When confronted with a decrease in work demands or adverse environmental conditions, most cells are able to revert to a smaller size and a lower and more efficient level of functioning that is compatible with survival. This decrease in cell size is called atrophy. Cell size, particularly in muscle tissue, is related to workload. As the workload of a cell diminishes, oxygen consumption and protein synthesis decrease. Cells that are atrophied reduce their oxygen consumption and other cellular functions by decreasing the number and size of their organelles and other structures. There are fewer mitochondria, myofilaments, and endoplasmic reticulum structures. When a sufficient number of cells are involved, the entire tissue or muscle atrophies.
Disuse atrophy occurs when there is a reduction in skeletal muscle use. An extreme example of disuse atrophy is seen in the muscles of extremities that have been encased in plaster casts. Because atrophy is adaptive and reversible, muscle size is restored after the cast is removed and muscle use is resumed. Denervation atrophy is a form of disuse atrophy that occurs in the muscles of paralyzed limbs. Lack of endocrine stimulation produces a form of disuse atrophy. In women, the loss of estrogen stimulation during menopause results in atrophic changes in the reproductive organs. With malnutrition and decreased blood flow, cells decrease their size and energy requirements as a means of survival.
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Involves the unregulated, enzymatic digestion ("autolysis") of a cell and its components.
Occurs as a result of irreversible cellular injury.
Different types of tissues tend to undergo different types of necrosis. Three main types of necrosis have been identified.
Digestive enzymes released by necrotic cells soften and liquefy dead tissue.
Occurs in tissues, such as the brain, that are rich in hydrolytic enzymes.
Dead tissue takes on a crumbly, "cheeselike" appearance. Dead cells disintegrate but their debris is not fully digested by hydrolytic enzymes.
Occurs in conditions like tuberculosis where there is prolonged inflammation and immune activity.
Dead tissues appear firm, gray and slightly swollen.
Often occurs when cell death results from ischemia and hypoxia. The acidosis that accompanies ischemia denatures cellular proteins and hydrolytic enzymes.
Seen with myocardial infarction, for example.
Pain is a subjective sensation of unpleasantness usually associated with actual or potential tissue damage. Pain can be protective, in that it causes an individual to back away from a dangerous stimulus, or it can serve no function, as is the case with chronic pain. Pain is sensed when specific pain receptors are activated. Description of pain is subjective and objective, based on the duration, the speed of sensation, and the location.
Receptors for Pain
Pain receptors are called nociceptors. Nociceptors include the free nerve endings, which respond to many stimuli, including mechanical pressure, deformation, temperature extremes, and various chemicals. With intense stimuli, other receptors such as the Pacinian corpuscles and Meissner's corpuscles also send information perceived as painful. Chemicals that cause or worsen pain include histamine, bradykinin, serotonin, several prostaglandins, potassium ion, and hydrogen ion. Each of these substances accumulates at sites of cellular injury, hypoxia, or death, alerting the individual to these happenings. Although all pain receptors are capable of responding to any type of tactile stimuli, each receptor appears to respond most readily to one specific type of stimulation.
Duration of Pain
Pain may be acute (lasting less than 6 months) or chronic (lasting longer than 6 months). Acute pain can be beneficial, serving to alert the individual to danger. Chronic pain is never beneficial.
Speed of Sensation
Fast pain is sensed less than 1 second (usually much less) after the application of a painful stimulus (e.g., touching a hot burner). Fast pain is well localized to the site and is frequently described as pricking or sharp. Fast pain is usually felt on or near the surface of the body. It is transmitted to the spinal cord by the A ÎÂ´ fibers.
Slow pain is felt 1 second or more after the application of a painful stimulus (e.g., pain that continues after a bump to the head). Slow pain is frequently described as dull, throbbing, or burning. It can intensify over the course of several minutes and may occur on the skin or in any deep tissue of the body. Slow pain can become chronic pain and lead to great disability. Slow pain is transmitted to the spinal cord by the slow C fibers. The C fibers are believed to release the neurotransmitter substance P when they synapse in the spinal cord. The neurotransmitter released by the A ÎÂ´ fibers is unknown.
