Exam 3 pages 54 - 84.pdf

7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/3/2023 Trichomoniasis Trichomoniasis is credited with being a far more prevalen...

7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/3/2023 Trichomoniasis Trichomoniasis is credited with being a far more prevalent STI than gonorrhea infection, and almost as common as chlamydia.13–15 In the United States, it has been estimated that 7.4 million new cases of trichomoniasis appear annually.14 Epidemiologically, Trichomonas vaginalis infections are commonly associated with other STIs and are therefore a marker for high-risk sexual behavior. An anaerobic protozoan that can be transmitted sexually, T. vaginalis, is shaped like a turnip and has three or four anterior flagella (see Fig. 46.5). Trichomonads can reside in the paraurethral glands of both sexes. Figure 46.5 Trichomoniasis— Women will have vaginal pruritus, thin or thick secretions, a foul vaginal odor, and possibly dysuria. (From Jensen S. (2015). Nursing health assessment: A best practice approach (2nd ed., p. 771, Table 24.3). Philadelphia, PA: Lippincott Williams & Wilkins.) Clinical Manifestations and Complications Men harbor the organism in the urethra and prostate and are asymptomatic. Although 10% to 25% of women are asymptomatic, trichomoniasis is a common cause of vaginitis when some imbalance allows the protozoan to proliferate.15 This extracellular parasite feeds on the vaginal mucosa and ingests bacteria and leukocytes. The infection causes a copious, frothy, malodorous, green or yellow discharge. There commonly is erythema and edema of the affected mucosa, with occasional itching and irritation. Sometimes, small hemorrhagic areas, called strawberry spots, appear on the cervix. Trichomoniasis can cause a number of complications.13 It is a risk factor for HIV transmission and infectivity in both men and women. In women, it increases the risk of tubal infertility and atypical pelvic inflammatory disease (PID), and it is associated with adverse outcomes such as premature birth in pregnant women.13 Trichomonads attach easily to mucous membranes. They may serve as vectors for the spread of other organisms, carrying pathogens attached to their surface into the fallopian tubes. In men, it is a common cause of nongonococcal urethritis and is a risk factor for infertility.14 Diagnosis and Treatment Diagnosis is made microscopically by identification of the motile protozoan on a wet-mount slide preparation. The pH of the discharge usually is greater than 6.0. Because the organism resides in other urogenital structures besides the vagina, systemic treatment is recommended. The treatment of choice is oral metronidazole or tinidazole, medications that are effective against anaerobic protozoans.13 Both drugs are chemically similar to disulfiram (Antabuse), a drug used in the treatment of alcohol addiction that causes nausea, vomiting, flushing of the skin, headache, palpitations, and lowering of the blood pressure when alcohol is ingested. Gastrointestinal disturbances and a metallic taste in the mouth are potential adverse effects of the drugs. Although metronidazole is considered safe for use during pregnancy, data on tinidazole use in pregnancy are limited.13 Sexual partners should be treated to avoid reinfection, and abstinence is recommended until the full course of therapy is completed. Exam Three: Why is it essential diagnose trichomonas early in PRINTED BY: [email protected]. Printing of Notes and pregnancy? Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 258/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/3/2023 Chlamydial Infections Chlamydial infection is the most prevalent STI in the United States, with an incidence estimated to be more than twice that of gonorrhea. Important 1/3/2023 C. trachomatis causes a wide variety of genitourinary infections, including nongonococcal urethritis in men and PID in women. The closely related organisms Chlamydia pneumoniae and Chlamydia psittaci cause mild and severe pneumonia, respectively. C. trachomatis is the most common sexually transmitted disease in North America.18 It can be serologically subdivided into types A, B, and C, which are associated with trachoma and chronic keratoconjunctivitis; types D through K, which are associated with genital infections and their complications; and types L1, L2, and L3, which are associated with LGV. C. trachomatis can cause significant ocular disease in neonates. It is a leading cause of blindness in underdeveloped countries. In these countries, the organism is spread primarily by flies, fomites, and nonsexual personal contact. In industrial countries, the organism is spread almost exclusively by sexual contact and therefore affects primarily the genitourinary structures. Exam Three: Why is it essential to identify chlamydial and gonorrheal infections in women of child-bearing age? Important 1/3/2023 Clinical Manifestations The signs and symptoms of chlamydial infection resemble those produced by gonorrhea. The most significant difference between chlamydial and gonococcal salpingitis is that chlamydial infections may be asymptomatic or clinically nonspecific. If there are symptoms in women, the most common symptom is a mucopurulent cervical discharge (Fig. 46.6). The cervix itself frequently hypertrophies and becomes erythematous, edematous, and extremely friable. This can lead to greater fallopian tube damage and increase the reservoir for further chlamydial infections. Exam Three: What is the most significant difference between chlamydia and gonorrhea? PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 259/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/3/2023 Diagnosis and Treatment Diagnosis of chlamydial infections takes several forms. The identification of polymorphonuclear leukocytes on Gram stain of penile discharge in the man or cervical discharge in the woman provides presumptive evidence. The direct fluorescent antibody test and the enzyme-linked immunosorbent assay that use antibodies against an antigen in the Chlamydia cell wall are rapid tests that are highly sensitive and specific. The positive predictive value of these tests is excellent among high-risk groups, but false- positive results occur more often in low-risk groups. The methodologic challenges of culturing this organism have led to the development of non–culture-based tests that amplify and detect C. trachomatis–specific DNA and RNA sequences.18 One of the newest sets of nonculture techniques, the nucleic acid amplification tests (NAATs), does not require viable organisms for detection and can produce a positive signal from as little as a single copy of the target DNA or RNA.18 Describe diagnostic lab tests for chlamydia. What are the benefits of using NAAT? Important 1/3/2023 The gonococcus is a pyogenic (i.e., pus-forming), gram-negative diplococcus.20 Humans are the only natural host for N. gonorrhoeae. The organism grows best in warm, mucus-secreting epithelia. The portal of entry can be the genitourinary tract, eyes, oropharynx, anorectum, or skin. Transmission usually is by sexual intercourse except for perinatal transmission.2 Autoinoculation of the organism to the conjunctiva is possible. Neonates born to infected mothers can acquire the infection during passage through the birth canal and are in danger of developing gonorrheal conjunctivitis, with resultant blindness unless treated promptly. An amniotic infection syndrome characterized by premature rupture of the membranes, premature delivery, and increased risk of infant morbidity and mortality has been identified as an additional complication of gonococcal infections in pregnancy. Genital gonorrhea in young children should raise the possibility of sexual abuse. The infection commonly manifests 2 to 7 days after exposure. It typically begins in the anterior urethra, accessory urethral glands, Bartholin or Skene glands, and the cervix. If untreated, gonorrhea spreads from its initial sites upward into the genital tract. In men, it spreads to the prostate and epididymis. In women, it commonly produces endometritis, salpingitis, and PID.2 Pharyngitis may follow oral–genital contact. The organism also can invade the bloodstream (i.e., disseminated gonococcal infection), causing serious sequelae such as bacteremic involvement of joint spaces, heart valves, meninges, and other body organs and tissues.2 Exam Three: Why is it essential to identify chlamydial