Introduction to Herpes zoster

Also called shingles, herpes zoster is an acute unilateral and segmental inflammation of the dorsal root ganglia caused by infection with the herpesvirus varicella-zoster, which also causes chickenpox. This infection usually occurs in adults. It produces localized vesicular skin lesions confined to a dermatome and severe neuralgic pain in peripheral areas innervated by the nerves arising in the inflamed root ganglia.
The prognosis is good unless the infection spreads to the brain. Eventually, most patients recover completely, except for possible scarring and, in corneal damage, visual impairment. Occasionally, neuralgia may persist for months or years.
Herpes zoster is found primarily in adults, especially those older than age 50. It seldom recurs.
Herpes zoster results from reactivation of varicella virus that has lain dormant in the cerebral ganglia (extramedullary ganglia of the cranial nerves) or the ganglia of posterior nerve roots since a previous episode of chickenpox.
Exactly how or why this reactivation occurs isn’t clear. Some believe that the virus multiplies as it’s reactivated and that it’s neutralized by antibodies remaining from the initial infection. However, if effective antibodies aren’t present, the virus continues to multiply in the ganglia, destroy the host neuron, and spread down the sensory nerves to the skin.
Signs and symptoms
Herpes zoster usually runs a typical course with classic signs and symptoms. Serious complications sometimes occur.

Onset of disease
Herpes zoster begins with fever and malaise. Within 2 to 4 days, severe deep pain, pruritus, and paresthesia or hyperesthesia develop, usually on the trunk and occasionally on the arms and legs in a dermatomal distribution. Pain may be continuous or intermittent and usually lasts from 1 to 4 Continue reading “Introduction to Herpes zoster”

Mastitis and breast engorgement

Mastitis (parenchymatous inflammation of the mammary glands) and breast engorgement (congestion) are disorders that may affect lactating females.

Mastitis occurs postpartum in about 1% of patients, mainly in primiparas who are breast-feeding. It occurs occasionally in nonlactating females and rarely in males. All breast-feeding mothers develop some degree of engorgement, but it’s especially likely to be severe in primiparas. The prognosis for both disorders is good.
Mastitis develops when a pathogen that typically originates in the nursing infant’s nose or pharynx invades breast tissue through a fissured or cracked nipple and disrupts normal lactation. The most common pathogen of this type is Staphylococcus aureus; less commonly, it’s Staphylococcus epidermidis or beta-hemolytic streptococci. Rarely, mastitis may result from disseminated tuberculosis or the mumps virus. Predisposing factors include a fissure or abrasion on the nipple; blocked milk ducts; and an incomplete let-down reflex, usually due to emotional trauma. Blocked milk ducts can result from a tight bra or prolonged intervals between breast-feedings.
Causes of breast engorgement include venous and lymphatic stasis and alveolar milk accumulation.
Signs and symptoms
Mastitis may develop anytime during lactation but usually begins 3 to 4 weeks postpartum with fever (101° F [38.3° C] or higher in those with acute mastitis), malaise, and flulike symptoms. The breasts (or, occasionally, one breast) become tender, hard, swollen, and warm. Unless mastitis is treated adequately, it may progress to breast abscess.
Breast engorgement generally starts with onset of lactation (day 2 to day 5 postpartum). The Continue reading “Mastitis and breast engorgement”

An Introduction to Epilepsy

Seizure disorder, or epilepsy, is a condition of the brain characterized by a susceptibility to recurrent seizures (paroxysmal events associated with abnormal electrical discharges of neurons in the brain). Epilepsy is believed to affect 1% to 2% of the population. The prognosis is good if the patient with epilepsy adheres strictly to his prescribed treatment.

