Pathology Terms

8/14/2019 Pathology Terms

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Key Terms

Chapter 19: Coagulation Disorders

Activated partial thromboplastin time (APTT)Laboratory measurement of the intrinsic and common coagulation pathways.

The normal range is 26 to 42 seconds. Prolonged in hemophilia A and B. Used

to guide heparin therapy.

Antithrombin III

A circulating anticoagulant that functions to inactivate thrombin.

Arterial spiders

Bright-red lesions with a pulsatile center and threadlike extensions radiating 5

to 10 mm in length.

Bleeding time

Laboratory procedure that tests both vascular status and platelet number and

function, but does not differentiate between the two. A controlled punctureincision is made in the free-hanging earlobe (Duke method) or on the volar

surface of the forearm (Ivy method). The length of time for bleeding to cease

is recorded. Normal bleeding time is 3 to 7 minutes.

Clotting factors

Plasma proteins that circulate in the blood (except III and IV) as inactive

molecules and complete the clotting process when activated to form a stable

fibrin clot (secondary hemostasis). All are designated by a Roman numeral

from I to XIII (there is no number VI).

Components of the blood coagulation system

(1) Blood vessels (contain the blood and constrict following injury to allow

formation of the platelet plug); (2) platelets (adhere to the exposed collagenand form a temporary platelet plug [primary hemostasis]); and (3) the 12

clotting factors (complete the clotting process when activated to form a stable

fibrin clot [secondary hemostasis]).

Contact factors

Factors including prekallikrein, high molecular weight kininogen (HMWK),

and factors XII and XI; activated at the time of injury by contact with tissue

surfaces; they also play a role in the dissolution of clots once they are formed.

Disseminated intravascular coagulation (DIC or consumption coagulopathy)

A complex syndrome characterized by diffuse thrombosis and occlusion of the

microvasculature with an accompanying fibrinolysis. Patients with DIC clot

and bleed simultaneously, and unless the underlying cause is removed, they

continue to do so and may die. DIC is initiated by the release of tissue

thromboplastin (tissue Factor III) secondary to tissue destruction (e.g.,

abruptio placentae, malignancies, chemotherapy, hemolytic transfusion

reaction, burns, crushing injury) with an initiation of the extrinsic coagulation

pathway. DIC can also be initiated by the intrinsic coagulation pathway, as in

sepsis and shock. Diagnostic tests reveal prolonged PT, PTT, TT, and fibrin

split products (FSP).

Ecchymosis (bruise)

An area of extravasated blood in the subcutaneous tissues and skin due to

injury.Extrinsic coagulation pathway


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Initiated by release of tissue thromboplastin (tissue factor III) from outside the

blood vascular system, which in turn activates factor VII in the extrinsic path

and then factors in the common pathway (X, V, II, I, XIII), resulting in the

formation of a stable fibrin clot.

Factor VIII

A complex clotting factor with 3 distinct subunits: (1) the antihemophiliacfactor (VIIIAHF), deficient in classic hemophilia A; (2) the von Willebrand

factor (VIIIVWF), deficient in von Willebrand's disease; and (3) a subunit

containing an antigenic site.

Factor XII (Hageman factor)

Plays a central role in linking three systems: (1) initiation of the intrinsic

coagulation system; (2) acceleration of the activation of plasminogen to

plasmin in the fibrinolytic system; and (3) change of kallikreinogen to

kallikrein in the inflammatory system. This role ensures a balance between

clot formation and digestion and ensures that clotting factors are localized at

the site of inflammation or bleeding and not disseminated throughout the body.

Fibrinolytic systemA countermechanism to blood clotting, activated to dissolve the fibrin clot and

restore blood vessel patency. The anticoagulant plasminogen circulates in the

blood in the inactive form. Three major activators of the fibrinolytic system

changing plasminogen to plasmin are: (1) tissue plasminogen activator (tPA),

released from the endothelial cells in the presence of thrombin and fibrin; (2)

urokinase, released from renal cells; and (3) streptokinase, released from

streptococci if infection is present. Within the clot, plasmin (a proteolytic

enzyme) digests fibrin, producing fibrin degradation (split) products (FSP or

FDP) and also breaks down fibrinogen in the plasma. Plasminogen activator

inhibitor (PAI-1) and alpha-macroglobulin inhibit tPA and limit plasmin

activity to the level of the platelet plug. The Hageman factor (XII) accelerates

activation of plasminogen to plasmin.

