Confirming diagnosis Severely diminished or absent T-cell number and function, as well as lymph node biopsy showing absence of lymphocytes, can confirm diagnosis of SCID.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Salivation, increased [Polysialia, ptyalism]:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
A patient who complains of increased salivation may have overproductive salivary glands or difficulty swallowing. To distinguish these, first test for a gag reflex and observe the patient’s ability to swallow and chew. Is he drooling? Is his chewing uncoordinated? An impaired gag reflex, drooling, and chewing incoordination suggest difficulty swallowing. Does he have related signs and symptoms, such as fatigue, fever, headache, or a sore throat? Ask about exposure to industrial toxins, such as mercury. Is the patient taking any medications? Note especially use of iodides, cholinergics, and miotics.
Inspect the mouth and mucous membranes for lesions. If present, are they painful? Put on gloves and palpate the lesions, which may be suppurative or infectious. Describe them in your notes. Next, inspect the uvula, gingivae, and pharynx. Palpate the lymph nodes, and determine if the parotid glands are swollen or sore.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Tearing, increased [Epiphora]:
History and physical examination
(Professional Guide to Signs & Symptoms (Fifth Edition))
If the patient complains of increased tearing, begin by fully exploring this sign. When did it begin? Is it constant or intermittent? Minimal or extensive? Is increased tearing accompanied by pain, irritation, or any other eye drainage or discharge? Next, ask about recent eye trauma and about ocular and systemic disorders. Then record which drugs the patient is taking. Note his occupation and the nature of his work. For example, does he read extensively, look at a computer screen frequently, or work with small or fine objects? Is he exposed to any chemicals or dust in the workplace?
After taking vital signs, examine both eyes—unless the history suggests a perforating or penetrating injury. Carefully inspect the external structures. Do the eyelashes contain debris? Examine the eyelids for lesions and edema. Ask the patient to look straight ahead at a fixed object while you check for ptosis. Are the lid margins turned inward or outward? Examine the eyeballs. Do they appear sunken or bulging? Examine the conjunctivae for redness and abnormal drainage. Also, note the color of the sclera. Hold a flashlight at the side of each eye and examine the cornea and iris for scars, irregularities, and foreign bodies. Evaluate extraocular muscle function by testing the six cardinal fields of gaze. (See Testing extraocular muscles, page 245.) Finally, test the patient’s visual acuity.
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Source: Professional Guide to Signs & Symptoms (Fifth Edition), 2006
Common variable immunodeficiency:
Diagnosis
(Handbook of Diseases)
Characteristic diagnostic markers in this disorder include decreased serum immunoglobulin (Ig) M, IgA, and IgG detected by immunoelectrophoresis, along with a normal circulating B-cell count. Antigenic stimulation confirms an inability to produce specific antibodies; cell-mediated immunity may be intact or delayed. X-rays usually show signs of chronic lung disease or sinusitis.
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Source: Handbook of Diseases, 2003
Human immunodeficiency virus infection:
Diagnosis
(Handbook of Diseases)
The CDC defines AIDS as an illness characterized by one or more “indicator” diseases coexisting with laboratory evidence of HIV infection and other possible causes of immunosuppression. The CDC’s current AIDS surveillance case definition requires laboratory confirmation of HIV infection in people who have a CD4+ T-cell count of 200 cells/µl or who have an associated clinical condition or disease.
Antibody tests
The most commonly performed tests, antibody tests indicate HIV infection indirectly by revealing HIV antibodies. The recommended protocol requires initial screening of individuals and blood products with an enzyme-linked immunosorbent assay (ELISA). A positive ELISA should be repeated and then confirmed by an alternate method, usually the Western blot or an immunofluorescence assay. However, antibody testing isn’t always reliable. Because the body takes a variable amount of time to produce a detectable level of antibodies, a “window” varying from a few weeks to as long as 35 months in one documented case allows an HIV-infected person to test negative for HIV antibodies.
Antibody tests are also unreliable in neonates because transferred maternal antibodies persist for 6 to 10 months. To overcome these problems, direct testing is performed to detect HIV. Direct tests include antigen tests (p24 antigen), HIV cultures, nucleic acid probes of peripheral blood lymphocytes with determination of HIV-1 ribonucleic acid levels, and the polymerase chain reaction.
Other tests
Additional tests to support the diagnosis and help evaluate the severity of immunosuppression include CD4+ and CD8+ T-lymphocyte subset counts, erythrocyte sedimentation rate, complete blood count, serum beta2-microglobulin, p24 antigen, neopterin levels, and anergy testing. Because many opportunistic infections in patients are reactivations of previous infections, patients are also tested for syphilis, hepatitis B, tuberculosis, toxoplasmosis and, in some areas, histoplasmosis.
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Source: Handbook of Diseases, 2003
Severe combined immunodeficiency disease:
Diagnosis
(Handbook of Diseases)
Clinical indications point to the diagnosis. Most infants with SCID suffer recurrent overwhelming infections within 1 year of birth. Some are diagnosed after a severe reaction to vaccination.