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Cutaneous pain is pain felt on the skin or in subcutaneous tissues (e.g., pain felt with a pinprick or a skinned knee). Cutaneous pain is well localized over a dermatome (an area of the skin innervated by a certain spinal cord segment) and is transmitted rapidly. Deep somatic pain is pain arising from bones and joints, tendons, skeletal muscles, blood vessels, and deep nerve pressure. A headache is considered deep somatic pain. Deep somatic pain is slow pain, which may radiate along a nerve route. Visceral pain is pain in the abdominal or thoracic cavity. Visceral pain is typically severe and may be well localized at one spot, but it may also be referred to different parts of the body. Visceral pain localizes over embryonic dermatomes and is caused by stimulation of several pain receptors.
Pain threshold is the level at which a stimulus is first perceived as pain. In general, humans have similar pain thresholds. An individual's pain threshold varies little over time.
Pain tolerance is an individual's ability to withstand a painful stimulus without demonstrating physical signs of pain. Pain tolerance is unique for each individual. It depends on past experience; cultural, familial, and role expectations; and the individual's current emotional and physical state. In some cultures it is considered weak to show pain, so pain tolerance is high. An individual who is depressed or anxious may have a reduced tolerance for pain. An individual who is distracted, or one who is in the middle of an emergency or an athletic challenge, may show a high tolerance for pain.
Central Nervous System Pathways for Pain
Once in the spinal cord, most pain fibers synapse on neurons in the dorsal horns of the segment they enter. However, some fibers may travel up or down several segments in the cord before synapsing. After activating cells in the spinal cord, information concerning painful stimuli is sent by one of two ascending pathways to the brain, the neospinothalamic tract or the paleospinothalamic tract.
Information carried to the spine in the fast-firing A ÎÂ´ fibers is transmitted ascendingly from the spinal cord to the brain via the fibers of the neospinothalamic tract. Some of these fibers terminate in the reticular activating system, alerting one to the occurrence of pain, but most travel to the thalamus. From the thalamus, signals are sent to the somatosensory cortex where the location of the pain is well localized. Cortical stimulation is required for the conscious interpretation of the pain signal.
Information carried to the spine in the slowly transmitting C fibers, as well as that carried in a few of the A ÎÂ´ fibers, is transmitted ascendingly to the brain via the fibers of the paleospinothalamic tract. These fibers travel to the reticular area of the brainstem and to an area of the mesencephalon called the periaqueductal gray area. Paleospinothalamic fibers that travel through the reticular area go on to activate the hypothalamus and the limbic system, influencing the function of these emotion-controlling areas. The periaqueductal gray area is an important integrating center for pain; the perception of pain is highly modified in this area. Pain carried in the paleospinothalamic tract is poorly localized and is responsible for causing the emotional distress associated with pain.
Gating of Pain in the Spinal Cord and the Brain
Experimental evidence suggests that the likelihood of transmitting painful stimuli from the spinal cord to the brain can be influenced by descending neurons firing on the cells of the spinal cord. Descending input to the spine may increase the transmission of a painful stimulus, or it might decrease the likelihood that a stimulus is perceived as painful. Reduced passage of a painful stimulus is called analgesia.
Descending neurons that affect pain transmission come from the cerebral cortex, the hypothalamus, the limbic system, and, especially, the periaqueductal gray area. The ability of upper brain areas to influence transmission of pain in the spinal cord is called gating. Gating occurs at each level of pain transmission (across both the neospinothalamic and the paleospinothalamic tracts) and in the brain as well. Fibers from the periaqueductal gray area that diffusely innervate the cerebral cortex, the limbic system, the hypothalamus, and the reticular formation are especially important in influencing pain transmission in the brain.
