Share Medical Knowledge

Varicella

sharemedicalexperience@gmail.com — Sun, 11 Apr 2010 14:43:29 PDT

Varicella or chickenpox is an acute disease caused by varicella-zoster virus (VZV) and characterized by generalized vesicular rash.

The incubation period is usually about 7- 14 days and this disease is known to be spread by direct contact. Airborne spread has also been demonstrated especially in hospitals.

Varicella is more common than other childhood diseases during the early months of life. After the first 2 weeks of life, the disease is generally mild. Maternal antibody transferred across the placenta may not be as effective in protecting infants against this disease as antibodies against other viruses.

Varicella is characterized by a generalized eruption that is centripetal in distribution with erythematous macules, papules, vesicles, and scabbed lesions. The vesicles are superficial, with varying amounts of erythema at their bases.

During the early phase of the eruption, lesions are found on the face, scalp, and trunk. Often, lesions can be detected in the scalp before their appearance on the skin by running the fingers through the hair. Later, new lesions appear on the extremities. By this time, the earlier lesions have dried and crusted. Excoriations are common, attesting to the pruritic nature of the lesions.

Mucous membranes of the conjunctiva and oropharynx are more frequently involved in adults than in children. New lesions continue to appear over a 3- or 4-day period, after which the rate of their appearance decelerates markedly.

Most children have a mild illness with few systemic complaints and an average maximal temperature of about 38.3° C. It is more common for adults to have considerable malaise, muscle ache, arthralgia, and headache. These may precede the first skin lesions by 24 to 48 hours.

The most common complication of Varicella is bacterial infections of the skin. The major complications of varicella in adults are encephalitis and pneumonia.

Infection produces a diffuse interstitial type of pneumonia with hypoxia resulting from poor diffusion of gases. Diffuse calcification of the lung parenchyma may be found years after recovery.

Encephalitis in childhood is most commonly manifested by a cerebellitis, which usually occurs at the end of the first week or during the second week after the onset of rash. This complication is almost always self-limited.

To help diagnose, serologic confirmation of the diagnosis can be made using a variety of techniques. The enzyme-linked immunosorbent assay (ELISA) and the latex agglutination assay are the most generally available. The laboratory director should be consulted regarding appropriate time of collection of specimens as well as interpretation of data.

Major therapeutic objectives are the prevention of superinfection and relief of pruritus. To relief pruritus can be accomplished frequently by application of calamine lotion. It is advisable to trim and file nails to reduce the damage from scratching. Bacterial superinfection can best be prevented by encouraging daily bathing with an antibacterial soap.

Relief of systemic symptoms may require additional medication such as acetaminophen, although this may increase pruritus.

Antiviral that usually used for adolescent and adults is acyclovir (800 mg per oral five times daily for 5-7 days).

Molluscum Contagiosum (Dimple Warts)

sharemedicalexperience@gmail.com — Thu, 18 Mar 2010 05:44:55 PDT

Molluscum contagiosum is a viral disease that caused pox virus family that clinically form papuls, and there are grooves on the surface with a mass contain molluscum bodies. Molluscum warts occur characteristically in small children and in young adults, although they may be seen occasionally in any age group. The incubation of this warts is estimated to vary from 14 days to 6 months.

This warts usually starts from single or small lesion and then spread wide to face, trunk, extremities. For Young adults more often present with lesions on the lower abdomen, pubic escutcheon, or inner thighs contracted during sexual transmission.

For children, molluscum warts are usually spread by close physical contact. Especially with their activities such as swimming in pool facilities, communal shower facilities, and contact sports.

For young adult, the most common of transmission is sexual contact.

For people with low immunity such as AIDs, Leukemia, people with chemotherapy, this warts can be the provoking factor too.

Histopathologic examination can help us to diagnose this disease. We can find molluscum bodies that contain virus particles from infected epidermis.

Patient should avoid communal swimming pools, baths, and shared clothing items. Because that activities can make contamination to other people.

The principle of treatment is to remove the mass containing molluscum bodies. We can use tools such as blackheads extractor, syringes, or curette. For young adults, should also be therapy for their sexual partner.