and gonorrheal PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created infections in women of child-bearing age? by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 260/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/3/2023 People with gonorrhea may be asymptomatic and may unwittingly spread the disease to their sexual partners. In men, the initial symptoms include urethral pain and a creamy yellow, sometimes bloody, discharge (Fig. 46.8). The disorder may become chronic and affect the prostate, epididymis, and periurethral glands.2 Rectal infections are common in homosexual men. In women, recognizable symptoms include unusual genital or urinary discharge, dysuria, dyspareunia, pelvic pain or tenderness, unusual vaginal bleeding (including bleeding after intercourse), fever, and proctitis (Fig. 46.9).2 Symptoms may occur or increase during or immediately after menses because the bacterium is an intracellular diplococcus that thrives in menstrual blood but cannot survive long outside the human body. There may be infections of the uterus and development of acute or chronic infection of the fallopian tubes (i.e., salpingitis), with ultimate scarring and sterility (Fig. 46.10). Important 1/3/2023 ationally, the highest rates of primary and secondary syphilis cases were among men aged 25 to 29 and 20 to 24 years, among men in the West, and in the South, and among Black men.22 T. pallidum is spread by direct contact with an infectious moist lesion, usually through sexual intercourse. Bacteria-laden secretions may transfer the organism during any type of intimate contact. Skin abrasions provide another possible portal of entry. There is rapid transplacental transmission of the organism from the mother to the fetus after 16 weeks’ gestation, so that active infection in the mother during pregnancy can produce congenital syphilis in the fetus. Untreated syphilis can cause prematurity, stillbirth, and congenital defects and active infection in the infant. Because the manifestations of maternal syphilis may be subtle, testing for syphilis is mandatory in all pregnancies. Once treated for syphilis, a pregnant woman usually is followed throughout pregnancy by repeat testing of serum titers. Exam Three: how does syphilis affect a fetus if untreated in the mother? PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 261/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/3/2023 linical Manifestations The clinical disease is divided into three stages: primary, secondary, and tertiary. Primary syphilis is characterized by the appearance of a chancre at the site of exposure, such as on the penis, vulva, anus, or mouth.2 Chancres typically appear within an average of 3 weeks of exposure but may incubate up to 3 months.2 The primary chancre begins as a single, indurated, papule up to several centimeters in diameter that erodes to create a clean-based ulcerated lesion on an elevated base. They also are solitary and have discrete raised borders.2 These lesions usually are painless and located at the site of sexual contact. Primary syphilis is readily apparent in the male, where the lesion is on the scrotum or penis (Fig. 46.11). Although chancres can develop on the external genitalia in females, they are more common on the vagina or cervix, and primary syphilis therefore may go untreated since they are not visible without a speculum examination. Often there is an accompanying inguinal lymphadenopathy. Exam Three: what the three stages of syphilis?Describe the clinical manifestation that characterizes the primary stage? Important 1/3/2023 The symptoms of a rash (especially on the palms, mucous membranes, meninges, lymph nodes, stomach, soles, and liver)2 (Fig. 46.12), fever, sore throat, stomatitis, nausea, loss of appetite, and inflamed eyes may come and go for a year but usually last for 3 to 6 months. Secondary manifestations may include some loss of hair and condylomata lata. These lesions are elevated, red-brown lesions that may ulcerate and produce a foul discharge. They are 2 to 3 cm in diameter, contain many spirochetes, and are highly infectious. Important 1/3/2023 Tertiary syphilis is a delayed response to the untreated disease. It can occur decades after the initial infection.2 When syphilis does progress to the symptomatic tertiary stage, it commonly takes one of three forms: development of localized destructive granuloma-like lesions called gummas, development of cardiovascular lesions, or development of central nervous system lesions. PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 262/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 8/25/2022 IN SUMMARY The vaginal–urogenital–systemic STIs—chlamydial infections, gonorrhea, and syphilis—can severely involve the genital structures and manifest as systemic infections. Gonorrheal and chlamydial infections can cause a wide variety of genitourinary complications in men and women, and both can cause ocular disease and blindness in neonates born to infected mothers. Syphilis is caused by a spirochete, T. pallidum. It can produce widespread systemic effects and is transferred to the fetus of infected mothers through the placenta. Important 8/25/2022 GERIATRIC Considerations Final exam content. Musculoskeletal changes in aging. Important 10/18/2022 People with compound fractures are more likely to experience complications in bone healing than those with other types of fractures. PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 263/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/20/2023 Impaired Healing Many factors can contribute to impaired bone healing, including the nature and extent of the injury, the health of the person with the fracture and his or her responses to injury, the adequacy of initial treatment, and pharmacologic factors. For large bone defects caused by trauma or a tumor, bone regeneration may need enhancement. Malunion is healing with deformity, angulation, or rotation that is visible on x-ray films. Early, aggressive treatment, especially of the hand, can prevent malunion and result in earlier alignment and return of function. Malunion is caused by inadequate reduction or alignment of the fracture. Delayed union is the failure of a fracture to unite within the normal period.38 Intra-articular fractures (i.e., those through a joint) may heal more slowly and may eventually produce arthritis. Nonunion is failure to produce union and cessation of the processes of bone repair.38 It is seen most often in the tibia, especially with open fractures or crushing injuries. It is characterized by mobility of the fracture site and pain on weight bearing. Muscle atrophy and loss of range of motion may occur. Nonunion usually is established 6 to 12 months after the time of the fracture. The complications of fracture healing are summarized in Table 48.2. TABLE 48.2 COMPLICATIONS OF FRACTURE HEALING Exam three content. Fractures. Impaired/poor healing. Important 10/18/2022 Complications of Fractures and Other Musculoskeletal Injuries Important 1/20/2023 Compartment Syndrome Compartment syndrome has been described as a condition of increased pressure within a limited space (e.g., abdominal and limb compartments) that compromises the circulation and function of the tissues in the space. Abdominal compartment syndrome alters cardiovascular hemodynamics, respiratory mechanics, and renal function. The discussion in this chapter is limited to a discussion of limb compartment syndromes. Exam three Content PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 264/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/20/2023 KEY POINTS BONE INFECTIONS Bone infections may be caused by a wide variety of microorganisms introduced during injury or operative procedures, or through the bloodstream. Once localized in bone, the microorganisms proliferate, produce cell death, and spread within the bone shaft, inciting a chronic inflammatory response with further destruction of bone. Bone infections are difficult to treat and eradicate. Measures to prevent infection include careful cleaning and debridement of skeletal injuries and strict operating room protocols. Osteomyelitis Osteomyelitis represents an acute or chronic infection of the bone. Osteo refers to bone, and myelo refers to the marrow cavity, both of which are involved in this disease. The infection can be caused by: Direct penetration or contamination of an open fracture or wound (exogenous origin) Seeding