Interpretation of the Gate Theory
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The gate theory of pain offers an explanation of how cultural and personal expectations, mood, and fear can influence an individual's perception and tolerance of pain. By emphasizing the ability of descending pathways to influence pain perception, the gate theory of pain explains how distraction or relaxation techniques may reduce pain, whereas focusing on a painful stimulus may increase the likelihood of the stimulus being passed into consciousness.
The gate theory of pain also explains how gating can occur with peripheral nervous stimulation to the spinal cord. Data suggest that when the large A Î” neurons carrying skin tactile information are stimulated at the same time that the A ÎÂ´ and C fibers are transmitting painful stimuli, spinal activation of both the neospinothalamic and the paleospinothalamic tracts is reduced. This reduced activation appears to result from lateral inhibition of the cells in the dorsal spine by the large A Î” neurons. Rubbing the head or skin after an injury stimulates the large A Î” fibers and produces some degree of analgesia. This is an example of gating the passage of a painful stimulus.
Endorphins, Enkephalins, and Serotonin
Some of the analgesic responses described above appear to result from the central nervous system production and release of the endogenous opiates: the endorphins and the enkephalins. Serotonin, another neurotransmitter, is also involved in producing analgesia.
Enkephalin is a small peptide released in the spinal cord from neurons descending from the periaqueductal gray area. Enkephalin causes presynaptic inhibition of types C and AÎ´ fibers in the spine. This inhibition reduces the passage of a painful stimulus beyond the spinal cord. Enkephalin is also present in the limbic system and the hypothalamus.
The endorphins and serotonin act as neurotransmitters in the brain to reduce the passage and perception of pain. The pituitary releases endorphin in response to intense exercise and during painful experiences such as labor and delivery. Endorphins also affect mood. Prolonged pain has been shown to deplete endorphin levels; perhaps this contributes to the despair and anguish seen in individuals who have chronic pain. Serotonin is produced in the brain and is released from descending fibers synapsing in the spinal cord. Drugs that increase brain serotonin levels, such as the tricyclic antidepressants, reduce pain perception.
Infants and children acutely feel pain and should never be exposed to painful therapies without pain medication. Infants may express pain differently than older children and adults.
Acute pain is characterized by increased heart rate, increased respiratory rate, facial grimacing, withdrawal, and crying. Dilated pupils and sweating occur. Usually, a person suffering acute pain is highly focused on the pain.
Chronic pain is associated with a return of heart and respiratory rate to normal. An individual who has chronic pain may appear quiet and subdued. Depression and despair may develop.
Rating scales from 1 to 10 allow an individual to evaluate pain and may help a clinician recognize the intensity of a person's pain. For children, a diagram showing a range of faces, from happy to very sad and crying, may be used to help identify level of pain.
Recognizing the subtle cues shown by an individual in pain is important for responding to pain when cultural, linguistic, or age barriers to communication exist.
Pain stimulates the stress response. Stress can reduce the functioning of the immune and inflammatory systems, and thus delay or impair healing.
Acute, severe pain may lead to cardiovascular collapse and shock.
Application of cool compresses may reduce pain associated with inflammation.
Comfort measures such as back rubs may reduce pain by stimulating the large AÎ´ fibers and by activating descending pathways stimulated by distraction.
Behavioral techniques, including distraction and imaging, may stimulate descending pathways that block the transmission of painful stimuli to the brain. The Lamaze method of breathing during labor is based on this principle.
Transcutaneous electrical nerve stimulation (electrodes on the skin) may relieve pain by stimulating the large type AÎ´ nerve fibers. Acupuncture may stimulate these fibers and reduce pain as well.
Analgesics such as acetaminophen can relieve mild pain, most likely by blocking the production of prostaglandins or other substances that sensitize pain receptors.
Nonsteroidal anti-inflammatory drugs, such as aspirin and ibuprofen, or steroids may be used for mild to moderate pain. These drugs block prostaglandin production both locally at sites of injury and in the central nervous system.