Fibrin split (or degradation) products (FSP or FDP)

Products of fibrin or fibrinogen degradation; elevated in DIC.

Hemarthrosis

Bleeding into a joint; suggests a factor VIII or IX deficiency.

Hematoma

A swelling or mass of blood confined to a space and caused by a break in a

blood vessel.

Hemophilia A (classic)

An X-linked recessive disorder resulting in deficiency of anti-hemophilicfactor VIII activity. Patients suffer joint and muscle hemorrhages and easy

bruising. Patients have normal bleeding times (primary hemostasis is intact),

normal prothrombin times (the extrinsic pathway clotting factors are normal),

and prolonged partial thromboplastin time (because factor VIII is an intrinsic

pathway clotting factor).

Hemophilia B (Christmas disease)

An X-linked recessive disorder caused by a deficiency of factor IX activity.

Less common than hemophilia A and usually less severe.

Heparin

An anticoagulant that prevents conversion of prothrombin to thrombin and

fibrinogen to fibrin by enhancing the inhibitory effects of antithrombin III.


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Used for the acute treatment of deep venous thrombosis (DVT) or pulmonary

embolism (PE) to keep the PTT 1.5 to 2.5 times the control value.

International normalized ratio (INR)

A method of standardizing the measurement of clotting activity, because the

measurement of the PT may vary from laboratory to laboratory; reduces the

risk of underdosing or overdosing patients on Coumadin therapy because ofthe changing sensitivity of tissue thromboplastins (used in the PT

measurement) from one laboratory to another. Normal INR: 1.0 to 2.0;

anticoagulated patients: 2.0 to 3.0; patients with mechanical heart valves or

those who continue to have clotting problems: 2.5 to 3.5.

Intrinsic coagulation pathway

Includes factors XII, XI, IX, and VIII. The Hageman factor (XII) initiates the

intrinsic coagulation pathway from inside the blood vessel when it comes in

contact with subendothelial exposed collagen when the blood vessel is

damaged. High molecular weight kininogen (HMWK) acts as a cofactor in the

conversion of prekallikrein to kallikrein, which in turn augments the

conversion of factor XII to XIIa. Once activated, XIIa in turn activates otherfactors in the intrinsic (XI, IX, VIII) and common pathway (X, V, II, I, XIII),

with the result that a stable fibrin clot is formed. Compared to the extrinsic

system, the intrinsic coagulation system is more sensitive, efficient, and

powerful, because it can generate large amounts of fibrin using the principle of

amplification. The intrinsic system is so powerful that there is enough clotting

potential in 1 ml of blood to clot all the fibrinogen in the body in 10 to 15

seconds if it were not carefully coupled to the fibrinolytic system.

Liver

Site of the synthesis of all the clotting factors except factor VIII and possibly

XI and XIII.

Partial thromboplastin time (PTT)

Screening test that measures the intrinsic and common pathway. Normal is 26

to 42 seconds. Prolonged in heparin therapy, hemophilia, DIC, vitamin K

deficiency, and liver disease. Used to guide dosage in heparin therapy to

decrease the risk of clotting, yet not cause hemorrhage.

Petechiae

Pinpoint hemorrhages (< 0.5 cm) into the dermis characteristic of platelet

disorders, especially thrombocytopenia.

Platelets (thrombocytes)

Nonnucleated cell fragments (1-4 (m in diameter) from megakaryocytes,

which stain light blue with red-purple granules. Platelets have a lifespan of 9to 10 days; 80% circulate in the blood and 20% are sequestered in the spleen.

Platelets play a vital role in primary hemostasis (temporary platelet plug),

secondary hemostasis (formation of the stable fibrin clot), and in clot

retraction; thus in thrombocytopenia all these functions are abnormal. The

normal serum platelet count is 150,000 to 400,000/mm.