through the bloodstream (hematogenous spread) Extension from a contiguous site Skin infections in people with vascular insufficiency Osteomyelitis can occur as an acute, subacute, or chronic condition. All types of organisms, including viruses, parasites, fungi, and bacteria, can produce osteomyelitis, but infections caused by certain pyogenic bacteria and mycobacteria are the most common. The specific agents isolated in pyogenic bacterial osteomyelitis are often associated with the age of the person or the inciting condition (e.g., trauma or surgery). Staphylococcus aureus is the most common cause, but organisms such as Escherichia coli, Neisseria gonorrhoeae, Haemophilus influenzae, and Salmonella species are also seen.36,49 Hematogenous Osteomyelitis Hematogenous osteomyelitis originates with infectious organisms that reach the bone through the bloodstream. Acute hematogenous osteomyelitis occurs predominantly in children.50 In adults, it is seen most commonly in debilitated people and in those with a history of chronic skin infections, chronic urinary tract infections, and intravenous drug use and in those who are immunologically suppressed. Intravenous drug users are at risk for infections with Streptococcus and Pseudomonas.36 Pathogenesis. The pathogenesis of hematogenous osteomyelitis differs in children and adults. In children, the infection usually affects the long bones of the appendicular skeleton. It starts in the metaphyseal region close to the growth plate, where termination of nutrient blood vessels and sluggish blood flow favor the attachment of blood-borne bacteria (Fig. 48.10). With advancement of the infection, purulent exudate collects in the rigidly enclosed bony tissue. Because of the bone’s rigid structure, there is little room for swelling and the purulent exudate finds its way beneath the periosteum, shearing off the perforating arteries that supply the cortex with blood, thereby leading to necrosis of cortical bone. Eventually, the purulent drainage may penetrate the periosteum and skin to form a draining sinus. In children 1 year of age and younger, the adjacent joint is often involved because the periosteum is not firmly attached to the cortex.36 From 1 year of age to puberty, subperiosteal abscesses are more common.36 As the process continues, periosteal new bone formation and reactive bone formation in the marrow tend to wall in the infection. Involucrum refers to a lesion in which bone formation forms a sheath around the necrotic sequestrum. It is seen most commonly in cases of chronic PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created osteomyelitis. Figure 48.10 Pathogenesis of hematogenous by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's osteomyelitis. (A) This epiphysis, metaphysis, and growth plate are prior permission. Violators will be prosecuted. normal. A small, septic microabscess is developing at the capillary about:blank 265/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology loop. (B) Expansion of the septic focus stimulates resorption of adjacent bony trabeculae. Woven bone begins to surround this focus. The abscess expands into the cartilage and stimulates reactive bone formation by the periosteum. (C) The abscess, which continues to expand through the cortex into the subperiosteal tissue, shears off the perforating arteries that supply the cortex with blood, thereby leading to necrosis of the cortex. (D) The extension of this process into the joint space, the epiphysis, and the skin produces a draining sinus. The necrotic bone is called a sequestrum. The viable bone surrounding a sequestrum is termed the involucrum. (From Strayer D. S., Rubin R. (Eds.) (2015). Rubin’s pathology: Clinicopathologic foundations of medicine (7th ed., Figure 30-17, p. 1325). Philadelphia, PA: Lippincott Williams & Wilkins.) In adults, the long bone microvasculature no longer favors seeding, and hematogenous infection rarely affects the appendicular skeleton. Instead, vertebrae, sternoclavicular and sacroiliac joints, and the symphysis pubis are involved. Infection typically first involves subchondral bone, then spreads to the joint space.36 With vertebral osteomyelitis, this causes sequential destruction of the endplate, adjoining disk, and contiguous vertebral body. Infection less commonly begins in the joint and spreads to the adjacent bone. Clinical Manifestations. The signs and symptoms of acute hematogenous osteomyelitis are those of bacteremia accompanied by symptoms referable to the site of the bone lesion. Bacteremia is characterized by chills, fever, and malaise. There often is pain on movement of the affected extremity, loss of movement, and local tenderness followed by redness and swelling. X- ray studies may appear normal initially, but they show evidence of periosteal elevation and increased osteoclast activity after an abscess has formed. Treatment. The treatment of hematogenous osteomyelitis begins with identification of the causative organism through blood and bone aspiration cultures.36,50 Antimicrobial agents are given first parenterally and then orally. The length of time the affected limb needs to be rested and pain control measures used are based on symptoms. Debridement and surgical drainage also may be necessary. Direct Penetration and Contiguous Spread Osteomyelitis Direct penetration or extension of bacteria from an outside (exogenous) source is now the most common cause of osteomyelitis in the United States.36 Bacteria may be introduced directly into the bone by a penetrating wound, an open fracture, or surgery. Inadequate irrigation or debridement, introduction of foreign material into the wound, and extensive tissue injury increase the bone’s susceptibility to infection. Iatrogenic bone infections are those inadvertently brought about by surgery or other treatments. These complications include pin tract infection in skeletal traction, septic (infected) joints in joint replacement surgery, and wound infections after surgery. Staphylococci and streptococci are still commonly implicated, but in 25% of postoperative infections, gram-negative organisms are detected.36 Measures to prevent these infections include preparation of the skin to reduce bacterial growth before surgery or insertion of traction devices or wires, strict operating room protocols, prophylactic use of antibiotics immediately before and for 24 hours after surgery and as a topical wound irrigation, and maintenance of sterile technique after surgery when working with drainage tubes and dressing changes. Pathogenesis. The PRINTED BY: [email protected]. Printing of Notes and pathogenesis of osteomyelitis resulting from direct penetration or Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this contiguous spread differs from hematogenous infection in that book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. virtually any traumatized bone may be involved. Although healthy about:blank 266/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology bone is highly resistant to infection, injury from local inflammation and trauma may devitalize bone and surrounding tissue, providing an inert matrix on which microorganisms introduced during trauma thrive. Clinical Manifestations. Osteomyelitis after trauma or bone surgery usually is associated with persistent or recurrent fever, increased pain at the operative or trauma site, and poor incisional healing, which often is accompanied by continued wound drainage and wound separation. Prosthetic joint infections often present with joint pain, fever, and cutaneous drainage. Diagnosis and Treatment. Diagnosis requires both confirming the infection and identifying the offending microorganism with culture and sensitivity studies. The diagnosis of skeletal infection entails use of various imaging strategies, including conventional radiology, nuclear imaging studies, CT scans, and MRI.50 Bone biopsy may be used to identify the causative microorganisms. Treatment includes antibiotics and selective use of surgical interventions. Antimicrobial agents are usually used prophylactically in people undergoing bone surgery. For people with osteomyelitis, early antimicrobial treatment, before there is extensive destruction of bone, produces the best results. The choice of agents and method of administration depend on the microorganisms causing the infection. In acute osteomyelitis that does not respond to antibiotic therapy, surgical decompression is used to release