Using loop diuretics (such as furosemide) and aminoglycoside antibiotics (such as gentamicin, tobramycin) together can increase the risk of damage to the inner ear leading to hearing loss.

• Open in Google Docs Viewer
• Open link in new tab
• Open link in new window
• Open link in new incognito window
• Download file
• Copy link address
• Edit PDF File on PDFescape.com

-noun Pharmacology .an antibiotic, C 2 1 H 3 9 N 7 O 1 2 , produced by a soil actinomycete, Streptomyces griseus, and used in medicine in the form of its white, water-soluble sulfate salt, chiefly in the treatment of tuberculosis.

Streptomycin is a water-soluble aminoglycoside derived from Streptomyces griseus. It is marketed as the sulfate salt of streptomycin. The chemical name of streptomycin sulfate is D-Streptamine, O-2-deoxy-2-(methylamino)-α-L-glucopyranosyl-(1→2)-O-5-deoxy-3-C-formyl-α-L-lyxofuranosyl-(1→4)-N,N1-bis(aminoiminomethyl)-,sulfate (2:3) (salt).The molecular formula for Streptomycin Sulfate is (C21H39N7O12)2-3H2SO4 and the molecular weight is 1457.41. It has the following structural formula:

Ibuprofen brand name: Advil, Children's Advil / Motrin, Medipren, Nuprin, Pediacare Fever etc.

Ibuprofen belongs to a class of drugs called non-steroidal anti-inflammatory drugs (NSAIDs). These drugs are used for the management of mild to moderate pain, fever, and inflammation. Prostaglandins are chemicals that are made by the body and are responsible for causing pain, fever and inflammation. Ibuprofen blocks the enzyme that makes prostaglandins (cyclooxygenase), resulting in lower levels of prostaglandins. As a consequence, inflammation, pain and fever are reduced.

Ibuprofen Drug Interactions

Ibuprofen is associated with several suspected or probable interactions that can affect the action of other drugs. Ibuprofen may increase the blood levels of lithium (Eskalith) by reducing the excretion of lithium by the kidneys. Increased levels of lithium may lead to lithium toxicity. Ibuprofen may reduce the blood pressure-lowering effects of drugs that are given to reduce blood pressure. This may occur because prostaglandins play a role in the regulation of blood pressure. When ibuprofen is used in combination with aminoglycosides (e.g., gentamicin) the blood levels of the aminoglycoside may increase, presumably because the elimination of aminoglycosides from the body is reduced. This may lead to aminoglycoside-related side effects. Individuals taking oral blood thinners or anticoagulants (e.g., warfarin) should avoid ibuprofen because ibuprofen also thins the blood, and excessive blood thinning may lead to bleeding.

Ibuprofen Side Effects

The most common ibuprofen side effects are rash, ringing in the ears, headaches, dizziness, drowsiness, abdominal pain, nausea, diarrhea, constipation and heartburn. Serious Ibuprofen side effect is ulceration of the stomach or intestine, and the ulcers may bleed. Sometimes, ulceration and bleeding can occur without abdominal pain, and black tarry stools, weakness, and dizziness upon standing (orthostatic hypotension) may be the only signs of a problem. Renal ibuprofen side effects include reduction of blood flow to the kidneys and impaired function of the kidneys. The impairment is most likely to occur in patients with preexisting impairment of kidney function or congestive heart failure, and use of ibuprofen in these patients should be done cautiously. People who are allergic to other NSAIDs, including aspirin, should not use ibuprofen. Individuals with asthma are more likely to experience allergic reactions to ibuprofen and other NSAIDs.

Hypomagnesemia means low levels of magnesium in the blood.

Low blood magnesium; Magnesium - low

Several conditions can cause hypomagnesemia, including:

• Alcoholism
• Chronic diarrhea
• High blood calcium levels
• Hyperaldosteronism
• Malabsorption
• Malnutrition
• Use of certain medications including amphotericin, cisplatin, and diuretics
• Excessive urination (polyuria)

Yu ASL. Disorders of magnesium and phosphorous. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007:chap 120.

Proximal renal tubular acidosis is a condition that occurs when the kidneys don't properly remove acids in the urine, leaving the blood too acidic.

Renal tubular acidosis - proximal; Type II RTA; RTA - proximal; Renal tubular acidosis type II

Your kidneys help regulate your body's acid-base balance (pH). Acidic substances in the body are buffered (counteracted) by alkaline substances, primarily bicarbonate.