Narcotics, such as morphine, can reduce intense pain. Morphine binds to opiate receptors in the central nervous system and alters pain perception.
Nerve block by injection of drugs or surgery may occasionally be used to treat severe pain.
Contact Dermatitis (Irritation)
Contact dermatitis is often sharply demarcated inflammation of the skin resulting from contact with an irritating chemical or atopic allergen (a substance producing an allergic reaction in the skin) and irritation of the skin resulting from contact with concentrated substances to which the skin is sensitive, such as perfumes, soaps, or chemicals.
Mild irritants: chronic exposure to detergents or solvents
Strong irritants: damage on contact with acids or alkalis
Allergens: sensitization after repeated exposure
Signs and Symptoms
Mild irritants and allergens: erythema and small vesicles that ooze, scale, and itch
Strong irritants: blisters and ulcerations
Classic allergic response: clearly defined lesions, with straight lines following points of contact
Severe allergic reaction: marked erythema, blistering, and edema of affected areas
Elimination of known allergens and decreased exposure to irritants, wearing protective clothing such as gloves, and washing immediately after contact with irritants or allergens
Topical anti-inflammatory agents (including corticosteroids), systemic corticosteroids for edema and bullae, antihistamines, and local applications of Burow's solution (for blisters)
administering systemic corticosteroid therapy (during extreme exacerbations)
applying weak tar preparations and ultraviolet B light therapy to increase thickness of stratum corneum
administering antibiotics (for positive culture for bacterial agent).
Inflammation is the response of a tissue to injury. Although painful, the inflammatory reaction is essential for preventing infection of the injured area as well as for initiating the process of healing.
There are five "cardinal signs" of inflammation:
Rubor- The redness that occurs as a result of the increased blood flow to the inflamed area.
Tumor- Swelling of the inflamed tissue as a result of increased capillary permeability and fluid accumulation.
Calor- The increase in temperature (heat) that occurs in the inflamed area as a result of increased blood flow.
Dolor- Pain that occurs in the inflamed area as a result of stimulation of sensory neurons.
Functio laesa- Alteration or loss of function in the inflamed tissues.
The inflammatory response may be divided into main two stages: the vascular response stage and the cellular response stage.
1. Vascular response
Rapid vasoconstriction of blood vessels occurs in the injured area and is followed by rapid vasodilatation.
An increase in capillary permeability occurs in the injured area leading to swelling and edema. The fluids that enter the injured area are useful for diluting out any bacterial toxins or irritants present in the tissue.
2. Cellular response
Phagocytic neutrophils are the first white blood cells to arrive in the injured area. Leukocytes are attracted to the injured area by certain bacterial substances as well as by cellular debris and cytokines (chemotaxis).
As fluid leaves the capillaries, the viscosity of blood increases and leukocytes precipitate to the walls of the capillary. This process is called margination. Leukocytes undergo a change in shape and squeeze through the now more permeable capillaries into the tissues. The movement of leukocytes through the capillary wall is called diapedesis.
Other white blood cells such as eosinophils and basophils also arrive at the injured area and release substances such as histamine that enhance the inflammatory reaction. Histamine is a powerful vasodilator that increases capillary permeability. Monocytes will also enter the inflamed tissues where they mature into phagocytic macrophages.
Cytokines such as interleukin and tumor necrosis factor are released to enhance the inflammatory and immune response. Prostaglandins are also released by many cells in the injured area and cause fever and vasodilation.
Hypersensitivity reactions are abnormal immune and inflammatory responses. There are four types of hypersensitivity reactions.