intramedullary pressure and remove drainage from the periosteal area. Prosthesis removal may be necessary in cases of an infected prosthetic joint. Exam three content. Osteomyelitis. Important 10/18/2022 OSTEONECROSIS After completing this section of the chapter, the learner will be able to meet the following objectives: Cite four major causes of osteonecrosis. Characterize the blood supply of bone and relate it to the pathologic features of the condition. Although this is not on the final exam it is a topic NPs need to be familiar with, esp. those who want to work in ortho or rheumatology practices. See table 48.1. Important 10/18/2022 CHART 48.1CAUSES OF OSTEONECROSIS PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 267/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 10/18/2022 Figure 48.12 Common sites of primary malignant bone tumors (chondrosarcoma, osteosarcoma, and Ewing sarcoma) and giant cell tumor, a locally aggressive benign tumor. Important 10/18/2022 Osteosarcoma Osteosarcoma is an aggressive and highly malignant bone tumor. It is the most common primary malignant bone tumor, and most often occurs in children.57 Osteosarcoma affects boys more than girls and accounts for about 56% of cases.36,57 Although osteosarcomas can develop in any bone, they most commonly arise in the vicinity of bone growth such as the knee, distal femur, or proximal humerus.36,57 Important 10/18/2022 Ewing Sarcoma Ewing sarcoma is a member of a group of small round cell, undifferentiated tumors thought to be of neural crest origin.36 The family of tumors includes Ewing sarcoma of the bone and soft tissue, extraosseous Ewing sarcoma, Askin tumor, and peripheral primitive neuroectodermal tumor (PPNET). Important 10/18/2022 Because Ewing sarcoma is a difficult diagnosis to establish, the diagnostic biopsy is very important. Important 10/18/2022 Chondrosarcoma Chondrosarcoma, a malignant tumor of cartilage, is the most common bone sarcoma among adults and the second most common primary malignant bone cancer overall.3 PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 268/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 10/18/2022 Metastatic Bone Disease Skeletal metastases, or secondary tumors, are more common than primary tumors.67,68 Approximately half of all people with cancer have bone metastasis at some point in their disease. Metastatic lesions are seen most often in the spine, femur, pelvis, ribs, sternum, proximal humerus, and skull and are less common in anatomic sites more distant from the trunk of the body. Predominant primary tumor sites with bone metastasis include prostate, colorectal, lung, and breast.69,70 The incidence of metastatic bone disease is highest in people older than 40 years of age. Clinical Manifestations and Diagnosis The major symptom of bone metastasis is pain in a specific bone area, and this is validated with evidence of an impending pathologic fracture. It usually develops gradually, over weeks, and is more severe at night. Pain is caused by stretching of the periosteum of the involved bone or by nerve entrapment, as when the nerve roots of the spinal cord are compressed by the vertebral body. The affected bone of the pathologic fracture appears to be eaten away on x-ray images; in severe cases, it crumbles on impact, much like dried toast. Many pathologic fractures occur in the femur, humerus, and vertebrae. Radiographic examinations are used along with CT, PET-CT, and bone scans to detect, diagnose, and localize metastatic bone lesions.71 Approximately, one third of people with skeletal metastases have positive bone scans without radiologic findings. Arteriography using radiopaque contrast media may be helpful in outlining the tumor margins. A bone biopsy usually is done when there is a question regarding the diagnosis or treatment. A closed-needle biopsy with CT localization is particularly useful with spine lesions. Serum levels of alkaline phosphatase and calcium often are elevated in people with metastatic bone disease. Treatment The primary goals in treatment of metastatic bone disease are to prevent pathologic fractures and promote survival with maximum functioning, allowing the person to maintain as much mobility and pain control as possible. Standard treatment methods include chemotherapy, irradiation, and surgical stabilization. Metastatic bone disease. No longer on final exam blueprint PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 269/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 8/25/2022 Hereditary and Congenital Deformities Congenital deformities are abnormalities that are present at birth. They range in severity from mild limb deformities, which are relatively common, to major limb malformations, which are relatively rare. The most common anomaly of the toes or fingers is polydactyly or the presence of an extra digit on the hand or foot. Macrodactyly occurs when one or more toes or fingers are hypertrophied and are significantly larger than the surrounding toes or fingers. There may also be a simple webbing of the fingers or toes (syndactyly) or the absence of a bone such as the phalanx, rib, or clavicle. Joint contractures and dislocations produce more severe deformity, as does the absence of entire bones, joints, or limbs. Surgery is done to relieve functional symptoms, such as pain or difficulty in fitting shoes. The cosmetic goal is to alter the grotesque appearance of the hand or foot and to achieve a similar size to the opposite extremity. Congenital deformities are caused by many factors, some unknown. These factors include hereditary influences, external agents that injure the fetus (e.g., radiation, alcohol, drugs, such as thalidomide taken by pregnant women with morning sickness in the 60s, and viruses), and intrauterine environmental factors. Many of the organic bone matrix components have been identified only recently, and their interactions were found to be more complex than originally thought. Hand and foot disorders associated with abnormalities in bone matrix include those with deficient collagen synthesis and decreased bone mass.12 Important 1/20/2023 Osteogenesis Imperfecta Osteogenesis imperfecta (OI) is a hereditary disease characterized by defective synthesis of type I collagen13,14 (Fig. 49.9). It is one of the most common hereditary bone diseases, with an estimated 20,00 to 50,000 people with OI in the United States.13 OI is usually transmitted as an autosomal dominant trait. Exam three content Important 10/18/2022 TABLE 49.1 Types of Osteogenesis Imperfecta PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 270/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 8/25/2022 Developmental Dysplasia of the Hip Developmental dysplasia of the hip (DDH), formerly known as congenital dislocation of the hip, is an abnormality in hip development that leads to a wide spectrum of hip problems in infants and children, including hips that are unstable, malformed, subluxated, or completely dislocated.16 In less severe cases, the hip joint may be unstable, with excessive laxity of the joint capsule, or subluxated, so that the joint surfaces are separated and there is a partial dislocation (Fig. 49.10). With dislocated hips, the head of the femur is located outside of the acetabulum. Figure 49.10 Normal (left) and abnormal relationships of hip joint structure in subluxation (middle) and dislocation (right). The results of newborn screening programs have shown that 1 of 100 infants have some evidence of hip instability, whereas dislocation of the hip is seen in 1 of every 1000 live births.10 The left hip is involved more frequently than the right hip because of the left occipital intrauterine positioning of most infants.10 The disorder occurs most frequently in first-born children and is six times more common in female than in male infants.16 Final exam content. Hereditary and congenital deformities. Important 8/25/2022 Diagnosis. Early diagnosis of DDH is important because treatment is easiest and most effective if begun during the first 6 months of life.16 Also, repeated dislocations cause damage to the femoral head and the acetabulum. There is no uniformly accepted method for diagnosis of DDH during the newborn period. However, there is evidence that ultrasound is most effective during the first month of life for screening hip joint problems.17 However, the U.S. Preventive Services Task Force (USPSTF) states that 90% of the hip abnormalities