The most effective in adult cases is Light freezing with liquid nitrogen (LN2). This treatment useful, non scaring and must be repeated every 10 to 14 days until clear.

The prognosis of this disease better if all the lesions have been removed.

Acute Pancreatitis

sharemedicalexperience@gmail.com — Fri, 12 Mar 2010 05:02:24 PST

Acute pancreatitis is an inflammatory process arising in the exocrine pancreas, with variable involvement of peripancreatic tissues or remote organ systems. Incidence of acute pancreatitis from about 10 to 50 case per 100,000 per year.

Gallstone disease and alcoholism are the most common etiology of this disease in industrialized country. Other etiologies are infection (ascariasis, mumps, cytomegalo virus infection), hyperlipidemia, chronic hypercalcemia, abdominal trauma (blunt or penetrating), surgery.

Acute pancreatitis primary complain is abdominal pain (about 95%). The characteristic of this pain are epigastric location and radiates to the back in one-half to two-thirds of patients and usually worsened by ingesting food or alcohol or by vomiting. Patient usually assume a knee-to-chest position to relief their pain. Other symptoms are nausea, vomiting and distention of abdominal.

On examination, abdominal tenderness is usually present. It may be mild and limited to the epigastrium or marked, diffuse, and accompanied by abdominal rigidity and rebound tenderness.

Fever, tachycardia, tachypnea and hypotension manifest depend of the severity of this disease. Patient with biliary obstruction usually present icterus.

Serum amylase consentration has been used to diagnose acute pancreatitis for more than 70 years. But serum amylase levels may also be elevated in several conditions that can closely mimic acute pancreatitis (e.g., cholangitis, gastrointestinal perforation or ischemia, ruptured ectopic pregnancy).

Abdominal CT scan also has a great contribution to help us diagnose acute pancreatitis. Abdominal ultrasonography may be useful in determining whether gallstones are the cause of an episode of acute pancreatitis.

Providing supportive care, Decreasing pancreatic inflammation and preventing the complications are the goal of treatment. For mild acute pancreatitis, patient need full bed rest, intravenous hydration and electrolytes, analgesia to relief pain. For severy acute pancreatitis, patient usually need an intensive care unit with careful attention to monitoring of hemodynamics , urine output, and respiratory and renal function. Patients should initially be kept at bed rest with no oral intake, and large amounts of intravenous narcotic analgesics are typically needed for pain relief as well as nasogastric suction for treatment of severe ileus, nausea, and vomiting. Several pharmacologic agents have been tried to inactivate trypsin and other serine proteases, decrease pancreatic secretion and reduce inflammation.

The most lethal complication is hypovolemia shock due to transudation and exudation of fluid into the retroperitoneum and peritoneum.

Learning about Antrax

sharemedicalexperience@gmail.com — Fri, 05 Mar 2010 05:09:30 PST

Antrax isi zoonotic infection caused by Bacillus anthracis (an aerobic, nonmotile, gram-positive bacillus). Antrax causes human disease by way of direct animal contact or through exposure to contaminated animal hides, meat or other products. No human-to-human transmission has been demonstrated.

In 1979, in Sverdlovsk in the former Soviet Union, the largest known epidemic of inhalational anthrax occurred; it was later found to have been the result of an accidental release of anthrax spores from a military research facility.

Antrax can manifest to cutaneus type (the most cases), inhalational, oropharyngeal, gastrointestinal, sepsis, and meningeal disease. The cutaneus type is beginning as a nonspecific, erythematous, painless, pruritic papule or macule that appears after an incubation period of 3 to 4 days. This type is usually more severe on the neck or face than on the trunk or extremities. The vesicle subsequently ulcerates and forms a characteristic centrally depressed black chancre (or malignant pustule).

For inhalation type or wool sorter's disease, this disease begins with an influenza-like prodrome that lasts for 1 to 6 days, followed by sudden deterioration with dyspnea, strider, cyanosis, and hypoxemia. Spesific clinical manifestation of this type is widening of the mediastinum due to hilar adenopathy.

Laboratory confirmation can be made by demonstration of the causative organism in blood, tissue fluids, and exudates by direct microscopic examination and culture, or by animal inoculation. Another laboratory studies are ELISA, PCR and a rapid hand-held immunochromatographic assay.