In about one-half of all epilepsy cases, the cause is unknown. Possible causes include:
  • birth trauma (inadequate oxygen supply to the brain, blood incompatibility, or hemorrhage)
  • perinatal infection
  • anoxia
  • infectious diseases (meningitis, encephalitis, or brain abscess)
  • ingestion of toxins (mercury, lead, or carbon monoxide)
  • brain tumors
  • inherited disorders or degenerative disease, such as phenylketonuria or tuberous sclerosis
  • head injury or trauma
  • metabolic disorders, such as hypoglycemia and hypoparathyroidism
  • stroke (hemorrhage, thrombosis, or embolism).
Signs and symptoms
The hallmark of epilepsy is recurring seizures, which can be classified as partial, generalized, status epilepticus, or unclassified (some patients may be affected by more than one type).
Partial seizures
Arising from a localized area of the brain, partial seizures cause focal symptoms. These seizures are classified by their effect on consciousness and whether they spread throughout the motor strip, causing a generalized seizure. When simple or complex seizures evolve to both sides of the brain, they’re termed secondary generalized seizures.
A simple partial seizure begins locally and generally doesn’t cause an alteration in consciousness. It isn’t uncommon for this type to present with sensory symptoms (lights flashing, Continue reading “An Introduction to Epilepsy”

Special Considerations in Patients with Laryngeal cancer

Special considerations
  • Psychological support and good preoperative and postoperative care can minimize complications and speed recovery.
Before partial or total laryngectomy:
  • Instruct the patient to maintain good oral hygiene. If appropriate, instruct a male patient to shave off his beard.
  • Encourage the patient to express his concerns before surgery. Help him choose a temporary nonspeaking method of communication (such as writing).
  • If appropriate, arrange for a laryngectomee to visit him. Explain postoperative procedures (suctioning, nasogastric [NG] tube feeding, and care of laryngectomy tube) and their results (the need to breathe through the neck, altered speech). Also, prepare him for other functional losses: He won’t be able to smell, blow his nose, whistle, gargle, sip, or suck on a straw.
After partial laryngectomy:
  • Give I.V. fluids and, usually, tube feedings for the first 2 days postoperatively; then give the patient oral fluids. Keep the tracheostomy tube (inserted during surgery) in place until edema subsides.
  • Keep the patient from using his voice until he has medical permission (usually 2 to 3 days postoperatively). Then caution him to whisper until healing is complete.
After total laryngectomy:

Introduction to Laryngeal cancer

The most common form of laryngeal cancer is squamous cell carcinoma (95%); rare forms include adenocarcinoma, sarcoma, and others. Such cancer may be intrinsic or extrinsic.
An intrinsic tumor is on the true vocal cord and tends not to spread because underlying connective tissues lack lymph nodes. An extrinsic tumor is on some other part of the larynx and tends to spread early.
Gender and Age
Laryngeal cancer is nine times more common in males than in females; most victims are between ages 50 and 65.
With laryngeal cancer, major predisposing factors include smoking and alcoholism; minor factors include chronic inhalation of noxious fumes and familial tendency.

Laryngeal cancer is classified according to its location:
  • supraglottis (false vocal cords)
  • glottis (true vocal cords)
  • subglottis (downward extension from the vocal cords [rare]).
Signs and symptoms
With intrinsic laryngeal cancer, the dominant and earliest indication is hoarseness that persists longer than 3 weeks; with extrinsic cancer, it’s a lump in the throat or pain or burning in the throat Continue reading “Introduction to Laryngeal cancer”

Brief Summary of Otitis externa

otitis externaAlso known as external otitis and swimmer’s ear, otitis externa is an inflammation of the skin of the external ear canal and auricle. It may be acute or chronic, and it’s most common in the summer. With treatment, acute otitis externa usually subsides within 7 days (although it may become chronic) and tends to recur.
Otitis externa usually results from bacterial infection with an organism, such as Pseudomonas, Proteus vulgaris, streptococci, or Staphylococcus aureus; sometimes it stems from a fungus, such as Aspergillus niger or Candida albicans (fungal otitis externa is most common in the tropics). Occasionally, chronic otitis externa results from dermatologic conditions, such as seborrhea or psoriasis. Predisposing factors include:
  • swimming in contaminated water (cerumen creates a culture medium for the waterborne organism)
  • cleaning the ear canal with a cotton swab, bobby pin, finger, or other foreign objects (irritates the ear canal and may introduce the infecting microorganism)
  • exposure to dust, hair care products, or other irritants (causes the patient to scratch his ear, excoriating the auricle and canal)
  • regular use of earphones, earplugs, or earmuffs (traps moisture in the ear canal, creating a culture medium for infection)
  • chronic drainage from a perforated tympanic membrane.
Signs and symptoms