The kidneys contain more than a million filtering units, called nephrons. Bicarbonate is reabsorbed into the blood in the initial (proximal) part of the tubule of each nephron. Proximal renal tubular acidosis (Type II RTA) occurs when bicarbonate is not properly reabsorbed by the proximal tubules, leaving the body in an acidic state (called acidosis).

Type II RTA is less common than Type I RTA. It most often occurs during infancy, and may go away by itself.

Causes of type II RTA include:

• Cystinosis
• Drugs such as ifosfamide (a chemotherapy drug), outdated tetracycline, aminoglycoside antibiotics, or acetazolamide
• Fanconi syndrome
• Inherited fructose intolerance
• Multiple myeloma
• Primary hyperparathyroidism
• Sjogren syndrome
• Wilson's disease

• Confusion or decreased alertness
• Dehydration
• Fatigue
• Increased breathing rate
• Osteomalacia
• Muscle pain
• Rickets
• Weakness

Other symptoms can include:

• Decreased urine output
• Increased heart rate or irregular heartbeat
• Muscle cramps
• Pain in the bones, back, flank, or abdomen
• Skeletal deformities

Arterial blood gas and blood chemistries may suggest metabolic acidosis and electrolyte imbalances, most often low levels of potassium or bicarbonate.

Other tests that may be done include:

• Blood pH level
• Urine pH
• Urinalysis may show abnormal levels of phosphate, calcium, glucose, and amino acids

This disease may also change the results of the following tests:

• Acid loading test (pH)
• Blood potassium level
• Urine calcium
• Urine citric acid
• Urine potassium level

The goal is to restore the normal pH (acid-base level) and electrolyte balance to the body. This will indirectly correct bone disorders and reduce the risk of osteomalacia and osteopenia in adults.

Some adults may need no treatment. All children need alkaline medication to prevent acid-induced bone disease, such as rickets, and to allow normal growth. The underlying cause should be corrected if it can be found.

Alkaline medications include sodium bicarbonate and potassium citrate. They correct the acidic condition of the body and correct low blood potassium levels. Thiazide diuretics may indirectly decrease bicarbonate loss but may worsen the low blood potassium levels.

Vitamin D and calcium supplements may be needed to help reduce skeletal deformities resulting from osteomalacia or rickets.

Although the underlying cause of proximal renal tubular acidosis may go away by itself, the effects and complications can be permanent or life-threatening. Treatment is usually successful.

• Electrolyte imbalances, such as hypokalemia
• Osteomalacia
• Rickets

Call your health care provider if you have symptoms of proximal renal tubular acidosis.

Get medical help immediately if you develop any of the following emergency symptoms:

• Decreased alertness or orientation
• Decreased consciousness
• Seizures

Most of the disorders that cause proximal renal tubular acidosis are not preventable.

Seifter JL. Acid-base disorders. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap 119.

Vertigo is a sensation of motion or spinning that is often described as dizziness.

Vertigo is not the same as light-headedness. People with vertigo feel as though they are actually spinning or moving, or that the world is spinning around them.

There are two types of vertigo:

• Peripheral vertigo occurs if there is a problem with the part of the inner ear that controls balance (vestibular labyrinth or semicircular canals) or with the vestibular nerve, which connects the inner ear to the brainstem.
• Central vertigo occurs if there is a problem in the brain, particularly in the brainstem or the back part of the brain (cerebellum).

Vertigo related to the inner ear may be caused by:

• Benign positional vertigo (also called benign paroxysmal positional vertigo)
• Drugs called aminoglycoside antibiotics
• Injury (such as head injury)
• Labyrinthitis
• Meniere's disease

Vertigo related to the vestibular nerve may be caused by:

• Inflammation (neuronitis)
• Nerve compression (usually a noncancerous tumor such as a meningioma or schwannoma)

Vertigo related to the brainstem may be caused by:

• Blood vessel disease
• Drugs (anticonvulsants, aspirin, alcohol)
• Migraine
• Multiple sclerosis
• Seizures(rarely)

The primary symptom is a sensation that you or the room is moving or spinning. With central vertigo, there are usually other symptoms from the condition causing the vertigo. Symptoms can include:

• Difficulty swallowing
• Double vision
• Eye movement problems
• Facial paralysis
• Slurred speech
• Weakness of the limbs

The spinning sensation may cause nausea and vomiting in some people.