Drug of choice of this disease is Penicillin that virtually eliminates the spread of cutaneous anthrax and essentially reduces the mortality rate to zero. Another alternative drugs are tetracycline, erythromycin, chloramphenicol, and ciprofloxacin.

To prevent Antrax, we should give vaccination of domestic livestock, prohibition of the slaughter of unvaccinated animals, and burning of animals suspected of having anthrax.

Brain Abscess

sharemedicalexperience@gmail.com — Wed, 03 Mar 2010 05:24:25 PST

Brain abscess affects the brain's parenchyma directly, whereas parameningeal infections produce suppuration in potential spaces covering the brain and spinal cord (epidural abscess and subdural empyema) or produce occlusion of the contiguous venous sinuses and cerebral veins (cerebral venous sinus thrombosis).

The condition that predispose to the development brain abscess are : otogenic (otitis media, mastoiditis), dental (dental abscess), penetrating or non penetrating head injury, cerebral infarction and tumor, post operative neurosurgical procedure, sinus (sinusitis), cardiac (infective endocarditis), pulmonary (lung abscess, bronchiectasis).

Clinical manifestation that usually present are fever, meningeal sign, increasing intracranial mass effect (nausea, depressed level of consciousness, and papilledema). Focal neurologic deficits depend on the site of the lesion, which in turn will be determined by the causal or predisposing condition. Headache is an important initial symptom in 80 to 90% of patients with bacterial abscess.

Examination of the cranium, ears, paranasal sinuses, oral cavity, heart, and lungs may provide important clues to the etiology. lumbar puncture is contraindicated for patients with signs of increased intracranial pressure. Cultures of blood and sputum may identify the organism and its antimicrobial sensitivity.

Magnetic resonance imaging (MRI) allows detection of early changes, such as brain edema, and is preferable to computed tomography (CT).

Brain abscess need urgent intervention. Because of the risk for cerebral herniation with large lesions, treatment of cerebral edema (intravenous dexamethasone) may be needed even while initiating surgical intervention.

Nonsurgical treatment may be considered in patients with : small lesion size, an already identified pathogen, no symptoms or signs of increased intracranial pressure requiring neurosurgical intervention, a deep or inaccessible lesion, multiple abscesses, a contraindication to surgery (e.g., a bleeding diathesis).

Factors associated with a poor prognosis include age, multiple abscesses, and diagnostic delay in the absence of systemic signs of infection.

Silicosis

sharemedicalexperience@gmail.com — Tue, 02 Mar 2010 06:52:46 PST

Silicosis refers to the parenchymal lung diseases associated with crystalline silica exposure, including acute, accelerated, and chronic or classic silicosis. For acute silicosis, an alveolar filling process follows heavy exposure within a few years. 5-10 years for accelerated silicosis and more than 10 years for chronic silicosis.

Free silica (SiO2), or crystalline quartz, is still a major occupational hazard. The major occupational exposures include: mining, employment in abrasive industries (e.g. stone, clay, glass, and cement manufacturing), packing of silica flour, stonecutting, foundry work.

People with acute silicosis presents with rapidly progressive dyspnea, they are also at increased risk for mycobacterial infection (with weight loss and fever manifestation).

The diagnosis of chronic silicosis is made on the basis of characteristic radiographic findings and history of employment in a job associated with exposure to silica-containing dust. But we must consider another differential diagnosis for lung masses such as lung cancer, mycobacterial infection.

The chest radiography of chronic silicosis shows small nodules that tend to predominate in the upper lobes. Calcification of the nodules is rare, as is so-called eggshell calcification of enlarged hilar nodes. In acute silicosis, we can find widespread consolidation in chest radiograph. CT may be helpful both in identifying nodules, which are preferentially located in the posterior aspect of the upper lobes, as well as in identifying larger opacities and more coalescence than might be noted on regular chest x-rays.

Treatment of silicosis are supportive therapy such as oxygen and rehabilitation. Diagnosis and treatment of mycobacterial infection also important, because silicosis can increase risk factor of this infection.