Protein C

A circulating plasma anticoagulant that functions to inactivate factors Va and

VIIIa. It is synthesized by the liver and is vitamin K-dependent. Protein S

enhances the anticoagulant activity of protein C.

Prothrombin time (PT)

Screening test that measures the extrinsic and common pathway. Normal is 10to 14 seconds. Prolonged in Coumadin therapy, liver disease, vitamin K


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hepatic synthesis of vitamin K-dependent coagulation factors (II, VII, IX, X).

The prothrombin time (PT) is used to adjust medication dosage to keep the

coagulation time 1.5 to 2 times the normal value. Recently the international

normalized ratio (INR) is used more frequently in place of the PT since it does

not vary from one laboratory to another.

Chapter 15: Human Immunodeficiency Virus (HIV) and Acquired

Immunodeficiency Syndrome (AIDS)

Acquired immunodeficiency syndrome (AIDS)

The late stage of HIV disease. AIDS involves the loss of function of the

immune system as CD4+ (T helper) cells are infected and destroyed, allowing

the body to succumb to opportunistic infections (Pneumocystis carinii

pneumonia, toxoplasmosis) that are generally not pathogenic in persons with

intact immune systems. The CDC defines AIDS as the presence of at least one

of several opportunistic infections or the presence of fewer than 200 CD4+

cells/mm3 in an HIV positive individual.

Acute HIV infection phase

An acute HIV syndrome experienced by more than half of patients 3 to 6

weeks after initial HIV infection, consisting of flu-like symptoms (fever,

headache, sore throat, rash). These symptoms result from a cellular immune

response that takes place before the immune system has had time to produce

antibodies. During this phase antibody status changes from seronegative toseropositive.

AIDS dementia complex

Deterioration of intellectual faculties, emotional disturbance, and

neuromuscular control as a result of HIV activity in the central nervous

system. AIDS-related dementia typically affects people in the latter stages of

the disease. Symptoms may include cognitive impairment (e.g., difficulty

concentrating, memory loss), mood and personality changes, speech and

vision difficulties, psychomotor dysfunction (e.g., lack of coordination,

incontinence), and paralysis.

Anergy

The lack of an immune response to a foreign antigen. Anergy may indicate aninability to mount a normal allergic or immune reaction, and may be a sign of

immunodeficiency. Patients with AIDS have cellular-mediated

immunodeficiency, which may be demonstrated with delayed-type

hypersensitivity skin tests (see Chapter 14).

Antibody-dependent complement-mediated cytotoxicity (ADCC)

An immune response in which antibodies bind to target cells and identify them

for attack by natural killer (NK) cells and macrophages-a mechanism of

removing HIV-infected CD4+ lymphocytes.

Apoptosis

A form of programmed cell death that is a normal mechanism for the

elimination of effete cells in fetal organogenesis as well as in the cellularproliferation that occurs during a normal immune response. Apoptosis is


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strictly dependent on cellular activation. It has been postulated that in HIV

infection, sequential signals delivered to CD4+ T cells induce apoptosis.

Asymptomatic phase

A period of clinical latency, which may last for several years in a relatively

intact immune system; however, continuous HIV replication occurs,

predominately in the lymphoid tissues.Candidiasis

A fungus infection, caused by a member of the genus Candida, especially in

immunocompromised individuals. In the mouth, candidiasis is called thrushand shows up as white patches; in the vagina, it is called vulvovaginal

candidiasis. Candidiasis can also attack the esophagus and lungs. Candidiasis

is considered an AIDS-defining condition in the United States.

Cervical dysplasia

Abnormal growth of cells in the cervix that can lead to cervical cancer;

associated with human papillomavirus. Cervical dysplasia is present in 40% of

HIV-infected women, who should receive a Papanicolaou smear and

colposcopic examination every 6 months for early detection of cervical cancer.Cluster of differentiation (CD)

A marker protein embedded in the surface of cell membranes or interior of

cells. CD molecules determine which other molecules can bind to a given cell

(e.g., the CD4+ marker allows HIV to invade certain types of cells). The T

helper cell has a CD4 marker on its surface, whereas the cytotoxic T cell has a

CD8 marker.

