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The term epitope refers to each specific portion of an antigen to which the immune system can respond blood pressure 50 purchase microzide 25mg line. Antigenic epitopes exist on both native "self" tissues as well as foreign "nonself" tissues blood pressure normal heart rate high discount 12.5 mg microzide with mastercard. A complex 3-dimensional protein has multiple antigenic epitopes that may be recognized as well as many other sites that remain "invisible" to the immune system arteria epigastrica cranialis superficialis commissura labiorum dorsalis purchase microzide cheap. The adaptive immune response arrhythmia long term effects order microzide 12.5 mg with visa, unlike the innate immune response discussed in Chapter 1, is a "learned" response to these highly variable but specific antigenic epitopes rather than a response to conserved patterns. The entire purpose of the adaptive immune system is to continuously sample antigenic epitopes, determine if they are self or nonself, and then either avoid mounting or mount, respectively, an immune response so that foreign antigens are eliminated from the system. Several immunologic concepts, especially those of the immune response arc, the primary adaptive immune response, and the secondary adaptive immune response, are involved in this process. Alveolar macrophages ingest the bacteria and transport the organisms to the hilar lymph nodes, where the processing phase begins. Over the next few days, as T and B lymphocytes are primed, the hilar nodes become enlarged because of the increased number of dividing T and B lymphocytes as well as the generalized increased trafficking of other lymphocytes through the nodes. The effector phase begins when the primed T lymphocytes recirculate and enter the infected lung. The T lymphocytes interact with the macrophage-ingested bacteria, and cytokines are released that activate neighboring macrophages to fuse into giant cells, forming caseating granulomas. Meanwhile, some of the effector T lymphocytes home to other lymph nodes throughout the body, where they become inactive memory T lymphocytes, trafficking and recirculating throughout the secondary lymphoid tissue. A secondary response in the skin is the basis of the tuberculin skin test used to diagnose tuberculosis (TB). The afferent phase of the secondary response begins when a purified protein derivative (PPD) reagent (antigens purified from mycobacteria) is injected into the dermis. The secondary processing phase begins when these PPD-stimulated macrophages migrate into the draining lymph node, where they encounter memory T lymphocytes from the previous lung infection, leading to reactivation of memory T lymphocytes. The secondary effector phase commences when these reactivated memory T lymphocytes recirculate and home back into the dermis, where they encounter additional antigen and macrophages at the injection site, causing the T lymphocytes to become fully activated and release cytokines. This process produces the typical indurated dermal lesion of the TB skin test, called the tuberculin form of delayed hypersensitivity (DH). Mycobacterium tuberculosis is difficult for macrophages to digest and process, sometimes resulting in a less robust immune response, explaining the situation of a negative PPD result in the face of active infection. In this testing method, peripheral blood is collected and exposed to tuberculin antigens. If a patient has been exposed to TB, circulating T lymphocytes that are TB antigen specific should be present. As described above, when exposed to TB antigen, these cells release interferon gamma, which can be measured either as the concentration of interferon gamma or as the number of cells releasing interferon gamma. Overview of the Immune Response Arc Analogous to the neural reflex arc, the immune response arc-the interaction between antigen and the adaptive immune system-can be subdivided into 3 phases: afferent, processing, and effector (Fig 21). Phases of the Immune Response Arc Afferent Phase the afferent phase of the immune response arc comprises the initial recognition, transport, and presentation of antigenic substances to the adaptive immune system. Recognition starts with antigenpresenting cells (APCs), which are specialized cells that bind and phagocytize antigen at a site. Phagocytosis occurs following receipt by the APC of stimulatory signals, such as exposure to complement, as discussed in Chapter 1. Following ingestion of antigen, APCs migrate via afferent lymphatics to lymph nodes. Afferent lymphatic channels, usually simply termed lymphatics, are veinlike structures that drain extracellular fluid (ie, lymph) from a site into a regional lymph node. Lymphatics serve 2 major purposes: to convey immune Figure 2-1 Comparison between the neural cells and to carry whole antigen from the site of reflex arc and the immune response arc. Each antigenic fragment is combined with a groove-shaped HLA peptide residing on the APC surface, and this surface complex forms a unique epitope. The combination of peptide and HLA protein is recognized by the T-lymphocyte receptors CD4 and CD8. HLA molecules vary in their capacity to bind various antigenic peptide fragments within their groove, and thus the HLA type determines the repertoire of peptide antigens capable of being presented to T lymphocytes. See Chapter 4 for a more thorough discussion of HLA molecules and disease susceptibility. Major histocompatibility complex (MHC) class I molecules (ie, HLA-A, -B, and -C) serve as the antigen-presenting platform for CD8+ T lymphocytes (Fig 2-2). Class I molecules are present on almost all nucleated cells and generally function in the processing of peptide antigens that have been synthesized by the host cell itself. If these presented antigens are recognized as self (ie, normal host protein), no immune reaction occurs. However, if there is an alteration of the normal host peptide (termed "altered self"), such as would occur with tumor or viral peptides after host cell invasion, an immune response is initiated. This process serves to provide surveillance for cancer or viral infection within the host. One could thus envision how a viral infection, a neoplasm, or simply a genetic mutation that alters protein structure could induce autoimmunity by stimulating an immune response that encompasses host tissue. MHC class II molecules (ie, HLA-DR, -DP, and -DQ) serve as the antigen-presenting platform for CD4+, or helper, T lymphocytes (Fig 2-3).