Type I Hypersensitivity Reactions
Type I hypersensitivity reactions are allergic reactions mediated by the IgE antibody. In type I reactions, an antigen"called an allergen" to which the individual is sensitive is recognized by a B cell, which is then stimulated to make IgE antibodies against the antigen. IgE binds the antigen as well as a nearby basophil or mast cell via a high-affinity IgE receptor present on those cells. The inciting allergen is typically multi-valent (has many IgE binding sites), so the allergen actually links several IgE antibodies together. This linking triggers a cascade of signals that cause degranulation of the mast cells and basophils, and the release of histamine, cytokines, chemokines, and leukotrienes. These mediators, as well as activated complement and eosinophil chemotactic factor, cause peripheral vasodilation and increased capillary permeability, leading to localized swelling and edema. Symptoms are specific according to where the allergic response occurs. Binding of the antigen in the nasal passages causes allergic rhinitis with nasal congestion and inflammation of the tissues, while binding of an antigen in the gut may cause diarrhea or vomiting.
A severe type I hypersensitivity reaction is termed an anaphylactic reaction. Anaphylaxis involves a rapid IgE mast cell response after exposure to an antigen to which the individual is highly sensitive. Histamine-induced dilation of the entire systemic vasculature can occur, leading to collapse of the blood pressure. A severe decrease in systemic blood pressure during an anaphylactic reaction is called anaphylactic shock. Because histamine is a potent constrictor of bronchiolar smooth muscle, anaphylaxis involves closure of the respiratory passages. Anaphylaxis in response to some drugs such as penicillin, or in response to a bee sting, may be fatal in highly sensitized individuals, as a result of circulatory collapse or respiratory failure. Symptoms of an anaphylactic reaction include itching, abdominal cramps, flushing of the skin, gastrointestinal (GI) upset, and breathing difficulties.
Type II Hypersensitivity Reactions
Type II hypersensitivity reactions occur when IgG or IgM antibodies attack tissue antigens. Type II reactions result from a loss of self-tolerance and are considered autoimmune reactions. The target cell is usually destroyed.
In a type II reaction, antibody-antigen binding causes complement activation, mast cell degranulation, interstitial edema, tissue destruction, and cell lysis. Type II hypersensitivity reactions lead to macrophage phagocytosis of the host cells. Examples of type II autoimmune diseases include Graves' disease, which involves antibodies produced against the thyroid gland; autoimmune hemolytic anemia, which involves antibodies produced against red blood cells; transfusion reactions, which involve antibodies produced against donor blood cells; and autoimmune thrombocytopenic purpura, which involves antibodies produced against platelets. Systemic lupus erythematosus (SLE) also has aspects of type II reactions.
Type III Hypersensitivity Reactions
Type III hypersensitivity reactions occur when circulating antibody-antigen complexes precipitate out in a blood vessel or in downstream tissue. Antibodies are not directed against those particular tissue sites, but are trapped in their capillary meshwork. In some cases, foreign antigens may adhere to tissues, causing formation of antibody-antigen complexes at those sites.
Type III reactions activate complement and mast cell degranulation, causing damage to the tissue or capillaries where they occur. Neutrophils are drawn to the area and begin to phagocytize the injured cells, causing release of cellular enzymes and the accumulation of cell debris. This continues the inflammation cycle.
Examples of type III hypersensitivity reactions include serum sickness, in which antibodies form against foreign blood, often in response to intravenous drug use. The antibody-antigen complexes deposit in the vascular system, joints, and kidneys. With glomerulonephritis, antibody-antigen complexes form in response to an infection, often by streptococcal bacteria, and deposit in the glomerular capillaries of the kidneys. With systemic lupus erythematosus, antibody-antigen complexes form against collagen and cellular DNA, and deposit in multiple sites of the body.
Type IV Hypersensitivity Reactions
Type IV hypersensitivity reactions are T cell-mediated reactions, in that cytotoxic (CD8) or helper (CD4) T cells are activated by an antigen, leading to destruction of the cells involved. Cytotoxic cell-mediated reactions are often against virally infected cells and can lead to extensive tissue damage. CD4 cell-mediated reactions are delayed, taking 24 to 72 hours to develop. They are characterized by the production of pro-inflammatory cytokines that stimulate macrophage phagocytosis and increase swelling and edema.