Colposcopy

Examination of the cervix with a lighted microscope (colposcope) to identify

abnormal cell growth and, if necessary, remove a tissue sample for biopsy.

Coreceptors

Different strains of HIV use two major coreceptors (CCR5 and CXCR4) along

with CD4 to bind to, fuse with, and enter target cells. Individuals who inherit

two defective copies of these coreceptors (homozygous) are resistant to the

development of HIV infection despite repeated exposure to the HIV virus

(about 1% of white Americans). Heterozygotes (one defective copy) for the

CCR5 or CXCR4 coreceptors (about 18% of white Americans) are not

protected from AIDS but may have a delayed onset.

Enzyme-linked immunosorbent assay (ELISA)

Generally the first screening test to detect HIV antibodies. If the test is

positive, the test is repeated, and when both tests are positive, a more specific

test, the Western Blot, is performed to confirm the diagnosis of HIV infection.False negative

A negative test for a person who does in fact have the disease or condition

being tested for. For example, an HIV-infected individual would have a

negative ELISA or Western Blot test during the window period (antibodies to

HIV generally appear in the circulation 2 to 12 weeks after infection but can

take up to 1 year).

False positive

A positive test result for a person who does not in fact have the disease or

condition being tested for. For example, an HIV antibody test (ELISA) on the

newborn of a HIV-positive mother would test positive (because maternal HIV

antibodies cross the placenta) when in fact the infant is not infected. Another


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test, such as the p24 antigen capture assay or RNA PCR test, should be used to

determine if the infant is infected.

Gag

The gene of the HIV that encodes the core proteins of the virus.

Highly active antiretroviral therapy (HAART)

A term for aggressive anti-HIV treatment, usually with two or more antiviralagents, such as protease inhibitors, nucleoside transcriptase inhibitors, and

nonnucleoside transcriptase inhibitors. HAART therapy has greatly reduced

mortality from AIDS in industrialized countries that have access to these

drugs.

HIV integrase

A viral enzyme that aids in the insertion of the viral cDNA into the host

nucleus.

HIV protease

A viral enzyme that cuts and assembles the virus protein into small segments

that surround the viral RNA, forming the infectious virus particles that bud

from the infected cell, thus essential to the HIV replication process.HIV RNA PCR

A test to determine the blood serum viral load in HIV-infected patients, using

polymerase chain reaction (PCR) as a technique. PCR amplifies cDNA

generated from HIV viral RNA (see Polymerase Chain Reaction, below).

Periodic assessment of the viral load is used to guide antiretroviral therapy and

for prognostic purposes, whereas monitoring the CD4+ T cell count is used to

assess the immune status. An HIV RNA count of 20,000 copies/ml is

considered by most experts as an indication to begin antiretroviral drug

therapy regardless of the CD4+ T cell count.

Invasive cervical cancer

A gynecologic malignancy associated with long-standing HIV disease,

included in the case definition since 1993.

Mycobacterium avium complex (MAC)

A disease caused by Mycobacterium avium orMycobacterium intracellulare(sometimes referred to as Mycobacterium avium-intracellulare or MAI),

bacteria found in soil and water. In immunosuppressed persons, the bacteria

can infect the lymph nodes, GI tract, liver, spleen, spinal fluid, and lungs.

MAC is the most common bacterial infection in persons with advanced AIDS

(usually with CD4+ T cell counts of < 50-75 cells/mm3). Symptoms include

diarrhea, wasting, fever, night sweats, fatigue, and splenomegaly. Rifabutin is

used as treatment and prophylaxis for MAC. MAC is considered an AIDS-defining condition in the United States.

P24 antigen capture assay

A test to detect the HIV p24 viral core protein in the blood of HIV-infected

persons where it exists either as a free antigen or complexed to anti-p24

antibodies.

Persistent glandular lymphadenopathy (PGL)

A condition in which the lymph nodes are persistently swollen in one or more

parts of the body; occurs during the early symptomatic phase of HIV infection.