It is more difficult to assess transmissibility in patients treated with topical corticosteroids heart attack one direction cheap microzide online american express, as they may appear quiet but still shed the virus blood pressure and dehydration order microzide overnight. DNA Viruses: Poxviruses the Poxviridae encompass a large family of enveloped heart attack troublemaker microzide 12.5mg, double-stranded DNA viruses arteria coronaria izquierda 12.5 mg microzide mastercard, with a distinctive brick or ovoid shape and a complex capsid structure. The best-known poxviruses are molluscum contagiosum, vaccinia, and smallpox (variola) virus. Molluscum Contagiosum Molluscum contagiosum virus is spread by direct contact with infected individuals. Infection produces 1 or more umbilicated nodules on the skin and eyelid margin and, less commonly, on the conjunctiva. Any chronic follicular conjunctivitis should instigate a careful search for eyelid margin molluscum lesions (Fig 4-20). Histologic examination of an expressed or excised nodule shows eosinophilic, intracytoplasmic inclusions (Henderson-Patterson bodies) within epidermal cells. Diagnosis is based on detection of the characteristic eyelid lesions in the presence of a follicular conjunctivitis. Treatment options include complete excision, cryotherapy, or incision of the central portion of the lesion. Extensive facial and eyelid molluscum lesions occur in association with AIDS (Fig 4-21). More recently, however, concerns of bioterrorism have prompted the reinstitution of a vaccination program, especially for military personnel. Ocular complications from self-inoculation have resulted, including potentially severe periorbital pustules, conjunctivitis, and keratitis. Use of vaccinia-immune globulin (VIG) is controversial but is indicated for severe disease. Concern about the use of VIG stems from limited rabbit studies that demonstrated a possible increase in corneal scarring. Individuals who are immunosuppressed, atopic, pregnant, breast-feeding, allergic to the vaccine, or living with a high-risk household contact should not receive the vaccine because of the risk of the possibly fatal, progressive vaccinia. Figure 4-21 Multiple molluscum contagiosum lesions on the eyelid of a patient with AIDS. DNA Viruses: Papovaviruses Human papillomaviruses (HPV) are small, nonenveloped, double-stranded DNA viruses with an icosahedral capsid. Persistent viral infection of susceptible epithelial cells induces cellular proliferation and can lead to malignant transformation. Papillomavirus proteins can induce transformation of the cell and loss of senescence. HPV subtypes 6 and 11 are maintained in a latent state within basal epithelial cells as circular episomes with very limited viral gene transcription and low copy number. Early viral gene products stimulate cell growth and lead to a skin wart or a conjunctival papilloma. As HPV-containing basal epithelial cells mature and differentiate into superficial epithelial cells, they become permissive for complete viral gene expression and produce infectious virus. In contrast, HPV 16 and 18 stereotypically integrate their viral genome into host chromosomal DNA, and this in turn is associated with malignant transformation and squamous cell carcinoma. Recently implemented immunization strategies specifically targeted against HPV oncogenes may result in a decreased incidence of these tumors in the future. Verrucae and papillomas are caused by papillomavirus infection of the skin and conjunctival epithelium (Fig 4-22). Venereally acquired conjunctival papillomas resemble those on the larynx and urogenital tract. Papillomavirus-associated conjunctival intraepithelial neoplasia and squamous cell carcinoma share many histologic features with similar lesions in the uterine cervix. Another neoplasm, Kaposi sarcoma of the skin or conjunctiva, is associated with infection by human herpesvirus type 8. RNA Viruses Picornaviruses are negative-sense, single-stranded RNA viruses with an icosahedral capsid and no envelope. Members of the family picornaviridae include the enteroviruses (poliovirus, coxsackievirus, echovirus, and enterovirus) and the rhinoviruses, the single most common etiology of the common cold. Togaviruses with general medical and ophthalmic importance include rubella, Figure 4-22 Conjunctival papillomas. Orthomyxoviruses such as influenza virus are negative-sense, single-stranded RNA viruses with an enveloped helical icosahedral capsid. Structurally similar to the orthomyxoviruses, paramyxoviruses of ocular importance include mumps virus, measles (rubeola) virus, parainfluenza virus, respiratory syncytial virus, and Newcastle disease virus (a cause of follicular conjunctivitis in poultry handlers). The paramyxovirus envelope contains