Acute otitis externa characteristically produces moderate to severe pain that’s exacerbated by manipulation of the auricle or tragus, clenching of the teeth, opening of the mouth, or chewing. Other signs and symptoms include fever, foul-smelling aural discharge, regional cellulitis, and partial hearing loss.
Fungal otitis externa may be asymptomatic, although A. niger produces a black or gray blotting paper–like growth in the ear canal. With chronic otitis externa, pruritus replaces pain, which may lead to scaling and skin thickening with a resultant narrowing of the lumen. An aural Continue reading “Brief Summary of Otitis externa”

Introduction to Osteoarthritis

Osteoarthritis, also known as hypertrophic osteoarthritis, osteoarthrosis, and degenerative joint disease, is the most common form of arthritis. A chronic disease, it causes deterioration of the joint cartilage and formation of reactive new bone at the margins and subchondral areas of the joints. This degeneration results from a breakdown of chondrocytes, usually in the hips and knees.
Osteoarthritis is widespread, occurring equally in both sexes until age 55. After age 55, incidence is higher in women. Incidence is after age 40; its earliest symptoms generally begin in middle age and may progress with advancing age.
The degree of disability depends on the site and severity of involvement; it can range from minor limitation of the fingers to severe disability in persons with hip or knee involvement. The rate of progression varies, and joints may remain stable for years in an early stage of deterioration.
Primary osteoarthritis, a normal part of aging, results from many things, including metabolic, genetic, chemical, and mechanical factors. Secondary osteoarthritis usually follows an identifiable predisposing event—most commonly trauma, congenital deformity, or obesity—and leads to degenerative changes.
Signs and symptoms
The most common symptom of osteoarthritis is a deep, aching joint pain, particularly after exercise or weight bearing, usually relieved by rest. Other symptoms include:
  • stiffness in the morning and after exercise (relieved by rest)
  • aching during changes in weather (joint pain in rainy weather)
  • “grating” of the joint during motion
  • altered gait contractures
  • limited movement.
These symptoms increase with poor posture, obesity, and occupational stress. Continue reading “Introduction to Osteoarthritis”

Lower Urinary tract infection

urinary tract infectionsCystitis and urethritis, the two forms of lower urinary tract infection (UTI), are nearly 10 times more common in women than in men and affect approximately 10% to 20% of all women at least once. Lower UTI is also a prevalent bacterial disease in children, with girls also most commonly affected.

In men and children, lower UTIs are frequently related to anatomic or physiologic abnormalities and therefore require extremely close evaluation. UTIs often respond readily to treatment, but recurrence and resistant bacterial flare-up during therapy are possible.
Most lower UTIs result from ascending infection by a single gram-negative enteric bacterium, such as Escherichia coli, Klebsiella, Proteus, Enterobacter, Pseudomonas, or Serratia. However, in a patient with neurogenic bladder, an indwelling urinary catheter, or a fistula between the intestine and bladder, lower UTI may result from simultaneous infection with multiple pathogens.
Infection may result from a breakdown in local defense mechanisms in the bladder that allow bacteria to invade the bladder mucosa and multiply. These bacteria cannot be readily eliminated by normal micturition.
The risk of cystitis is higher when the bladder or urethra becomes blocked and urine flow stops. It can occur when instruments are inserted into the urinary tract during procedures such as catheterization or cystoscopy. Other risks include pregnancy, diabetes, and a history of analgesic or reflux nephropathy. The elderly are at increased risk for developing UTIs due to incomplete emptying of the bladder; this is associated with conditions such as benign prostatic hyperplasia (BPH), prostatitis, and urethral strictures. Also, lack of adequate fluids, bowel incontinence, immobility or decreased mobility, indwelling urinary catheters, and placement in a nursing home all place the person at risk for developing an infection.
Bacterial flare-up
During treatment, bacterial flare-up is generally caused by the pathogenic organism’s resistance to the prescribed antimicrobial therapy. The presence of even a small number (less than 10,000/ml) of bacteria in a midstream urine sample obtained during treatment casts doubt on the treatment’s Continue reading “Lower Urinary tract infection”