identified by ultrasound resolve on their own.17 Clinical examination of the hips is recommended at birth and every several months during the first year of life.17 Important 8/25/2022 Follow-up clinical examinations should be done in the presence of an abnormality. In infants, signs of DDH include asymmetry of the hip or gluteal folds, shortening of the thigh so that one knee (on the affected side) is higher than the other hip, and limited abduction of the affected hip (Fig. 49.11). The asymmetry of gluteal folds is not definitive but indicates the need for further evaluation. The USPSTF states that evidence is insufficient to recommend routine screening of asymptomatic infants as a means of preventing adverse outcomes.16 PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 271/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 8/25/2022 Figure 49.11 Congenital dysplasia of the left hip with shortening of the femur, as indicated by legs in abduction and asymmetric gluteal and thigh folds (arrows). Several examination techniques can be used to screen for a dislocatable hip.5,16,18 Two specific maneuvers for assessing hip stability in the newborn are the Ortolani maneuver (for reducible dislocation) (Fig. 49.12) and the Barlow maneuver (for the dislocatable hip) (Fig. 49.13).5,16,18 The Barlow maneuver involves a manual attempt to dislocate and reduce the abnormal hip while the infant is in the supine position with both knees flexed. With gentle downward pressure being applied to the knees, the knee and thigh are manually abducted as an upward and medial pressure is applied to the proximal thigh. In infants with the disorder, the initial downward pressure on the knee produces a dislocation of the hip, a positive Barlow sign. This is followed by a palpable or audible click (i.e., Ortolani sign) as the hip is reduced and moves back into the acetabulum. The sensitivity of these tests is improved significantly with the use of trained and experienced examiners. The Galeazzi test is a measurement of the length of the femurs that is done by comparing the height at the knees while they are flexed at 90 degrees. An inequality in the height of the knees is a positive Galeazzi sign and is usually caused by hip dislocation or congenital femoral shortening. This test is not useful in detecting bilateral DDH because both leg lengths will be equal. In an older child, instability of the hip may produce a delay in standing or walking and eventually cause a characteristic waddling gait. When the thumbs are placed over the anterior iliac crest and the hands are placed over the lateral pelvis in examination, the levels of the thumbs are not even; the child is unable to elevate the opposite side of the pelvis (positive Trendelenburg test). Important 8/25/2022 Figure 49.12 You will learn more about the DDH exam in the FNP courses. Important 8/25/2022 Juvenile Osteochondroses The three osteochondroses listed here are recommened study for the FNP board certification exam. You will learn more about these in the FNP courses. PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 272/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 8/25/2022 Legg–Calvé–Perthes Disease Important 8/25/2022 affecting primarily those, mostly boys, between ages 3 and 12 years, with a median age of 7 years.22 Important 8/25/2022 Osgood–Schlatter Disease Important 8/25/2022 Slipped Capital Femoral Epiphysis PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 273/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/20/2023 Gout Gout is a group of disorders characterized by increased serum uric acid and urate crystal deposits in kidneys and joints.2 Gout is more prevalent in males (70% of cases), particularly in males of African American descent, and the peak age of occurrence is between ages 40 and 50.4 High uric acid levels or hyperuricemia (>7 mg/dL in males and 6 mg/dL in females) are present in 5% to 10% of the population of the United States.4 Asymptomatic hyperuricemia is a laboratory finding and not a disease. About one in five people with hyperuricemia will develop gout.4 Most people with hyperuricemia do not develop gout. Only one third of people with hyperuricemia have primary gout and the other two thirds have secondary gout.2 Gout disorders include acute gouty arthritis with recurrent attacks of severe articular and periarticular inflammation; tophi or the accumulation of crystalline deposits in articular surfaces, bones, soft tissue, and cartilage; gouty nephropathy or renal impairment; and uric acid kidney stones. The term primary gout is used to designate cases in which the cause of the disorder is unknown or caused by an inborn error in metabolism and is characterized primarily by hyperuricemia and gout. Primary gout is predominantly a disease of males, with a peak incidence in the fourth to sixth decade.2 In secondary gout, the cause of the hyperuricemia is known but the gout is not the main disorder. Pathogenesis The pathogenesis of gout resides in an elevation of serum uric acid levels. Uric acid is the end product of purine metabolism.38 Two pathways are involved in purine synthesis: 1. A de novo pathway in which purines are synthesized from nonpurine precursors. 2. The salvage pathway in which purine bases are recaptured from the breakdown of nucleic acids derived from exogenous (dietary) or endogenous sources. The elevation of uric acid and the subsequent development of gout can result from overproduction of purines, decreased salvage of free purine bases, augmented breakdown of nucleic acids because of increased cell turnover, or decreased urinary excretion of uric acid (Fig. 50.10). Primary gout, which constitutes 90% of cases, may be a consequence of enzyme defects that result in an overproduction of uric acid or inadequate elimination of uric acid by the kidney.38 In most cases, the reason is unknown. In secondary gout, the hyperuricemia may be caused by the increased breakdown of nucleic acids, as occurs with rapid tumor cell lysis during treatment for lymphoma or leukemia. Other cases of secondary gout result from chronic renal disease. Some of the diuretics, including the thiazides, can interfere with the excretion of uric acid. Figure 50.10 Pathogenesis of hyperuricemia and gout. Purine nucleotides are synthesized de novo from nonpurine precursors or derived from preformed purines in the diet. Purine nucleotides are catabolized to hypoxanthine or incorporated into nucleic acids. The degradation of nucleic acids and dietary purines also produces hypoxanthine. Hypoxanthine is converted into uric acid, which in turn is excreted into the urine. Hyperuricemia and gout from (1) increased de novo purine synthesis, (2) increased cell turnover, (3) decreased salvage of dietary purines and hypoxanthine, and (4) decreased uric acid excretion by the kidneys. (From Strayer D., Rubin R. (Eds.) (2015). Rubin’s pathology: Clinicopathologic foundations of medicine (7th ed., Figure 30-60, p. 1367). Philadelphia, PA: Lippincott PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created Williams & Wilkins.) An attack of gout occurs when monosodium by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's urate crystals precipitate in the joint and initiate an inflammatory prior permission. Violators will be prosecuted. response. Synovial fluid is a poorer solvent for uric acid than plasma, about:blank 274/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology and uric acid crystals are even less soluble at temperatures below 37 °C. Crystal deposition usually occurs in peripheral areas of the body, such as the great toe, where the temperatures are cooler than in other parts of the body. With prolonged hyperuricemia, crystals and microtophi (i.e., small, hard nodules with irregular surfaces that contain crystalline deposits of monosodium urate) accumulate in the synovial lining cells and in the joint cartilage.4 The released crystals are chemotactic to leukocytes and also activate complements. Phagocytosis of urate crystals by polymorphonuclear leukocytes occurs and leads to polymorphonuclear cell death with the release of lysosomal enzymes. As this process continues, the inflammation causes destruction of the cartilage and subchondral bone. Repeated or untreated attacks of acute arthritis eventually lead to chronic arthritis and the formation of the large, hard nodules called tophi4,38 (Fig. 50.11). They are found most commonly in the synovium, olecranon