hemagglutinin-neuraminidase protein spikes and a hemolysin, which mediate viral fusion with the host cell membrane. Eye infections due to RNA viruses present to the ophthalmologist less often than those due to DNA viruses, and they most commonly manifest as follicular conjunctivitis associated with an upper respiratory tract infection. However, certain RNA virus infections may cause pathologic changes in virtually any ocular tissue. For example, influenza virus can induce inflammation in the lacrimal gland, cornea, iris, retina, optic nerve, and other cranial nerves. In measles (rubeola) virus (a paramyxovirus) infection, the classic triad of postnatally acquired measles-cough, coryza, and follicular conjunctivitis-can be observed. Less common are optic neuritis, retinal vascular occlusion, and pigmentary retinopathy. Mumps virus (a paramyxovirus) infection may result in dacryoadenitis, sometimes concurrent with parotid gland involvement. Follicular conjunctivitis, epithelial and stromal keratitis, iritis, trabeculitis, and scleritis have all been reported within the first 2 weeks after onset of parotitis.
Large pulse pressure def purchase microzide 12.5 mg otc, yellowish KPs are called mutton-fat KPs and are usually associated with granulomatous types of inflammation blood pressure medication make you feel better buy generic microzide on line. Perilimbal vascular engorgement (ciliary flush) or diffuse injection of the conjunctiva prehypertension spanish cheap generic microzide uk, episclera heart attack upper back pain buy 12.5mg microzide overnight delivery, or both is typical with acute anterior uveitis. Flare may be graded similarly, and the SUN group adopted the method described previously by Hogan and colleagues (Table 5-9). Table 5-8 Figure 5-2 Large "mutton-fat" keratic precipitates in a patient with sarcoidosis. Large keratic precipitates such as these generally indicate a granulomatous disease process. Note the 3 types of iris nodules: A, Koeppe nodules (pupillary border); B, Busacca nodules (midiris); and C, Berlin nodules (iris angle). With uveitic involvement of the ciliary body and trabecular meshwork, intraocular pressure (IOP) is often low, secondary to decreased aqueous production or increased uveoscleral outflow, but IOP may increase precipitously if the meshwork becomes clogged by inflammatory cells or debris or if the trabecular meshwork itself is the site of inflammation (trabeculitis). Intermediate Segment Signs in the intermediate anatomical area of the eye include vitreal inflammatory cells, which are graded in density from 0 to 4+: the SUN group did not achieve consensus regarding a grading system for vitreous cells. The vitreous grading scale shown here was used in the Multicenter Uveitis Steroid Treatment Trial. The consensus is that cells in the vitreous strands are old, and cells in the syneretic areas may be new. The National Institutes of Health (NIH) grading system for vitreous haze, which was adopted by the SUN group, may be a better indicator of disease activity than cell counts alone. With this method, standardized photographs are used for comparison with clinical images to ultimately arrive at the level of vitreous haze. Additional uveitic changes may be observed in the vitreous, namely, snowball opacities, which are common in sarcoidosis or intermediate uveitis exudates over the pars plana (snowbank). As pars planitis becomes inactive, the pars plana appears gliotic or fibrotic and smooth; thus, these changes are not referred to as snowbanks. Posterior Segment Signs in the posterior segment of the eye include retinal or choroidal inflammatory infiltrates inflammatory sheathing of arteries or veins exudative, tractional*, or rhegmatogenous* retinal detachment retinal pigment epithelial hypertrophy or atrophy* atrophy or swelling of the retina, choroid, or optic nerve head* preretinal or subretinal fibrosis* retinal or choroidal neovascularization* An asterisk is used to indicate structural complications. Standardization of vitreal inflammatory activity in intermediate and posterior uveitis. A comprehensive history and review of systems is of paramount importance in helping to elucidate the cause of uveitis. In this regard, a diagnostic survey for uveitis as shown in the appendix can be very helpful. The age, sex, sexual practices, and racial background of the patient are important elements in some uveitic syndromes. Table 5-10 Although ocular inflammation may be an isolated process involving only the eye, it can also be associated with a systemic condition. However, ocular inflammation frequently does not correlate with inflammatory activity elsewhere in the body, so it is important for the clinician to carefully review systems. In some cases, the uveitis may actually precede the development