A physical exam may reveal:

• Eye movement problems, involuntary eye movements (nystagmus)
• Lack of coordination and balance, difficulty walking
• Hearing loss
• Weakness

Tests to determine the cause of vertigo may include:

• Blood tests
• Brainstem auditory evoked potential studies
• Caloric stimulation
• EEG
• Electronystagmography
• Head CT
• Lumbar puncture
• MRI scan of head and MRA scan of blood vessels of the brain

Medications to treat peripheral vertigo may include:

• Anticholinergics (such as scopolamine)
• Antihistamines (such as meclizine)
• Benzodiazepines (such as diazepam or lorazepam)
• Promethazine (to treat nausea and vomiting)

Benign positional vertigo is most often treated with physical maneuvers that help reposition small structures in the semicircular canals of the inner ear. This reduces or stops the vertigo.

The cause of central vertigo should be identified and treated as appropriate.

Try to avoid head positions that cause vertigo. Use caution in situations such as driving, walking, or operating heavy equipment. Even short episodes of vertigo may be dangerous.

The outcome depends on the cause.

Persistent, unrelieved vertigo can interfere with driving, work, and lifestyle. It can also cause falls, which can lead to many injuries, including hip fractures.

Call for an appointment with your health care provider if vertigo is persistent or troublesome.

Baloh RW. Hearing and equilibrium. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap 454.

Bauer CA, Jenkins HA. Otologic symptoms and syndromes. In: Cummings CW, Flint PW, Haughey BH, et al., eds. Otolaryngology: Head & Neck Surgery. 4th ed. Philadelphia, Pa: Mosby Elsevier; 2005; chap 126.

Electronystagmography is a test to look at voluntary and involuntary eye movements. It evaluates the acoustic nerve, which runs from the brain to the ears (and control hearing and balance) and the occulomotor nerve, which runs from the brain to the eyes.

ENG

Patches called electrodes (similar to those used with ECG, but smaller) are placed above, below, and to the side of each eye. They may be attached by adhesive or by a band around the head. Another electrode is attached to the forehead.

The electrodes record eye movements that occur when the inner ear and nearby nerves are stimulated by delivering cold and warm water to the ear canal at different times. Sometimes, the test is done using air instead of water. Each ear is tested separately.

When cold water enters the ear, it should cause rapid, side-to-side eye movements called nystagmus. The eyes should move rapidly away from the cold water and slowly back. Next, warm water is placed into the ear. The eyes should now move rapidly toward the warm water then slowly away.

Patients may also be asked to use their eyes to track objects, such as flashing lights.

The electrodes detect the length and speed of eye movements, and a computer records the results.

The test takes about 90 minutes.

Electronystagmography provides exact measurements of eye movements detected by the electrical changes the movements produce. It is more objective than simply watching the eyes after flushing warm or cold water into the ears. It can record behind closed eyelids or with the head in a variety of positions.

No preparation is necessary. Check with your health care provider if you are taking any medications.

There is minimal discomfort. You may find cold water in the ear uncomfortable. Brief dizziness (vertigo) may occur during the test.

The test is used to determine whether a balance or nerve disorder is the cause of dizziness or vertigo.

Your doctor may order this test if you have dizziness or vertigo, impaired hearing, or suspected damage to the inner ear from certain medications.

Distinct involuntary eye movements should occur after instillation of warm or cold water into the ear canal.

Note: Normal value ranges may vary slightly among different laboratories. Talk to your doctor about the meaning of your specific test results.

Abnormal results may be a sign of damage to the nerve of the inner ear or other parts of the brain that control eye movements.

Any disease or injury that damages the acoustic nerve can cause vertigo. This may include:

• Blood vessel disorders with bleeding (hemorrhage), clots, or atherosclerosis of the blood supply of the ear
• Cholesteatomaand other ear tumors
• Congenital disorders
• Injury
• Medications that are toxic to the ear nerves, including aminoglycoside antibiotics, some antimalarial drugs, loop diuretics, and salicylates
• Multiple sclerosis
• Movement disorders such as progressive supranuclear palsy
• Rubella
• Some poisons

Additional conditions under which the test may be performed:

• Acoustic neuroma
• Benign positional vertigo
• Labyrinthitis
• Meniere's disease

There is a small risk associated with the caloric stimulation part of the test. Excessive water pressure can injure a previously damaged eardrum, but this rarely occurs. Caloric stimulation should not be performed if your eardrum has been perforated recently because of the risk of causing ear infection.