bursa, Achilles tendon, subchondral bone, and extensor surface of the forearm and may be mistaken for rheumatoid nodules. Tophi usually do not appear until 10 years or more after the first gout attack. This stage of gout, called chronic tophaceous gout, is characterized by more frequent and prolonged attacks, which often are polyarticular. Figure 50.11 Gout. (A) Gouty tophi of the hands appear as multiple rubbery nodules, one of which is ulcerated. (B) A cross-section of a digit demonstrates a tophaceous collection of toothpaste-like urate crystals. (From Strayer D., Rubin R. (Eds.) (2015). Rubin’s pathology: Clinicopathologic foundations of medicine (7th ed., Figure 30-61A and B, p. 1368). Philadelphia, PA: Lippincott Williams & Wilkins.) Clinical Manifestations Gout is categorized into four phases: 1. The asymptomatic hyperuricemia 2. Acute gout arthritis 3. Intercritical gout 4. Chronic tophaceous gout2 The first phase may not even be identified or may be detected during an annual physical examination because the person has no symptoms. The typical acute attack of gout is monoarticular and usually affects the first metatarsophalangeal joint. The tarsal joints, insteps, ankles, heels, knees, wrists, fingers, and elbows also may be initial sites of involvement. Acute gout often begins at night and may be precipitated by excessive exercise, certain medications or foods, alcohol, or dieting. The onset of pain typically is abrupt, and redness and swelling are observed. The attack may last for days or weeks. Pain may be severe enough to be aggravated even by the weight of a bedsheet covering the affected area. In the early stages of gout after the initial attack has subsided, the person is asymptomatic, and joint abnormalities are not evident. This is the third phase or the intercritical gout. After the first attack, it may be months or years before another attack. As attacks recur with increased frequency, joint changes occur and become permanent. This fourth phase is called chronic tophaceous gout. Gout has been linked with cardiovascular disease, obesity, metabolic syndrome, hyperlipidemia, excessive alcohol use, and renal insufficiency. Therefore, these potential comorbidities need to be ruled out and, if they are ruled out, should be prevented.39 Diagnosis and Treatment Although hyperuricemia is the biochemical hallmark of gout, the presence of hyperuricemia cannot be equated with gout because many people with this condition never develop gout. A definitive diagnosis of gout can be made only when monosodium urate crystals are in the synovial fluid or in tissue PRINTED BY: [email protected]. Printing of Notes and sections of tophaceous deposits. Synovial fluid analysis is useful in Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this excluding other conditions, such as septic arthritis, pseudogout, and book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. RA. Diagnostic methods may include measures to determine if the about:blank 275/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology disorder is related to overproduction or to underexcretion of uric acid.38,39 This is done through measurement of serum uric acid levels and collection of a 24-hour urine sample for determination of urate excretion in the urine.38,39 The objectives for treatment of gout include the termination and prevention of the acute attacks of gouty arthritis and the correction of hyperuricemia, with consequent inhibition of further precipitation of sodium urate and absorption of urate crystal deposits already in the tissues. Pharmacologic management of acute gout is directed toward reducing joint inflammation. Exam three content. Crystal-induced arthropathies. Gout. Important 1/20/2023 Superficial Fungal Infections Fungi are free-living, saprophytic plantlike organisms, certain strains of which are considered part of the normal skin flora. Some fungi cause deep infections and others are superficial. There are two types of fungi, yeasts, and molds. Yeasts, such as Candida albicans, grow as single cells and reproduce asexually9 (see Fig. 52.1). Molds grow in long filaments, called hyphae.9 There are thousands of known species of yeasts and molds, but only about 100 of them cause disease in humans and animals.9 Fungal or mycotic infections of the skin are traditionally classified as superficial or deep. The superficial mycoses, more commonly known as tinea or ringworm, invade only the superficial keratinized tissue (skin, hair, and nails). Deep fungal infections involve the epidermis, dermis, and subcutaneous tissue. Infections that typically are superficial may exhibit deep involvement in people who are immunosuppressed.5 Figure 52.1 Superficial fungal infection. Candida in skin fold. (From Jensen S. (2015). Nursing health assessment: A best practice approach (2nd ed., p. 275). Philadelphia, PA: Wolters Kluwer.) Exam three content. Fungal infections. Candidal infections. Risk factors and associated systemic disorders. PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 276/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 8/25/2022 ost of the superficial mycoses, also called dermatophytoses, are caused by the dermatophytes, a group of closely related fungi. These fungi are classified into three genera: Microsporum (M. audouinii, M. canis, M. gypseum) Epidermophyton (E. floccosum) Trichophyton (T. schoenleinii, T. violaceum, T. tonsurans)5 Two of these, Microsporum and Trichophyton, affect the hair.5 Another way of classifying the dermatophytes is according to their ecologic origin—human, animal, or soil. Anthropophilic species (M. audouinii, M. tonsurans, T. violaceum) are parasitic on humans and are spread by other infected humans. Zoophilic species (M. canis and T. mentagrophytes) cause parasitic infections in animals, some of which can be spread to humans. Geophilic species originate in the soil but may infect animals, which in turn serve to infect humans. Pathogenesis and Clinical Manifestations. The fungi that cause superficial mycoses live on the dead keratinized cells of the epidermis. They emit an enzyme that enables them to digest keratin, which results in superficial skin scaling, nail disintegration, or hair breakage, depending on the location of the infection.5 An exception to this is the invading fungus of tinea versicolor, which does not produce a keratolytic enzyme. Deeper reactions involving vesicles, erythema, and infiltration are caused by the inflammation that results from exotoxins liberated by the fungus. Fungi also are capable of producing an allergic or immune response.5 Superficial fungal infections affect various parts of the body, with the lesions varying according to site and fungal species. Tinea can affect the body (tinea corporis), face and neck (tinea faciale), scalp (tinea capitis), hands (tinea manus), feet (tinea pedis), nails (tinea unguium), or genitalia (tinea cruris).5 Diagnosis and Treatment. Diagnosis of superficial fungal infections is primarily done by microscopic examination of skin scrapings for fungal spores, the reproducing bodies of fungi. Potassium hydroxide (KOH) preparations are used to prepare slides of skin scrapings. KOH disintegrates human tissue and leaves behind the threadlike filaments or hyphae that grow from the fungal spores. Cultures also may be done using a dermatophyte test medium or a microculture slide that produces color changes and allows for direct microscopic identification. The Wood light (UV light) is another method that can assist with the diagnosis of tinea. Some types of fungi (e.g., M. canis and M. audouinii) fluoresce yellow-green when the light is directed onto the affected area.5 Superficial fungal infections may be treated with topical or systemic antifungal agents. Treatment usually follows diagnosis confirmed by KOH preparation or culture, particularly if a systemic agent is to be used. Topical agents, both prescription and over-the-counter preparations, are commonly used in the treatment of tinea infections. However, success often is limited because of the lengthy duration of treatment, poor compliance, and high rates of relapse at specific body sites. Mycoses are commonly seen in clinical practice. PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 277/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 8/25/2022 Tinea of the Body or Face. The tineas are also commonly seen by NPs. Important 1/20/2023 Bacterial Infections Bacteria are considered normal