The prognosis of accelerated silicosis and acute silicosis is poor because of progressiveness loss of lung function. For chronic silicosis, it can lead to progressive impairment and respiratory failure.

Learning about Marfan Syndrome

sharemedicalexperience@gmail.com — Fri, 26 Feb 2010 22:37:33 PST

Marfan syndrome is caused by mutation in gene for structural molecules of the extracellular matrix especially fibrilin-1 (FBN1) on chromosome 15 that lead abnormalities in microfibrillar assembly and stability. This disease also reduce microfibrils in elastic or non elastic tissues.

Incidence of Marfan Syndroem is about 1 in 10,000 in most racial and ethnic groups. The disorder is inherited as an autosomal dominant trait. At least 25 percents of people wih Marfan Syndrome do not have an affected parent, and therefore probably represent new mutations.

The specific diagnoses of Marfan Syndrome will continue to be made in the clinic rather than the molecular genetics laboratory.

All of clinical manifestation depend on whether the molecular defect resides in a gene for collagen, fibrillin, elastin, or other matrix protein, the bones, ligaments, joints, blood vessels, eyes, or skin are affected to various degrees.

Clinical features are tall stature with long and thin extremities, low subcutaneous fat, arm span >8cm excess of height, arachnodactyly, long and narrow face, high arched palate, dental crowding, scoliosis, pectus excavatum or carinatum, pes planus, protrusion acetabuli, joint laxity. Treatment for this disorder are corrective surgery for scoliosis, orthodontia for dental crowding.

This syndrome also can manifest aneurysma dilatation of aorta ascending, aortic regurgitation, mitral valve prolapse, aortic dissection. The treatment for this manifestation are β-adrenergic blockade, composite aortic graft.

Another clinical features are ectopia lentis, myopia, flat cornea, retinal detachment. The treatment for this disorder are corrective lenses.

Post Traumatic Stress Disorder (PTSD)

sharemedicalexperience@gmail.com — Fri, 26 Feb 2010 04:52:26 PST

PTSD is a condition marked by the development of symptoms with duration more than a month after exposure to traumatic life events. People with this disorder will reacts to this experience with fear and helplessness, persistently relives the event, and tries to avoid being reminded of it. Their reaction significantly affect important area of life (e.g family, work).

This disorder usually arise from experiences in war, torture, natural catastrophes (tsunami, hurricane, earthquake), assault, rape, and serious accidents, for example, in cars and in burning buildings.

The National Comorbidity Study found that 60 percent of males and 50 percent of females had experienced some significant trauma. The mental status examination often reveals feelings of guilt, rejection, and humiliation. Patients may also describe dissociative states and panic attacks, illusions and hallucinations may be present. Associated symptoms can include aggression, violence, poor impulse control, depression, and substance-related disorders. Cognitive testing may reveal that patients have impaired memory and attention.

Keys to correctly diagnosing PTSD involve a careful review of the time course relating the symptoms to a traumatic event. PTSD is also associated with reexperiencing and avoidance of a trauma, features typically not present in panic or generalized anxiety disorder.

The major approaches for people with PTSD are support, encouragement to discuss the event, and education about a variety of coping mechanisms (e.g., relaxation). Sedatives and hypnotics drugs can also be helpful.

Learn about Breast Tumor in Teenage Girls

sharemedicalexperience@gmail.com — Thu, 25 Feb 2010 02:21:41 PST

If teenage girls and women during their early reproductive years found tumor in their breast. The first one we must think about Fibroadenoma mammae (FAM). Because Fibroadenoma is the most common breast tumor in this age. They are rarely seen in women after the age of 40 or 45. Fibroadenomas are benign solid tumors composed of stromal and epithelial elements. Clinically, they may increase in size over a period of several months. They easily palpable and may be lobulated form.

Fibroadenomas do not have malignant potential, although neoplasia may develop in the epithelial elements within them, just as in epithelium elsewhere in the breast. Cancer in a newly discovered fibroadenoma is exceedingly rare.

On excision, fibroadenomas are well-encapsulated masses that may detach easily from surrounding breast tissue. A tissue diagnosis is required to rule out malignancy.