Pneumocystis carinii pneumonia (PCP)The most frequently diagnosed serious infection in patients with AIDS caused

by a protozoan. PCP is a common infection that can cause severe illness inimmunocompromised people (especially with CD4+ T cell counts less than


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200 cells/mm); it is a leading cause of death in persons with AIDS. Symptoms

include dry cough, fever, chest tightness, and dyspnea. First-line treatment and

prophylaxis is TMP-SMX (Bactrim, Septra); other drug treatment options

include pentamidine or dapsone. PCP is an AIDS-defining condition in the

United States.

Polymerase chain reaction (PCR)A highly sensitive test that can detect small amounts of RNA or DNA in blood

or tissue samples using an amplification technique that multiplies the existing

RNA or DNA so that it can be detected more readily.

Progressive multifocal leukoencephalopathy (PML)

A rapidly progressing viral infection of the brain believed to be caused by the

papovavirus. Symptoms include memory loss, loss of strength, coma, and

death. PML is considered an AIDS-defining condition in the United States.

Protease inhibitor

A class of anti-HIV drug that prevents creation of an HIV-specific protease.

Retroviruses

Viruses that use ribonucleic acid (RNA) rather than deoxyribonucleic acid(DNA) as their genetic material. HIV are retroviruses and use reverse

transcriptase to convert their genome RNA into double-stranded proviral DNA

after they enter the host cell.

Reverse transcriptase

The enzyme, located in the HIV virion, that transcribes viral RNA into DNA

after the virus enters the target cell. It is essential to HIV replication in the

invaded target cell.

Symptomatic phase of HIV infection

The stage in which CD4+ cell counts have usually dropped below 300 cells/L.

Symptoms indicating immunosuppression are present and continue until the

person develops an AIDS-related condition-opportunistic infections,

secondary neoplasms, and neurologic manifestations.

Toxoplasmosis

An opportunistic infection caused by Toxoplasma gondii, a protozoan found in

undercooked meat and cat feces. A frequent manifestation of the disease is

toxoplasmic encephalitis, characterized by cerebral edema, dementia, lethargy,

seizures, and coma. Symptoms may include fever, severe headache and

lymphadenopathy. Toxoplasmosis is considered an AIDS-defining condition in

the United States.

Western blot test

Most common confirmatory test (detects anti-HIV antibodies) for HIVinfection; less likely to give a false-positive or false-negative reading than

ELISA.


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hapter 10: Bronchial Asthma: Allergic and Otherwise

Acute phase asthmatic response

In allergic asthma, this response begins within minutes of exposure to an

inhaled antigen and resolves in approximately 1 hour. Consists of

bronchoconstriction due to increased responsiveness of bronchial smoothmuscle; hypersecretion of mucus leading to plugging of airways; and mucosal

edema (owing to increased vascular permeability that leads to narrowing of

airways. Mast cells in the bronchial epithelium also release leukotrienes and

cytokines that cause the influx of leukocytes, neutrophils and monocytes, and

especially eosinophils.

Allergic (extrinsic; atopic) asthma

Initiated by a type I hypersensitivity reaction induced by exposure to an

extrinsic antigen, such as house dust mite, animal danders, feathers, pollens,

molds, foods, food preservatives (sulfiting agents added to fruit and salads in

restaurants).

Asthma

Clinically defined condition marked by recurrent episodes of reversible

bronchial narrowing, often separated by periods of more normal ventilation.

Classic triad of signs and symptoms in an acute asthmatic attack

Dyspnea, cough, and prolonged wheezing respirations (at first more prominent

during expiration but later evident both during expiration and inspiration).

Common denominator underlying predisposition to asthmatic attacks

Nonspecific hyperreactivity of the tracheobronchial tree. Asthmatic airways

behave as if their beta-adrenergic receptors (which help preserve airway

patency) are incompetent; bronchoconstrictor influences mediated by

parasympathetic and alpha-adrenergic pathways are therefore predominant.Dyspnea

Abnormal shortness of breath.