Examples of conditions caused by type IV reactions include autoimmune thyroiditis (Hashimoto's disease), in which T cells are produced against thyroid tissue, graft and tumor rejection, and delayed allergic reactions, such as the reaction to poison ivy. The tuberculin skin test indicates the presence of delayed cell-mediated immunity against the tuberculin bacillus.
Shock is the collapse of systemic arterial blood pressure. With a severe fall in blood pressure, blood flow does not adequately meet the energy demands of tissues and organs. In addition, the body responds by diverting blood away from most tissues and organs to ensure that vital organs, "that is, the brain, heart, and lungs" receive blood. The tissues and organs that are deemed expendable are severely jeopardized, especially the kidneys, the gut, and the skin. If the individual survives the shock episode, renal failure, gastric ulcers, intestinal infarction, and a sloughing of the skin often follow.
The Baroreceptor Response to Shock
With the beginning of shock, baroreceptor reflexes are activated and the body tries to compensate for the drastically reduced blood pressure. If the cause of shock continues, compensation will become inadequate and deterioration of all organs, including the lungs, heart, and brain, will progress. As the heart and lungs deteriorate, a deadly cycle is initiated. Oxygenation and cardiac output progressively fall, and shock worsens, soon becoming irreversible. Irreversible shock results in death of the individual.
Causes of Shock
Blood pressure depends on the product of the cardiac output (heart rate Ã- stroke volume) and TPR. Therefore, anything that causes heart rate, stroke volume, or TPR to plummet can cause shock.
There are six major causes of shock.
Cardiogenic shock can occur following collapse of the cardiac output, which often results from a myocardial infarct, fibrillation, or congestive heart failure.
Hypovolemic shock can occur if there is a loss of circulating blood volume, causing a severe drop in cardiac output and blood pressure. Hemorrhage and dehydration can cause hypovolemic shock.
Anaphylactic shock can occur following a widespread allergic response associated with mast cell degranulation and the release of inflammatory mediators, such as histamine and prostaglandin. These inflammatory mediators cause widespread systemic vasodilatation and edema, which cause TPR and blood pressure to fall dramatically.
Septic shock can occur following a massive systemic infection and the subsequent release of vasoactive mediators of inflammation. These substances initiate widespread vasodilation and edema, causing TPR and blood pressure to collapse. Septic shock may occur with a blood-borne bacterial infection or result from the release of gut contents, for example, with gastrointestinal perforation or a burst appendix. Some bacteria seem to be superantigens capable of rapidly stimulating septic shock.
Neurogenic shock occurs following sudden loss of vascular tone throughout the body. Neurogenic shock may result from an injury to the cardiovascular center of the brain, a spinal cord injury, or deep general anesthesia. It may also occur as a result of a burst of parasympathetic stimulation to the heart that slows the heart rate, with a corresponding decrease in sympathetic stimulation to the blood vessels. This type of occurrence may explain sudden fainting during a severe emotional disturbance.
Burn shock occurs following a severe burn involving a substantial amount of total body surface area. Burn shock is an interesting combination of shock due to the systemic release of the vasodilatory mediators of inflammation causing a fall in TPR, and a collapse of the blood volume as plasma leaks across suddenly porous capillary membranes.
Specific manifestations will depend on the cause of shock, but all, except neurogenic shock, will include the following:
Cool, clammy skin.
Increased heart and respiratory rate.
Dramatically decreased blood pressure.
Individuals with neurogenic shock will have a normal or slow heart rate, and will be warm and dry to the touch.
A measured severe decrease in blood pressure.
Decreased or absent urine output.
Tissue hypoxia, cell death, and multi-organ failure following a prolonged decrease in blood flow.
Adult respiratory distress syndrome from hypoxic destruction of the alveolar-capillary interface.
Most patients who die of shock do so because of disseminated intravascular coagulation resulting from extensive tissue hypoxia and subsequent tissue death that leads to massive stimulation of the coagulation cascade.