Summary of Bladder cancer

Bladder tumors can develop on the surface of the bladder wall (benign or malignant papillomas) or grow within the bladder wall (generally more virulent) and quickly invade underlying muscles. Most bladder tumors (90%) are transitional cell carcinomas, arising from the transitional epithelium of mucous membranes. Less common are adenocarcinomas, epidermoid carcinomas, squamous cell carcinomas, sarcomas, tumors in bladder diverticula, and carcinoma in situ. Bladder tumors are most prevalent in men older than age 50 and are more common in densely populated industrial areas, but women are diagnosed at more advanced stages.

Certain environmental carcinogens—such as 2-naphthylamine, benzidine, tobacco, and nitrates—predispose people to transitional cell tumors. Thus, workers in certain industries (rubber workers, weavers, leather finishers, aniline dye workers, hairdressers, petroleum workers, and spray painters) are at high risk for such tumors. The period between exposure to the carcinogen and development of symptoms is about 18 years.
Squamous cell carcinoma of the bladder is most common in geographic areas where schistosomiasis is endemic. It’s also associated with chronic bladder irritation and infection (for example, from kidney stones, indwelling urinary catheters, and cystitis caused by cyclophosphamide).

Signs and symptoms
In early stages, about 25% of patients with bladder tumors have no symptoms. Commonly, the first sign is gross, painless, intermittent hematuria (often with clots in the urine). Patients with invasive lesions often have suprapubic pain after voiding. Other symptoms include bladder irritability, urinary frequency, nocturia, and dribbling.

Only cystoscopy and a biopsy can confirm bladder cancer. Cystoscopy should be performed when hematuria first appears. When it’s performed under anesthesia, a bimanual examination is usually done to determine if the bladder is fixed to the pelvic wall. A thorough history and physical examination may help determine whether the tumor has invaded the prostate or the lymph nodes.
The following tests can provide essential information about the tumor:

Drug abuse and dependence National Institute on Drug Abuse defines drug abuse and dependence as the use of a legal or an illegal drug that causes physical, mental, emotional, or social harm. Examples of abused drugs include narcotics, stimulants, depressants, anxiolytics, and hallucinogens.

Chronic drug abuse, especially I.V. use, can lead to life-threatening complications, such as cardiac and respiratory arrest, intracranial hemorrhage, acquired immunodeficiency syndrome, tetanus, subacute infective endocarditis, hepatitis, vasculitis, septicemia, thrombophlebitis, pulmonary emboli, gangrene, malnutrition and GI disturbances, respiratory infections, musculoskeletal dysfunction, trauma, depression, increased risk of suicide, and psychosis. Materials used to “cut” street drugs can also cause toxic or allergic reactions.

Drug abuse can occur at any age. Experimentation with drugs commonly begins in adolescence or even earlier. Drug abuse commonly leads to addiction, which may involve physical or psychological dependence or both. The most dangerous form of abuse occurs when users mix several drugs simultaneously—including alcohol.

Drug abuse commonly results from a combination of low self-esteem, peer pressure, inadequate coping skills, and curiosity. There is also evidence of familial patterns of addiction.
Most people who are predisposed to drug abuse have few mental or emotional resources against stress, an overdependence on others, and a low tolerance for frustration. Taking the drug gives them pleasure by relieving tension, abolishing loneliness, allowing them to achieve a temporarily peaceful or euphoric state, or simply relieving boredom.
Drug dependence may follow experimentation with drugs in response to peer pressure. It may also follow the use of drugs to relieve physical pain, but this is uncommon.
Signs and symptoms
Indications of acute intoxication vary, depending on the drug. Continue reading “Drug abuse and dependence”