Exercise-induced asthma (EIA)

Asthmatic attack triggered by exercise, especially sprint running.

FEV1.0The maximum amount of air that can be exhaled as forcefully and as rapidly

as possible during the first second after a maximum inspiration (normally,

83%). FEV1.0 is reduced in obstructive disorders, such as asthma. FEV1.0 is

used to assess the severity and progression of the asthmatic episode and also to

periodically assess the patient's response to treatment.

Idiopathic (intrinsic) asthmaInitiated by diverse nonimmunologic mechanisms, including ingestion of

aspirin; respiratory infections; air pollutants (e.g., cigarette smoke, perfumes,

aerosol sprays); inhalation of dry, cold air; and exercise.

Late phase asthmatic response

Begins several hours after exposure to an inhaled antigen but lasts much

longer than the acute response; characterized by inflammation and

inflammatory cells (PMNs, eosinophils, basophils), which can cause epithelial

damage and airway constriction.

Leukotrienes

Extremely potent mediators that cause prolonged bronchoconstriction as well

as increased vascular permeability and increased mucus production (formerlycalled slow reactive substance of anaphylaxis (SRS-A).


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Status asthmaticus

Severe asthma that has persisted for at least 24 hours and is not substantially

managed by optimal doses of epinephrine and theophylline; may result in

death from acute respiratory insufficiency.

Chapter 9: Familiar (IgE-Mediated) Allergic Disorders: Anaphylaxis

and the Atopic Diseases

Allergen

A substance (antigen) that can produce an allergic reaction in the body of

sensitive individuals but is harmless to most people; for example, plant

pollens, excreta of house dust mites, animal dander, feathers, certain foods.

Allergic rhinitis

A condition characterized by sneezing; rhinorrhea (runny nose); obstruction of

the nasal passages; conjunctival and nasal itching; and lacrimation, all

occurring in a temporal relationship to allergen exposure. It can be seasonal

(hay fever) and commonly related to exposure to airborne plant pollens or

perennial in an environment of chronic exposure (e.g., a research technician

who handles animals every day and is exposed to animal danders to which he

or she becomes sensitized).

Allergy

The capacity to react in an abnormal way to a specific substance acquired

through prior contact with that substance. Three important aspects of allergy

are (1) it is specific (reaction only to a specific antigen); (2) it is acquired

rather than inherent; and (3) prior contact with the specific antigen isnecessary to become sensitized (develop memory B or T lymphocytes).

Anaphylactic kit

Kit containing a tourniquet and preloaded syringes of epinephrine, and

antihistamines for emergency self-treatment by individuals who are

hypersensitive to insect venom and are at high risk of systemic anaphylaxis.

Anaphylaxis

An acute systemic hypersensitivity reaction to an antigen (usually injected) to

which there has been prior sensitization, such as insect venom or penicillin.

Type I hypersensitivity reaction is mediated by IgE attached to basophils and

mast cells in smooth muscles of bronchioles and in connective tissue around

blood vessels, resulting in the release of histamine and other vasoactivesubstances. Onset of symptoms is immediate (within minutes) after injection

of the antigen and can be fatal. Manifested by respiratory distress

(bronchospasm, laryngeal edema occluding airways) followed by vascular

collapse or hypotensive shock. Cutaneous manifestations include intense

itching and hives with or without angioedema. GI manifestations include

nausea, vomiting, abdominal cramps, and diarrhea. Emergency treatment

includes removing the offending substance (tourniquet proximal to injection

site); establishing a patent airway (intubate if needed); administration of 0.3

ml 1:1000 epinephrine subcutaneously or IV; and support blood pressure by

restoring plasma volume with IV normal saline.

Angioedema


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A well-demarcated, localized edema involving the deeper layers of the skin

and subcutaneous tissue.

Animal dander

An allergen source from animals, including hair, epidermal scales, feathers,

fur, silk, wool, saliva, lacrimal secretions, and even urine.

AntihistaminesDrugs commonly used for the symptomatic relief of allergies; mechanism of

action involves competition with histamine for tissue receptors (unlike

cromolyn sodium, antihistamines do not block the release of histamine from

mast cells).