Griggs RC, Jozefowicz RF, Aminoff MJ. Approach to the patient with neurologic disease. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier. 2007: chap 418.

Acute tubular necrosis is a kidney disorder involving damage to the tubule cells of the kidneys, resulting in acute kidney failure.

Necrosis - renal tubular; ATN; Necrosis - acute tubular

Acute tubular necrosis (ATN) is caused by lack of oxygen to the kidney tissues (ischemia of the kidneys).

The internal structures of the kidney, particularly the tissues of the kidney tubule, become damaged or destroyed. ATN is one of the most common structural changes that can lead to acute renal failure.

ATN is one of the most common causes of kidney failure in hospitalized patients. Risks for acute tubular necrosis include:

• Blood transfusion reaction
• Injury or trauma that damages the muscles
• Recent major surgery
• Septic shock or other forms of shock
• Severe low blood pressure (hypotension) that lasts longer than 30 minutes

Liver disease and kidney damage caused by diabetes (diabetic nephropathy) may make a person more susceptible to the condition.

ATN can be caused by:

• Exposure to medications that are toxic to the kidneys (such as aminoglycoside antibiotics)
• Antifungal agents (such as amphotericin)
• Dye used for x-ray (radiographic) studies

• Decreased consciousness
  • Coma
  • Delirium or confusion
  • Drowsy, lethargic, hard to arouse
• Decreased urine output or no urine output
• General swelling, fluid retention
• Nausea, vomiting

Note: Other symptoms of acute kidney failure may also be present.

Examination usually indicates acute kidney failure. There may be signs of fluid overload, including abnormal sounds on listening to the heart and lungs with a stethoscope (auscultation).

Other signs include:

• BUN and serum creatinine levels may increase
• Fractional excretion of sodium and of urea may be relatively high
• Kidney biopsymay show acute tubular necrosis (but a biopsy is rarely done)
• Urinalysis may show casts, kidney tubular cells, and red blood cells
• Urine sodiummay be high
• Urine specific gravity and osmolarity urine indicate dilute urine

In most people, acute tubular necrosis is reversible. The goal of treatment is to prevent life-threatening complications of acute kidney failure during the time the lesion is present.

Treatment focuses on preventing the excess build-up of fluids and wastes, while allowing the kidneys to heal. Patents should be watched for deterioration of kidney function.

Treatment can include:

• Identifying and treating the underlying cause of the problem
• Restricting fluid intake to a volume equal to the volume of urine produced
• Restricting substances normally removed by the kidneys (such as protein, sodium, potassium) to minimize their buildup in the body
• Taking medications to help control potassium levels in the bloodstream
• Taking water pills (diuretics) to increase fluid removal from the kidney

Dialysis can remove excess waste and fluids. This can make you feel better, and may make the kidney failure easier to control. Dialysis may not be necessary for all people, but is often lifesaving, especially if serum potassium is dangerously high.

Dialysis may be needed in the following cases:

• Decreased mental status
• Fluid overload
• Increased potassium levels
• Pericarditis
• Total lack of urine production
• Uncontrolled buildup of nitrogen waste products

The duration of symptoms varies. The decreased urine output phase may last from a few days to 6 weeks or more. This is occasionally followed by a period of high urine output, where the healed and newly functioning kidneys try to clear the body of fluid and wastes.

One or two days after urine output rises, symptoms reduce and laboratory values begin to return to normal.

• Chronic renal failure
• End-stage renal disease
• Gastrointestinal loss of blood
• Hypertension
• Increased risk of infection

Call your health care provider if your urine output decreases or stops, or if you develop other symptoms of acute tubular necrosis.

Promptly treating conditions that can lead to decreased blood flow and/or decreased oxygen to the kidneys can reduce the risk of acute tubular necrosis.

Blood transfusions are crossmatched to reduce the risk of incompatibility reactions.

Control conditions such as diabetes, liver disorders, and cardiac disorders to reduce the risk of acute tubular necrosis.

Carefully monitor exposure to medications that can be toxic to the kidney. Have your blood levels of these medications checked regularly. Drink a lot of fluids after having any radiocontrast dyes to allow them to be removed from the body and reduce the risk of kidney damage.

Goldman L, Ausiello D. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders; 2007 Chapter 121