flora of the skin. Most bacteria are not pathogenic, but when pathogenic bacteria invade the skin, superficial or systemic infections may develop. Bacterial skin infections are commonly classified as primary or secondary infections. Primary infections are superficial skin infections such as impetigo or ecthyma. Secondary infections consist of deeper cutaneous infections, such as infected ulcers. Diagnosis usually is based on cultures taken from the infected site. Treatment measures include antibiotic therapy and measures to promote comfort and prevent the spread of infection. Impetigo. Impetigo is a common, superficial bacterial infection caused by staphylococci or group A beta-hemolytic streptococci, or both.4 Impetigo is common among infants and young children, although older children and adults occasionally contract the disease. Its occurrence is highest during warm summer months or in warm, moist climates. Impetigo initially appears as a small vesicle or pustule or as a large bulla on the face or elsewhere on the body. As the primary lesion ruptures, it leaves a denuded area that discharges a honey-colored serous liquid that hardens on the skin surface and dries as a honey-colored crust (Fig. 52.5). New vesicles erupt within hours. Pruritus often accompanies the lesions, and skin excoriations that result from scratching multiply the infection sites. Although a very low risk, a possible complication of untreated streptococcal impetigo is poststreptococcal glomerulonephritis. Topical mupirocin (Bactroban) is effective in treating impetigo and has few side effects. In most instances, it is the first choice but if a larger area is involved then a systemic antibiotic may be necessary.10 Figure 52.5 Impetigo of the face results from S. aureus commonly. (From Jensen S. (2015). Nursing health assessment: A best practice approach (2nd ed., p. 274). Philadelphia, PA: Wolters Kluwer.) Another form of impetigo exists, bullous impetigo, which is usually caused by Staphylococcus aureus.4 Bullous impetigo is common among children. It is due to the epidermolytic toxin and is not generally contaminated by streptococci.4,11 Thin bullae erupt that appear clear to cloudy and coalesce. The bullae open, leaving the original bullous rim with central thin, flat, honey-colored crusts, or in some cases denuded areas. The face is often affected, but bullous impetigo may occur anywhere on the body. The treatment measures are the same as for nonbullous impetigo. Exam three content. Impetigo. PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 278/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/20/2023 Cellulitis is a deeper infection affecting the dermis and subcutaneous tissues. It is usually caused by group A beta-hemolytic streptococci or S. aureus, but can be caused by bacteria specific to certain activities, such as fish handling, swimming in fresh water, or swimming in salt water, or from animal bites or scratches. Preexisting wounds (e.g., ulcers, erosions) and tinea pedis are often portals of entry. Legs are the most common sites, followed by the hands and pinnae of the ears, but cellulitis may be seen on many body parts. The lesion consists of an expanding red, swollen, tender plaque with an indefinite border, covering a small to wide area (Fig. 52.7). Cellulitis is frequently accompanied by fever, erythema, heat, edema, and pain. Cellulitis often involves the lymph system, and, once compromised, repeat infections may impair lymphatic drainage, leading to chronically swollen legs, and eventually dermal fibrosis and lymphedema. Incorrectly treated, it may result in septicemia, nephritis, or death. Treatment measures (oral and intravenous antibiotics) are aimed at the invasive organisms and the extent of the infection. Figure 52.7 Cellulitis on leg infected with S. aureus and Pseudomonas. Exam three content. Cellulitis. PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 279/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/20/2023 Herpes Zoster. Herpes zoster (shingles) is an acute, localized vesicular eruption distributed over a dermatomal segment of the skin. It is caused by the same herpesvirus, varicella–zoster, which causes chickenpox. It is believed to be the result of reactivation of a latent varicella–zoster virus infection that was dormant in the sensory dorsal root ganglia since a primary childhood infection. During an episode of herpes zoster, the reactivated virus travels from the ganglia to the skin of the corresponding dermatome. Although herpes zoster is not as contagious as chickenpox, the reactivated virus can be transmitted to nonimmune contacts. Herpes zoster occurs in 10% to 20% of all people.4 It can occur at any time during the life span but tends to happen in older adults more frequently. The incidence is much less among African Americans. Other people at risk because of impaired T-cell–mediated immunity are those with conditions such as HIV infection and certain malignancies, chronic corticosteroid users, and those undergoing chemotherapy and radiation therapy. The lesions of herpes zoster typically are preceded by a prodrome consisting of a burning pain, a tingling sensation, extreme sensitivity of the skin to touch, and pruritus along the affected dermatome. Among the dermatomes, the most frequently involved are the thoracic, the cervical, the trigeminal, and the lumbosacral. Prodromal symptoms may be present for 1 to 3 days or longer before the appearance of the rash. During this time, the pain may be mistaken for a number of other conditions, such as heart disease, pleurisy, musculoskeletal disorders, or gastrointestinal disorders. The lesions appear as an eruption of vesicles with erythematous bases that are restricted to skin areas supplied by sensory neurons of a single or associated group of dorsal root ganglia. In immunosuppressed people, the lesions may extend beyond the dermatome. Eruptions usually are unilateral in the thoracic region, trunk, or face. New groups of vesicles erupt for 3 to 5 days along the nerve pathway. The vesicles dry, form crusts, and eventually fall off. The lesions usually clear in 2 to 3 weeks, although they can persist up to 6 weeks in some older adults. Serious complications can accompany eruptions. Eye involvement can result in permanent blindness and occurs in a large percentage of cases involving the ophthalmic division of the trigeminal nerve (Fig. 52.10). Postherpetic neuralgia, which is pain that persists longer than 1 to 3 months after the resolution of the rash, is an important complication of herpes zoster. It is seen most commonly in people older than 60 years of age, increasing age being the greatest risk factor. Given the aging population in the United States, the incidence of herpes zoster is expected to increase dramatically over the next two decades. Affected people complain of sharp, burning pain that often occurs in response to nonnoxious stimuli. Even the slightest pressure of clothing and bedsheets may elicit pain. It usually is a self-limited condition that persists for months, with symptoms abating over time. Figure 52.10 Dermatomal distribution of herpes zoster rash due to varicella–zoster virus. (From Hinkle J. L., Cheever K. H. (2018). Brunner & Suddarth’s Textbook of medical–surgical nursing (14th ed., p. 1819). Philadelphia, PA: Wolters Kluwer.) The treatment of choice for herpes zoster is the administration of an antiviral agent (e.g., acyclovir, valacyclovir, PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created famciclovir). The treatment is most effective when started within 72 by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's hours of rash development. When given in the acute vesicular stage, prior permission. Violators will be prosecuted. the antiviral drugs have been shown to decrease the amount of lesion about:blank 280/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology development and pain. Narcotic analgesics, tricyclic antidepressants, gabapentin, anticonvulsant drugs, and nerve blocks have been used for management of postherpetic neuralgia. Local application of capsaicin cream or lidocaine patches may be used in selected cases. Zoster vaccine (Zostavax) is effective in either preventing or lessening the severity of herpes zoster.14 This vaccine is highly recommended for people greater than 50 years of age and anyone with high risk for herpes zoster.15 Exam three content. Herpes Zoster. PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 