Defective humoral immunity is difficult to detect before an infant is 5 months old. Before age 5 months, even normal infants have very small amounts of the serum immunoglobulins (Ig) IgM and IgA, and normal IgG levels merely reflect maternal IgG. However, severely diminished or absent T-cell number and function and lymph node biopsy showing absence of lymphocytes can confirm the diagnosis of SCID.
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Source: Handbook of Diseases, 2003
Hyper-aldosteronism:
Diagnosis
(Handbook of Diseases)
Persistently low serum potassium levels in a nonedematous patient who isn’t taking diuretics, doesn’t have obvious GI losses (from vomiting or diarrhea), and has a normal sodium intake suggest hyperaldosteronism.
If hypokalemia develops in a hypertensive patient shortly after starting treatment with potassium-wasting diuretics (such as thiazides), and if it persists after the diuretic has been discontinued and potassium replacement therapy has been instituted, evaluation for hyperaldosteronism is necessary.
A low plasma renin level that fails to increase appropriately during volume depletion (upright posture, sodium depletion) and a high plasma aldosterone level during volume expansion by salt loading confirm primary hyperaldosteronism in a hypertensive patient without edema.
The serum bicarbonate level is commonly elevated, with ensuing alkalosis due to hydrogen and potassium ion loss in the distal renal tubules.
Other tests show markedly increased urine aldosterone levels and increased plasma aldosterone levels. In secondary hyperaldosteronism, plasma renin levels are increased.
A suppression test is useful to differentiate between primary and secondary hyperaldosteronism. During this test, the patient receives desoxycorticosterone I.M. for 3 days while plasma aldosterone levels and urine metabolites are continuously measured. These levels decrease in secondary hyperaldosteronism but remain the same in primary hyperaldosteronism. Simultaneously, renin levels are low in primary hyperaldosteronism and high in secondary hyperaldosteronism.
Other findings include electrocardiogram signs of hypokalemia (ST-segment depression and flattened U waves), chest X-ray showing left ventricular hypertrophy from chronic hypertension, and localization of the tumor by adrenal angiography, computed tomography scans, or magnetic resonance imaging.
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Source: Handbook of Diseases, 2003
Hyper-parathyroidism:
Diagnosis
(Handbook of Diseases)
Findings differ in primary and secondary disease.
Primary disease
In primary disease, a high concentration of serum PTH on radioimmunoassay with accompanying hypercalcemia confirms the diagnosis. In addition, X-rays show diffuse demineralization of bones, bone cysts, outer cortical bone absorption, and subper-iosteal erosion of the phalanges and distal clavicles.
Microscopic examination of the bone with such tests as X-ray spectrophotometry typically demonstrates increased bone turnover. Laboratory tests reveal elevated urine and serum calcium, chloride, and alkaline phosphatase levels and decreased serum phosphorus levels.
Hyperparathyroidism may also raise uric acid and creatinine levels and increase basal acid secretion and serum immunoreactive gastrin. Increased serum amylase levels may indicate acute pancreatitis.
Secondary disease
Laboratory findings in secondary hyperparathyroidism show normal or slightly decreased serum calcium levels and variable serum phosphorus levels, especially when hyperparathyroidism is due to rickets, osteomalacia, or kidney disease. The patient history may reveal familial kidney disease, seizure disorders, or drug ingestion.
Other laboratory values and physical examination findings identify the cause of secondary hyperparathyroidism.
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Source: Handbook of Diseases, 2003
Hyper-lipoproteinemia:
Diagnosis
(Handbook of Diseases)
Diagnostic findings vary among the five types of hyperlipoproteinemia.
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Source: Handbook of Diseases, 2003
Salivation, increased:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
Ask the patient about related signs and symptoms, such as fatigue, fever, headache, or a sore throat. Also ask about exposure to industrial toxins such as mercury. Is the patient taking any medications? Note especially use of iodides, cholinergics, and miotics.
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
Tearing, increased:
History
(Signs & Symptoms: A 2-in-1 Reference for Nurses)
If the patient complains of increased tearing, begin by fully exploring this sign. When did it begin? Is it constant or intermittent? Minimal or extensive? Is increased tearing accompanied by pain or irritation? Is there any other drainage or discharge from the eye? Next, ask about recent eye trauma and about ocular and systemic disorders. Then record what drugs the patient is taking. Note his occupation and the nature of his work. For example, does he read extensively, look at a computer screen frequently, or work with small or fine objects. Is he exposed to any chemicals or dust in the workplace?
» READ BOOK EXCERPT ONLINE »
Source: Signs & Symptoms: A 2-in-1 Reference for Nurses, 2007
ALKALOSIS (INCREASED pH):
Approach to the Diagnosis
(Differential Diagnosis in Primary Care)
Taking a drug history and noting hyperventilation or vomiting during
the clinical evaluation will assist in the diagnosis. Serial electrolytes,
arterial blood gases, and drug screen are first-line laboratory tests to
assist in the diagnosis.
» READ BOOK EXCERPT ONLINE »
Source: Differential Diagnosis in Primary Care, 2007
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