Atopic diseases

Term used to describe a group of hypersensitivity (allergic) diseases in which

hereditary factors are known to be involved; it is the predisposition that isinherited and not sensitivity a particular allergen. About 75% of atopicindividuals have elevated IgE levels. Atopic diseases include: (1) allergic

seasonal and perennial rhinitis; (2) allergic (extrinsic) asthma; (3) atopic

(eczematous) dermatitis; 4) urticaria (hives); and (5) angioedema.Dermatographism

The appearance of a linear wheal at the site of a brisk stroke with a firm

object; a type of physical urticaria.

Eosinophil chemotactic factor of anaphylaxis (ECF-A)

Chemical mediator that attracts eosinophils to an area of inflammation in type

I hypersensitivity (allergic) reactions.

Epinephrine

Drug of choice for the emergency treatment of anaphylaxis.

Hay fever

Seasonal rhinitis, commonly associated with exposure to airborne allergens

such as tree pollen, grasses, fungi, or ragweed pollen.

IgE

Immunoglobulin (antibody) involved in most type I allergic reactions. IgE is a

cytophilic molecule whose Fc fragment (stem of the Y) is affixed to mast cells

and basophils (IgE levels in the blood serum are low). When an allergen

combines with the Fab site (tail fins of the Y) of IgE, IgE causes histamine and

other vasoactive chemicals to be released from the mast cell or basophil,

resulting in an inflammatory response.

Immunotherapy (hyposensitization)

Procedure involving subcutaneous injections of gradually increasing

concentrations of extracts of a clearly known and documented allergen towhich the patient is sensitive over prolonged periods. The goal is to relieve the

symptoms to the specific allergen. The probable mechanism of

hyposensitization is an increase in IgG which serves as a blocking antibody for

IgE by competing with IgE for the allergen at mucosal surfaces; mast cells

release less and less histamine as the patient is desensitized. The nurse or

physician administering the treatment must keep an emergency dose of

epinephrine on hand in the event of an anaphylactic reaction (this treatment

could result in sensitizing rather than desensitizing the patient to the allergen).

Laryngeal edema

In a systemic anaphylactic reaction, edema of the vocal cords and epiglottis in

mild cases may be experienced as a "lump in the throat", hoarseness, or stridoror may be severe enough to cause complete mechanical obstruction of the


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airways, terminating in death. The edema is caused by the release of histamine

and other vasoactive mediators from mast cells in the respiratory tract,

resulting in increased permeability of blood vessels and exudation of fluid into

the soft tissues of the upper airways.

Mast cells

Effector cells in type I hypersensitivity reactions; found throughout the bodyin loose connective tissue. Mast cells are covered with IgE receptors on their

cell surface and filled with vesicles or granules containing chemical mediators,

such as histamine, that produce inflammation when released; basophils in the

blood have similar chemical mediators.

Nasal polyps

Edematous mucosal protrusions with variable degrees of infiltration by

eosinophils commonly found in patients with perennial rhinitis; may cause

obstruction of breathing through the nose.

Pruritus

Itching.

Rhinitis medicamentosaA complication of improper self-medication (overuse) with sympathomimetic

amines (e.g., Neo-Synephrine nose drops) resulting in rebound congestion of

the nasal mucosa. Treatment involves withdrawal of the medication and

substitution of a topical corticosteroid nasal spray for a few weeks.

Rhinorrhea

Watery discharge from the nose; excessive nasal secretion.

Skin testing (for allergies)

Two types of skin testing are used to test for potential allergens: (1) the

epidermal (prick) test, which uses highly diluted allergen in a solvent and may

be read in 15 minutes; and 2) the intracutaneous injection (0.02 ml) of the

diluted allergen. A control site with the solvent only is also tested. Epinephrine

must be kept on hand to use in case of an acute systemic anaphylactic reaction.

Contrary to popular belief, a positive wheal and flare reaction provides no

insurance that the patient's symptoms arise from exposure to the allergen inquestion. Individuals with atopy commonly react to numerous allergens usedin skin testing but may not react to the same allergen when encountered in the

environment. The value of allergen skin tests is to support or oppose

impressions formed during clinical assessment.