281/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/20/2023 Atopic Dermatitis. Atopic dermatitis (atopic eczema) is an itchy, inflammatory skin disorder that is characterized by poorly defined erythema with edema, vesicles, and weeping at the acute stage and skin thickening (lichenification) in the chronic stage.34 Although often described as an immunoglobulin E (IgE)-mediated hypersensitivity (atopic) disease, allergic causation is difficult to document, and the disorder is increasingly viewed as a skin disease that predisposes to allergies.34 Approximately 30% of children with atopic dermatitis develop asthma, and 35% will develop allergies in adolescence and adulthood.34 Atopic dermatitis presents differently at different ages (infantile and adult) and in people of different races. Approximately 70% of cases of atopic allergy start in children younger than 5 years of age.34 The infantile form of atopic dermatitis is characterized by vesicle formation, oozing, and crusting with excoriations. It usually begins on the cheeks and may progress to involve the scalp, arms, trunk, and legs (Fig. 52.16). The skin of the cheeks may be paler, with extra creases under the eyes, called Dennie-Morgan folds. The infantile form may become milder as the child ages, often disappearing by the age of 15 years. However, many people have resultant eczematous disorders and rhinitis symptoms throughout life. Figure 52.16 Atopic eczema on an infant’s face. (From Jensen S. (2015). Nursing health assessment: A best practice approach (2nd ed., p. 848). Philadelphia, PA: Wolters Kluwer.) Adolescents and adults usually have dry, red patches affecting the face, neck, and upper trunk, but without the thickening and discrete demarcation associated with psoriasis. The bends of the elbows and knees are usually involved. In chronic cases, the skin is dry, leathery, and lichenified. People with dark skin may have a papular eruption and poorly demarcated hypopigmentation patches on the cheeks and extremities. In people with black skin, pigmentation may be lost from lichenified skin. Acute flares may present with red patches that are weepy, shiny, or lichenified (i.e., thickened, with more prominent markings) and with plaques and papules. Itching may be severe and prolonged with both childhood and adults forms of atopic dermatitis. Secondary infections are common. Treatment of atopic eczema is designed to target the underlying abnormalities: dryness, pruritus, infection, and inflammation. The guidelines derived from a combined review of the American Academy of Allergy, Asthma, and Immunology; American College of Allergy, Asthma, and Immunology Joint Task Force 2012; Atopic Dermatitis Practice Parameter; and the American Academy of Dermatology highlight therapies and outline basic principles of atopic dermatitis management.35 Underlying all treatment measures is a comprehensive education program regarding the cause of the disorder, treatment measures, and avoidance of temperature changes and stress to minimize vascular and sweat responses. Basic therapy begins with optimal skin care, addressing the skin barrier defect with continuous use of emollients and skin hydration, along with avoiding exposure to environmental irritants and foods that cause exacerbations of the symptoms. The person should bathe with warm water and mild soap. Bathing dries the skin, yet it is important to maintain a low level of microorganisms to prevent infection. A key feature of atopic dermatitis is severe dryness of the skin caused by PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created dysfunction of the skin barrier with transepidermal water loss. This is by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's accompanied by intense pruritus and inflammation. Application of prior permission. Violators will be prosecuted. moisturizers increases hydration of the skin.36 A number of clinical about:blank 282/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology trials have shown that they lessen the symptoms and signs of atopic dermatitis, including erythema, fissuring, and pruritus.35 Topical corticosteroids remain an important treatment for acute flare-ups but can cause local and systemic side effects. Potency of topical corticosteroids is classified by the potential for vasoconstriction. In general, only preparations that have weak or moderate potency are used on the face and genital areas, whereas those that have moderate or high potency are used on other areas of the body.34 Lower-potency corticosteroids may be sufficient on all areas of the body in younger children. One of the main concerns of topical corticosteroid use is skin thinning. Another concern is secondary adrenal suppression and the suppression of growth in children resulting from systemic absorption.34,36 Wet-wrap therapy, in which a wet dressing is applied over emollients in combination with topical antiseptics (e.g., triclosan, chlorhexidine) or topical corticosteroids, has been shown to be beneficial in some cases of severe atopic dermatitis.36,37 Secondary infection with S. aureus is common and usually treated with short courses of antibiotics.34 Short-term corticosteroids are also used during acute flare-ups with adult people. Cyclosporine and azathioprine, both immunosuppressive agents, may also be used, keeping in mind their potentially harmful effects. Antihistamines are useful for their sedative effects and may be helpful during severe pruritus episodes. Phototherapy alone or in combination with corticosteroids during acute flares is often practiced, with beneficial results. Studies have examined the use of probiotics, foods containing live microorganisms, such as Lactobacillus acidophilus or Bifidobacterium bifidum. There is sufficient data to document the role of probiotics in preventing atopic dermatitis, but their effect on atopic dermatitis is not as clear. Probiotics are believed to reduce IgE-mediated reactions.38 Probiotic preparations are available to the consumer in the form of powders, tablets, drinks, and fermented dairy products.38 Exam three content. Atopic dermatitis. Eczema. PRINTED BY: [email protected]. Printing of Notes and Highlights is for personal, private use only. Notes created by user are not part of publisher content. No part of this book may be reproduced or transmitted without publisher's prior permission. Violators will be prosecuted. about:blank 283/288 7/19/24, 6:06 PM Highlights & Notes: Lippincott CoursePoint for Norris: Porth's Pathophysiology Important 1/20/2023 Thermal Injury About 490,000 people in the United States require medical care for burns each year, with 40,000 requiring hospitalization.47 The effects and complications of burns fully illustrate the essential function that the skin performs as it protects the body from the damaging elements in the environment while serving to maintain the constancy of the body’s internal environment. The massive loss of skin tissue not only predisposes a person to invasion from microbes that are present in the environment but also allows for a substantial loss of body fluids leading to interference with temperature regulation, challenges for the immune system, and excessive demands imposed on the metabolic and reparative processes that are needed to restore the body's interface with the environment. Burns are caused by a number of sources. Flame burns occur because of exposure to direct fire. Scald burns result from hot liquids spilled or poured on the skin surface. In a child, a scald burn may be indicative of child abuse. Chemical burns occur from industrial agents used in occupational sites. Electrical burns occur from contact with live electrical wires in fields or in the home. Electrical burns are usually more extensive because of internal tissue injury and the presence of entrance and exit wounds. Lightning, electromagnetic radiation, and ionizing radiation also can cause skin burns. Classification of Burns Burns are typically classified according to the depth of involvement as first-degree, second-degree, and third- degree burns. The depth of a burn is largely influenced by the duration of exposure to the heat source and the temperature of the heating agent. First-Degree Burns. First-degree burns (superficial partial- thickness burns) involve only the outer layers of the epidermis. They are red or pink, dry, and painful. There usually is no blister formation. A mild sunburn is an exa