of inflammation at other body sites. Immunocompromise, use of intravenous drugs, hyperalimentation, and certain occupations are just a few risk factors that can direct the investigation. Differential Diagnosis of Uveitic Entities the differential diagnosis of uveitis is broad and includes infectious agents (viruses, bacteria, fungi, protozoa, and helminths), noninfectious entities of presumed immunologic or allergic origin, masquerade syndromes such as endophthalmitis and neoplastic disease, and unknown or idiopathic causes. Intraocular lymphoma, retinoblastoma, leukemia, and malignant melanoma may all be mistaken for uveitis. In addition, juvenile xanthogranuloma, pigment dispersion syndrome, retinal detachment, retinitis pigmentosa, and ocular ischemia syndrome all must be considered in the differential diagnosis of uveitis. Although pattern recognition alone is frequently sufficient to establish a definitive diagnosis, accurate biomicroscopic and funduscopic descriptions of posterior segment inflammatory conditions are extremely helpful in forming the differential diagnosis and in distinguishing individual entities because the distribution and evolution of these findings may be quite characteristic. However, many patients do not present with the classic signs and symptoms of a particular disease. Some patients require ongoing monitoring, as the clinical appearance may be unclear or change with time and treatment. The presentation of a disease can also be modified by previous therapy or by a delay in evaluation by the physician. This naming-meshing system first classifies the type of uveitis based on anatomical criteria and associated factors (eg, acute versus chronic, unilateral versus bilateral) and then matches the pattern of uveitis exhibited by the patient with a list of potential uveitic entities that share similar characteristics. Epidemiology of Uveitis Uveitis is responsible for 10% of all blindness cases in the United States, and the incidence of blindness attributable to uveitis is approximately 15 new cases/100,000 persons per year. Prevalence varies by geographic location, age of study population, academic center, and study date. An epidemiologic study of uveitis in northern California suggests an incidence of 52.
Fuchs adenoma (also called pseudoadenomatous hyperplasia) is usually an incidental finding at autopsy and rarely becomes apparent clinically blood pressure levels chart order microzide 25 mg on line. It appears as a glistening heart attack high bride in a brothel buy 25mg microzide visa, white or tan pulse pressure in athletes cheap 12.5mg microzide overnight delivery, irregular tumor arising from the ciliary crest blood pressure chart daily order microzide once a day. Acquired Hyperplasia Hyperplasia of the pigmented ciliary epithelium or the RPE usually develops in response to trauma, inflammation, or other ocular insults (Fig 17-13A). Because of their location, ciliary body lesions often do not become evident clinically. Occasionally, however, they may reach a large size and simulate a ciliary body melanoma. Posteriorly located lesions may be more commonly recognized and can lead to diagnostic uncertainty. In the early management of these atypical lesions, observation is often appropriate to document stability of the lesion. Simple Hamartoma Simple hamartoma of the RPE is a small (up to 1 mm), sharply demarcated transretinal lesion that is located close to the center of the macula, arising from the RPE (Fig 17-13B). Combined Hamartoma Combined hamartoma of the RPE and retina is a rare disorder that occurs most frequently near the optic nerve head margin, though it may also be observed in the peripheral fundus. Typically, the hamartoma appears as a pigmented, slightly elevated lesion with vitreoretinal traction and tortuous retinal vessels (Fig 17-13C, see a l s o Fig 11-49). Glial cells within this lesion may contract, producing traction lines seen clinically in the retina. Exudative complications associated with the vascular component of the lesion may be seen. These lesions have been mistaken for melanomas because of their pigmentation, slight elevation, and propensity to Figure 17-13 Lesions of the RPE. C, Clinical appearance and D, fluorescein angiogram of a peripapillary combined hamartoma of the retina and RPE. Note obscuration of the retinal vessels in superior aspect of the lesion, moderate deep pigmentation, and secondary change in young individuals. The fluorescein angiogram shows the vascular component of the hamartoma, composed of small capillary-like telangiectatic vessels. Note the relative hypofluorescence superior to the optic nerve head due to the RPE component of this lesion. A circumscribed choroidal hemangioma typically occurs in patients with no systemic disorders. This