

Epstein-Barr virus can lead to B-cell lymphomas in those patients who are immunosuppressed.

Malignant tumors have no capsule, which allows them to spread readily. They have rapid

growth rates and specific microscopic alterations. They are poorly differentiated and spread to

distant tissues.

Some tumors initially described as benign can progress to cancer and then are referred to as

malignant tumors

Malignant tumors have cells that vary in both size and shape, and they grow rapidly.

Benign tumors are well encapsulated and well differentiated, but actually do retain some

normal tissue. They do not spread to regional lymph nodes, nor are they generally resistant to

treatment

Point mutations are small changes in one or a few nucleotides.

Tumor-suppressor genes encode proteins that in their normal state negatively regulate

proliferation.

Oncogenes are mutant genes that in their normal nonmutant state direct synthesis of protein

that positively accelerates proliferation.

Telomeres are protective ends, or caps, on each chromosome.

Proto-oncogene is an oncogene in its nonmutant state.