Type I immune disorders (anaphylactic, immediate hypersensitivity)

Disorders that are usually mediated by IgE of the humoral immune system.

Urticaria (hives)Well circumscribed wheals with erythematous borders and pale centers

involving the superficial skin; distinctly pruritic but usually self-limited,

lasting for 36 hours or less.

Chapter 8: Disturbances in Growth, Cellular Proliferation, and

Differentiation

Adenocarcinoma

A malignant neoplasm arising from the parenchyma of a gland.Adenoma


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normal columnar epithelium in the respiratory tract to squamous epithelium in

a chronic cigarette smoker.

Metastasis (pl., metastases)

A secondary malignant growth that originates from a primary tumor and is

distant from the primary site. Cancer spread takes place through three routes:

lymphatic system (most common); blood circulatory system; and seeding ofbody cavities and surfaces. A fourth potential route of spread is by direct

implantation on surgical gloves or instruments used during surgery or biopsy.

Neoplasm (tumor)

An abnormal mass of proliferating cells.

Oncogenes

Cancer-causing genes derived from protooncogenes. Protooncogenes can be

transformed into oncogenes by four basic mechanisms: a point mutation, gene

amplification, chromosomal rearrangement, or insertion of a viral genome.

Oncogenes produce abnormal oncoproteins that fail to regulate the cell

replication cycle, resulting in excessive cell multiplication.

OsteomaA benign neoplasm of bone.

Osteosarcoma

A malignant neoplasm arising from bone.

Papanicolaou smear (exfoliative cytology)

A cytologic test for malignant changes, mainly in the female genital tract

(cervix, endometrium, vagina).

Papilloma

A growth projecting into the lumen of an organ in fingerlike projections.

Point mutation

A mechanism that involves a single base substitution in the DNA chain

resulting in a miscoded protein that has one amino acid substituted for another.

Poorly differentiated

A situation in which the resemblance of neoplastic cells to comparable normal

cells is slight, such that the tumor consists largely of primitive-appearing,

unspecialized proliferating cells.

Protooncogenes

Cellular genes whose function is to promote the normal growth and

differentiation of cells; they code for proteins involved in the regulation of the

cell cycle.

Sarcoma

A malignant neoplasm derived from supporting tissue.Scirrhous tumor

A type of tumor that contains an extremely dense fibrous stroma.

Stroma

Supporting framework.

Telomerase

An enzyme that repairs telomeres and may be the key to immortality.

Embryonic stem cells and germ cells secrete telomerase, explaining their

extensive ability to replicate, but somatic cells do not (explaining their finite

lifespan). Cancer cells also secrete telomerase, which may be the key to their

ability to divide indefinitely.

Telomeres


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The end caps on chromosomes, essential for chromosomal stability during cell

replication. Telomeres shorten with each somatic cell replication until a critical

length is reached and the cell is no longer able to replicate. Telomere

shortening is believed to be the basis of aging (acts like a molecular clock

keeping track of our lifespan).

TNM staging systemA method of staging a malignant tumor as an indication of how far it has

spread. T refers to the size of the primary tumor and the number denotes its

local extent and varies according to site; N refers to lymph node involvement,

and a high number indicates an increasing extent of involvement; and M refers

to the extent of distant metastases. The TNM system can be applied to many

different types of tumor, although the criteria are different for each tumor site

(e.g., the TNM criteria would be different for prostate and breast carcinoma).

Tumor suppressor genes

Genes that inhibit or "put the brakes on" the cell replication cycle in contrast

to protooncogenes that encode proteins that promote cell growth. Mutation of

tumor suppressor genes has the effect of removing the brakes in the regulationof the cell cycle resulting in a higher rate of uncontrolled growth-cancer.

Most malignancies involve mutations in tumor suppressor genes and

oncogenes.

Well-differentiated

A condition in which the resemblance of neoplastic cells to their normal

ancestors is close.

Pathology Terms

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