Fibroadenoma has two subtypes. The first one is Giant Fibroadenoma that attains an unusually large size, typically greater than 5 cm. And latter is Juvenile Fibroadenoma that occurs in adolescents and young adults and histologically is more cellular than the usual fibroadenoma. Although these lesions may display remarkably rapid growth, surgical removal is curative.

Black Widow Spider Bites

sharemedicalexperience@gmail.com — Wed, 24 Feb 2010 05:26:20 PST

We can found Widow spiders (genus Latrodectus) throughout the world. At least one of five species inhabits all areas of the United States except Alaska. The most popular widow spider is the black widow (Latrodectus mactans).

Female spiders (Black widow) has a leg span of 1 to 4 cm and a shiny black body with a distinctive red ventral marking (often hourglass shaped). Variations in color occur among other species, some of them appearing brown or red and some without the ventral marking. The nonaggressive female widow spider bites in defense. Males are too small to bite through human skin.

Widow spiders produce neurotoxic venom with minimal local effects with major component is α-latrotoxin that acts at presynaptic terminals by enhancing release of neurotransmitters.

When they bite us, may be felt painless or felt as a “pinprick.” Local findings are minimal.

Neuromuscular symptoms may occur as early as 30 minutes after the bite such as :

· Severe pain and spasms of large muscle groups

· Abdominal cramps and rigidity

· Dyspnea as the result from chest wall muscle tightness

· Hypertension, diaphoresis, and tachycardia as the result of autonomic stimulation.

· Other symptoms : nausea, vomiting, headache, paresthesias, fatigue, and salivation.

· Symptoms usually peak at several hours and resolve in 1 to 2 days.

· Death is an unusual result of widow spider bites.

For mild bites, we can treat with local wound care such as cleansing, intermittent application of ice, and tetanus prophylaxis as needed. In some cases, we can use narcotics and benzodiazepines to relieve muscular pain.

In the United States, antivenom derived from horse serum is available (Black Widow Spider Antivenin, Merck & Co., West Point, PA). We must be careful use this antivenom because this antivenom can cause anaphylactoid reactions or serum sickness. So, before use antivenom, better we do skin testing for possible allergy. In some studies have demonstrated that antivenom can decrease hospital stay.

Sexual Sado-Masochism

sharemedicalexperience@gmail.com — Tue, 23 Feb 2010 01:07:58 PST

Sexual Sadism

The terminology of this disorder was named after the Marquis de Sade, an 18th century French author and military officer who was repeatedly imprisoned for his violent sexual acts against women.

Most persons with sexual sadism are male and before the age of 18 years.

Sadism is a defense against fears of castration; persons with sexual sadism do to others what they fear will happen to them and derive pleasure from expressing their aggressive instincts.

Sexual sadism is related to rape, although rape is more aptly considered an expression of power. Some sadistic rapists, however, kill their victims after having sex (so-called lust murders).

According to John Money, there are five contributory causes of sexual sadism :

· Hereditary predisposition

· Hormonal malfunctioning

· Pathological relationships

· History of sexual abuse

· The presence of other mental disorders.

DSM-IV-TR Diagnostic Criteria for Sexual Sadism :

A. Over a period of at least 6 months, recurrent, intense sexually arousing fantasies, sexual urges, or behaviors involving acts (real, not simulated) in which the psychological or physical suffering (including humiliation) of the victim is sexually exciting to the person.

B. The person has acted on these sexual urges with a nonconsenting person, or the sexual urges or fantasies cause marked distress or interpersonal difficulty.

Sexual Masochism

Masochism’s terminology from the activities of Leopold von Sacher-Masoch, a 19th century Austrian novelist whose characters derived sexual pleasure from being abused and dominated by women.

According to DSM-IV-TR, persons with sexual masochism have a recurrent preoccupation with sexual urges and fantasies involving the act of being humiliated, beaten, bound, or otherwise made to suffer.

Sexual masochistic practices are more common among men than among women.

Psychodynamic

SigmundFreud believed masochism resulted from destructive fantasies turned against the self.

In some cases, persons can allow themselves to experience sexual feelings only when punishment for the feelings follows. Persons with sexual masochism may have had childhood experiences that convinced them that pain is a prerequisite for sexual pleasure. About 30% of those with sexual masochism also have sadistic fantasies.

