Symptoms

Signs

 

 

 

Content 12

 

 

Alcohol

Alcohol can interfere with the function of each of these components, thereby causing impotence, infertility, and reduced male secondary sexual characteristics.1 In the testes, alcohol can adversely affect the Leydig cells, which produce and secrete the hormone testosterone. Studies found that heavy alcohol consumption results in reduced testosterone levels in the blood. Alcohol also impairs the function of the testicular Sertoli cells that play an important role in sperm maturation. In the pituitary gland, alcohol can decrease the production, release, and/or activity of two hormones with critical reproductive functions, luteinizing hormone and follicle-stimulating hormone. Finally, alcohol can interfere with hormone production in the hypothalamus.

 

 

 

 

 

 

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Complications of Injecting Drug Use

  • Local problems—Abscess (Figures 240-2 
    Image not available.

    A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of ­Richard P. Usatine, MD.)

    and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2
    • IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
    • Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
  • IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
    • Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.

 

Content 3

Content 13

Content 11

 


Question 1 of 10

All of the following statements regarding the epidemiology of schistosomal infection are true EXCEPT:

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The answer is A. (Chap. 259) Human schistosomiasis is caused by five species of parasitic trematodes. Schistosoma mansoni, Schistosoma japonicum, Schistosoma mekongi, and Schistosoma intercalatum are intestinal species, whereas Schistosoma haematobium is a urinary species. There are reportedly up to 300 million individuals infected with Schistosoma. (See Figure IV-278.) S haematobium is not seen in South America. All forms of schistosomiasis are initiated by penetration of infective cercariae released from infected snails into fresh water. After entering skin, the schistosome migrates via venous or lymphatic vessels to either the intestinal or urinary venous system depending on species. Acute skin infection causes dermatitis (swimmer’s itch) within 2–3 days. Katayama fever, acute schistisomal serum sickness related to migration, may develop in 4–8 weeks. Eosinophilia is common in acute infection. This has become a more common global health problem as travelers are exposed while swimming or boating in infected fresh water bodies. Chronic schistosomiasis depends on the species and the location of infection. The intestinal species are responsible for portal hypertension. S haematobium causes urinary symptoms and a higher risk of urinary tract carcinoma. There are immunologic tests available to diagnose schistosomiasis, and in some cases, stool or urine examination may be positive.

 

Image not available.

FIGURE IV-278 Global distribution of schistosomiasis. A. Schistosoma mansoni infection (dark blue) is endemic in Africa, the Middle East, South America, and a few Caribbean countries. S intercalatum infection (green) is endemic in sporadic foci in West and Central Africa. B. S haematobium infection (purple) is endemic in Africa and the Middle East. The major endemic countries for S japonicum infection (green) are China, the Philippines, and Indonesia. S mekongi infection (red) is endemic in sporadic foci in Southeast Asia.

 

A 75-year-old triathlete complains of gradually worsening vision over the past year. It seems to be involving near and far vision. The patient has never required corrective lenses and has no significant medical history other than diet-controlled hypertension. He takes no regular medications. Physical examination is normal except for bilateral visual acuity of 20/100. There are no focal visual field defects and no redness of the eyes or eyelids. Which of the following is the most likely diagnosis?

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Age-related macular degeneration is a major cause of painless, gradual bilateral central visual loss. It occurs as nonexudative (dry) or exudative (wet) forms. Recent genetic data have shown an association with the alternative complement pathway gene for complement factor H. The mechanism link for that association is unknown. The nonexudative form is associated with retinal drusen that leads to retinal atrophy. Treatment with vitamin C, vitamin E, beta-carotene, and zinc may retard the visual loss. Exudative macular degeneration, which is less common, is caused by neovascular proliferation and leakage of choroidal blood vessels. Acute visual loss may occur because of bleeding. Exudative macular degeneration may be treated with intraocular injection of a vascular endothelial growth factor antagonist (bevacizumab or ranibizumab). Blepharitis is inflammation of the eyelids usually related to acne rosacea, seborrheic dermatitis, or staphylococcal infection. Diabetic retinopathy, now a leading cause of blindness in the United States, causes gradual bilateral visual loss in patients with long-standing diabetes. Retinal detachment is usually unilateral and causes visual loss and an afferent pupillary defect.

 

Mr. Jenson is a 40-year-old man with a congenital bicuspid aortic valve who you have been seeing for more than a decade. You obtain an echocardiogram every other year to follow the progression of his disease knowing that bicuspid valves often develop stenosis or regurgitation requiring replacement in middle age. Given his specific congenital abnormality, what other anatomic structure is important to follow on his biannual echocardiograms?

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The answer is A. (Chap. 282) Bicuspid aortic valve is among the most common of congenital heart cardiac abnormalities. Valvular function is often normal in early life and thus may escape detection. Due to abnormal flow dynamics through the bicuspid aortic valve, the valve leaflets can become rigid and fibrosed, leading to either stenosis or regurgitation. However, pathology in patients with bicuspid aortic valve is not limited to the valve alone. The ascending aorta is often dilated, misnamed “poststenotic” dilatation; this is due to histologic abnormalities of the aortic media and may result in aortic dissection. It is important to screen specifically for aortopathy because dissection is a common cause of sudden death in these patients.

 


 

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