Malabsorption results from damage to the small-bowel epithelium or bypass or loss of absorptive surface area. 

Intestinal malabsorption of ingested nutrients produces osmotic diarrhea, steatorrhea, or specific deficiencies (e.g., iron; folate; B12; vitamins A, D, E, and K).

Among the disorders that result in inadequate absorption of vitamin K from the intestinal tract are cystic fibrosis, celiac disease, Crohn disease, ulcerative colitis, dysentery, and extensive resection of bowel. Because drugs that reduce the bacterial population of the bowel are used frequently in many of these disorders, the availability of the vitamin may be further reduced. For immediate correction of the deficiency, parenteral vitamin K should be given.

 

Common causes of intestinal malabsorption.


COMMON CAUSES OF MALABSORPTION

Maldigestion: Chronic pancreatitis, cystic fibrosis, pancreatic carcinoma
Bile salt deficiency: Cirrhosis, cholestasis, bacterial overgrowth (blind loop syndromes, intestinal diverticula, hypomotility disorders), impaired ileal reabsorption (resection, Crohn’s disease), bile salt binders (cholestyramine, calcium carbonate, neomycin)
Inadequate absorptive surface: Massive intestinal resection, gastrocolic fistula, jejunoileal bypass
Lymphatic obstruction: Lymphoma, Whipple’s disease, intestinal lymphangiectasia
Vascular disease: Constrictive pericarditis, right-sided heart failure, mesenteric arterial or venous insufficiency
Mucosal disease: Infection (esp. Giardia, Whipple’s disease, tropical sprue), inflammatory diseases (esp. Crohn’s disease), radiation enteritis, eosinophilic enteritis, ulcerative jejunitis, mastocytosis, tropical sprue, infiltrative disorders (amyloidosis, scleroderma, lymphoma, collagenous sprue, microscopic colitis), biochemical abnormalities (gluten-sensitive enteropathy, disaccharidase deficiency, hypogammaglobulinemia, abetalipoproteinemia, amino acid transport deficiencies), endocrine disorders (diabetes mellitus, hypoparathyroidism, adrenal insufficiency, hyperthyroidism, Zollinger-Ellison syndrome, carcinoid syndrome)

Protein-losing enteropathy may result from several causes of malabsorption; it is associated with hypoalbuminemia and can be detected by measuring stool α1-antitrypsin or radiolabeled albumin levels. Therapy is directed at the underlying disease.

 

 

 

 

 

 

 

 

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.

 

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A

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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The correct answer is A. You answered A.

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 correct answer is A. You answered A.

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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