dome-shaped, often inconspicuous vascular hamartoma is generally located in the postequatorial fundus, often in the macular area (Fig 18-1A, B). It may initially be difficult to distinguish from the surrounding fundus, but eventually degenerative changes occur in the overlying retinal pigment epithelium (RPE). These tumors also cause cystoid degeneration of the overlying outer retinal layers. In some cases, the tumors produce a secondary exudative retinal detachment that often extends into the foveal region, resulting in blurred vision and metamorphopsia. Circumscribed choroidal hemangioma may be difficult to diagnose, because it can resemble other choroidal lesions, including amelanotic choroidal melanoma choroidal osteoma carcinoma metastatic to the choroid granuloma of the choroid Ancillary diagnostic studies are helpful in evaluating both types of choroidal hemangiomas. A-scan ultrasonography shows a high-amplitude initial echo and high-amplitude broad internal echoes (high internal reflectivity; Fig 18-1C). B-scan ultrasonography reveals localized or diffuse choroidal thickening with prominent internal reflections without choroidal excavation or acoustic shadowing. Diffuse choroidal hemangioma is generally seen in patients with Sturge-Weber syndrome (ie, Figure 18-1 Circumscribed choroidal hemangioma. A, Dome-shaped tumor (inferior edge outlined by arrows) resembles the surrounding fundus in color. It may also be fundus photograph in which the eye is associated with congenital ocular melanocytosis (ie, illuminated transclerally from one side shows phakomatosis pigmentovascularis). C, Ascan ultrasonography shows characteristic diffuse reddish-orange coloration of the fundus, resulting high internal reflectivity (arrow). D, Optical i n an ophthalmoscopic pattern referred to as tomato coherence tomography shows a very-lowketchup fundus (Fig 18-2). ILM = internal limiting membrane; RPE = retinal pigment exudative retinal detachment often develop in eyes with epithelium. See also Chapter 12 in this volume, BCSC the arterial phase shows intratumoral vessels. Secti on 1 2, Retina and Vitreous, and Section 6, F, In the late phase of the angiogram, the tumor is hyperfluorescent. Symptomatic circumscribed choroidal hemangiomas were traditionally managed with laser photocoagulation that created chorioretinal adhesions. The primary treatment of choice for symptomatic circumscribed choroidal hemangioma is photodynamic therapy (PDT). PDT for circumscribed choroidal hemangioma is administered using the same standard parameters as Figure 18-2 Diffuse choroidal hemangioma, PDT for exudative age-related macular degeneration. The saturated red color of Most hemangiomas respond to PDT with resolution of the affected fundus (A) contrasts markedly with the subretinal fluid and regression of the lesion, often the color of the unaffected fundus (B) of the same patient.
Injection and telangiectasis of the anterior and posterior eyelid margins blood pressure what do the numbers mean discount microzide 12.5mg overnight delivery, white lashes (poliosis) heart attack jokes order microzide 25 mg amex, lash loss (madarosis) arteria tapada sintomas buy 25 mg microzide mastercard, and trichiasis may be seen in varying degrees heart attack quotes discount 25 mg microzide with visa, depending on the severity and duration of the blepharitis. Staphylococcal blepharoconjunctivitis may present as a chronic (>4-week duration) unilateral or bilateral conjunctivitis. Clinical findings include a papillary reaction of the tarsal conjunctiva, particularly the inferior tarsal conjunctiva near the eyelid margin, as well as injection of the bulbar and tarsal conjunctivae. Specific clinical signs in patients with chronic conjunctivitis may implicate certain bacterial species. Moraxella lacunata may produce a chronic angular blepharoconjunctivitis, with crusting and ulceration of the skin in the lateral canthal angle and papillary or follicular reaction on the tarsal conjunctiva, sometimes with adjacent keratitis. Moraxella angular blepharoconjunctivitis is frequently associated with concomitant S aureus blepharoconjunctivitis. Several forms of keratitis may develop in association with staphylococcal blepharoconjunctivitis. Punctate epithelial keratopathy manifests as erosions that stain with fluorescein; these erosions are often distributed across the inferior cornea, coinciding with the contour of the eyelids across the corneal surface. A diffuse pattern may also be observed, and asymmetric or unilateral keratopathy is not uncommon. The degree of corneal involvement can be markedly disproportionate to the severity of the eyelid disease, a circumstance that can lead to diagnostic confusion. Marginal corneal infiltrates may be the most distinctive clinical finding (Fig 3-18). Phlyctenulosis is a local corneal and/or conjunctival inflammation that is believed to represent a cellmediated, or delayed, hypersensitivity response induced by microbial antigens such as the cell-wall components of staphylococcus. Phlyctenulosis is frequently associated with S aureus in developed countries and is classically associated with Mycobacterium tuberculosis in malnourished children in areas of the world with endemic tuberculosis. Phlyctenules typically present unilaterally at or near the limbus, on the bulbar conjunctiva or cornea, as 1 or more small, rounded, elevated, gray or yellow, Figure 3-18 Staphyloccocal marginal corneal hyperemic, focal inflammatory nodules accompanied by infiltrate. Conjunctival phlyctenules do not lead to scarring, but residual wedge-shaped fibrovascular corneal scars form along the limbus; when such scars are bilateral and inferior, they may suggest previous phlyctenulosis. Corneal involvement is recurrent, and centripetal migration of successive inflammatory lesions may eventually develop, affecting vision if untreated. Occasionally, such inflammation leads to corneal thinning and, in rare cases, perforation. Eyelid and conjunctival cultures can be performed in suspected cases of staphylococcal blepharoconjunctivitis when the initial diagnosis is in doubt, the treatment response is poor, or the infection is worsening. In cases of chronic unilateral conjunctivitis that is refractory to therapy, masquerade syndrome (conjunctival malignancy) and factitious illness should be ruled out. The characteristic laboratory finding in staphylococcal blepharoconjunctivitis is a heavy, confluent growth of S aureus. Susceptibility testing may be useful in guiding treatment in cases that have been refractory to empiric antibiotic therapy. Eyelid hygiene, with either commercially available eyelid scrub kits or warm water with diluted baby shampoo, may help reduce bacterial colonization and the accumulation of Figure 3-19 Confluent phlyctenules secondary to staphylococcal blepharitis. With these treatments, patients should focus their attention on the base of the lashes, where colonization and seborrhea are the greatest. Topical bacitracin, erythromycin, and azithromycin may be applied to the eyelid margin to reduce both the bacterial load and inflammation. Concomitant ATD and/or lipid-induced tear-film instability may also occur and should be treated to improve comfort. Cases with prominent infectious conjunctivitis should be treated with an antibiotic solution. Since treatment of staphylococcal blepharitis is likely to be prolonged and repeated, special attention to minimizing drug toxicity and resistance is necessary. A well-tolerated, narrow-spectrum antimicrobial agent effective against the majority of staphylococci should be selected, used at therapeutic doses, and discontinued as soon as feasible. Anti-inflammatory therapy consists of limited and judicious use of mild doses of topical corticosteroids in selected cases. Patients with routine staphylococcal blepharitis or blepharoconjunctivitis obtain more rapid symptomatic relief with the use of adjunct topical corticosteroids, but their use should be weighed against the risk of side effects and, less likely, further proliferation of the pathogen. Although corticosteroids provide little therapeutic benefit for toxic-related punctate epithelial keratopathy, marginal infiltrates and phlyctenulosis have a strong immunologic component and thus respond promptly to topical corticosteroid therapy. In the case of phlyctenulosis, corticosteroids are usually necessary early in the course of treatment. Eyelid hygiene and antibiotic therapy alone may be sufficient in cases of marginal infiltrates, but corticosteroids may be introduced earlier if the diagnosis is certain. If epithelial defects are noted over the infiltrates, diagnostic cultures should be considered before corticosteroid treatment is begun. Those occurring on the anterior eyelid in the glands of Zeis or lash follicles are called external hordeola, or styes. Hordeola occurring on the posterior eyelid from meibomian gland inspissation are termed internal hordeola. Both types are associated with a localized purulent abscess, usually caused by S aureus. The l e s i on disappears in weeks to months, when the sebaceous contents drain either externally through the eyelid skin or internally through the tarsus or when the extruded lipid is phagocytosed and the granuloma dissipates. Occasionally, patients with a chalazion experience blurred vision secondary to astigmatism induced by its pressure on the globe. It should be noted that basal cell, squamous cell, and sebaceous cell carcinoma can masquerade as chalazia or chronic blepharitis.
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