The cause of shock must be identified and reversed if possible.
Plasma volume replacement is essential, except with cardiogenic shock. What is used for replacement depends on the cause of shock.
Supplemental oxygen or artificial ventilation may be required.
Vasopressor agents are given in order to return blood pressure toward normal.
An allergy is an overstimulation of inflammatory reactions that occurs in response to a specific environmental antigen. An antigen that causes an allergy is called an allergen. Allergic reactions may be antibody mediated or T cell mediated. Type I hypersensitivity reactions are examples of antibody-mediated allergies, whereas Type IV hypersensitivity reactions are examples of T cell mediated allergies.
An individual with a Type I hypersensitivity allergic response has developed sensitized IgE antibodies to an allergen. When the allergen is encountered by the antibody, the antibody is overexpressed, causing excessive mast cell degranulation and release of histamine and other inflammatory mediators (leukotrienes, chemokines, and cytokines). Type IV hypersensitivity reactions occur after transdermal (across the skin) transport of an allergen that is presented to T cells sensitized to that allergen. Manifestations of an allergic response depend on where the allergen is encountered whether in food, in inhaled particles, or through the skin. The timing of an allergic reaction varies depending on if the response is type I (immediate) or type IV (delayed). A type I reaction involving the skin is called atopic dermatitis; a type IV reaction is called allergic contact dermatitis. The skin response to poison ivy is a type of allergic contact dermatitis.
Cause of Allergies
The cause of allergies is unclear, although there appears to be a genetic predisposition. A predisposition may involve excessive IgE binding, easily provoked mast cell degranulation, or excessive helper T cell response. Recent work suggests that a deficiency in T regulatory cells may contribute to over-responsiveness of the immune system and allergy. Overexposure to certain allergens at any time, including during gestation, may cause an allergic response.
Infants and children exposed to cigarette smoke are at greater risk of developing asthma and other respiratory allergies.
Localized swelling, itching, and redness of the skin, with skin exposure to an allergen. Type IV reactions are often characterized by blistering and crusting over of the affected area.
Diarrhea and abdominal cramps, with exposure to a gastrointestinal allergen.
Allergic rhinitis, characterized by itchy eyes and runny nose, with exposure to a respiratory allergen. Swelling and congestion occur. Breathing difficulties may occur because of histamine-mediated constriction of the bronchiolar smooth muscle of the airways.
Skin tests help in diagnosing an allergy. A small amount of the suspected allergen is injected under the skin. Individuals allergic to that allergen will respond with marked erythema, swelling, and itching at the injection site.
Serum immunoglobulin analysis may indicate increased basophil and eosinophil count.
A severe allergic reaction may result in anaphylaxis, which is characterized by a decrease in blood pressure and closure of the airways. Itching, cramping, and diarrhea may occur. Without intervention, severe reactions can lead to cardiovascular shock, hypoxia, and death.
Allergic contact dermatitis (e.g., with a poison ivy reaction) may lead to secondary infection from excessive scratching.
Antihistamines and drugs that block mast cell degranulation may reduce the allergy symptoms.
Corticosteroids, inhaled, administered nasally, or taken systemically, act as anti-inflammatory agents and can reduce the symptoms of an allergy. Inhaled or intranasal therapy needs to be used for extended periods of time before becoming effective. Inhaled corticosteroids exert their effects only on the respiratory passages and may have few systemic effects.
Inhaled mast cell stabilizers reduce mast cell degranulation and may reduce type I allergic symptoms.
Desensitization therapy, involving repeated injections of small amounts of an allergen to which an individual is sensitive, may cause the individual to build IgG antibodies, called blocking antibodies, against the allergen. These blocking antibodies also bind the allergen and by doing so interfere with the ability of the allergen to covalently link multiple IgE molecules together; this prevents mast cell degranulation so allergic symptoms are reduced. IgG antibodies are produced each time the allergen is encountered and eventually may stop the allergic response.