Moral masochism involves a need to suffer, but is not accompanied by sexual fantasies.

DSM-IV-TR Diagnostic Criteria for Sexual Masochism :

A. Over a period of at least 6 months, recurrent, intense sexually arousing fantasies, sexual urges, or behaviors involving the act (real, not simulated) of being humiliated, beaten, bound, or otherwise made to suffer.

B. The fantasies, sexual urges, or behaviors cause clinically significant distress or impairment in social, occupational, or other important areas of functioning.

Treatment

1. Psychotherapy

· Insight-oriented psychotherapy : to help them understand the dynamics of behavioral patterns. Supportive psychotherapy : to help them repair the interpersonal, social, or occupational damage that occurs.

· Cognitive behavioral therapy : helps them recognize dysphoric states that precipitate sexual acting out.

· Marital therapy or couples therapy : to help them regain self-esteem.

2. Pharmacotherapy

Prognosis

Because of the chronic course of sexual masochism and the uncertainty of its causes, treatment is often difficult. The fact that many masochistic fantasies are socially unacceptable or unusual leads some people who may have the disorder not to seek or continue treatment. Severe or difficult cases of sexual masochism should be referred to professionals who have experience treating such cases.

Prevention

Because it is sometimes unclear whether sadomasochistic behavior is within the realm of normal experimentation or indicative of a diagnosis of sexual masochism, prevention is a tricky issue. Often, prevention refers to managing sadomasochistic behavior so it primarily involves only the simulation of severe pain and it always involves consenting partners familiar with each other's limitations.

Wilms Tumor

sharemedicalexperience@gmail.com — Sat, 20 Feb 2010 03:39:55 PST

Definition

Wilms tumor is the most common primary malignant renal tumor of childhood and is the paradigm for multimodal management of a pediatric malignant solid tumor.

Epidemiology

The incidence of Wilms tumor is 10 cases per million among white children younger than 15 years, and the male to female ratio is low. The incidence is approximately three times higher for blacks in the United States and Africa than for eastern Asians.

Clinical Manifestation

• Abdominal swelling or abdominal mass (most common complain).
• Abdominal mass
• Gross hematuria
• Fever
• Hypertension (about 25% of cases).

Differential Diagnosis

• Splenomegaly
• Neuroblastoma (often arises in the celiac axis or extends across the midline because of lymph node involvement).

Imaging Studies

• Ultrasonography
The patency of the inferior vena cava.
• CT Scans of the abdomen with contrast
To evaluate the nature and extent of the mass, may suggest apparent extension of the tumor into adjacent structures, such as the liver, spleen, or colon.
• Plain chest radiographs, CT scans of chest
To determine whether pulmonary metastasis is present.
• Brain CT scans or MRI
For all children with clear cell sarcoma of the kidney or rhabdoid tumor of the kidney

Staging

Treatment

Surgery
• Surgical removal of the primary tumor remains the cornerstone of Wilms tumor therapy.
• Assessment of tumor spread at surgery is essential for accurate staging and for subsequent determination of the need for radiation therapy and administration of the appropriate chemotherapeutic regimen. Every effort must be made to remove the tumor without causing spread or spill.

Radiotherapy
• The National Wilms Tumor Studies have shown that patients with stage I and II tumors and favorable histologic findings who receive vincristine and actinomycin D do not need postoperative irradiation.

Chemotherapy
According to National Wilms Tumor Study Group findings, the chemotherapy regimens recommended for children with favorable histologic findings of Wilms tumor depend on tumor stage:
• Stage I or II, vincristine and actinomycin D for 18 weeks
• Stage III or IV, a combination of vincristine, actinomycin D, and doxorubicin for 21 weeks.

Prognosis

The most important determinant of prognosis :
• Tumor size
• Age of the patient
• Presence of lymph node metastasis
• Local features of the tumor, such as capsular or vascular invasion.

Bacterial Vaginosis

sharemedicalexperience@gmail.com — Fri, 19 Feb 2010 05:15:03 PST

Definition

Bacterial vaginosis (BV) has previously been referred to as nonspecific vaginitis or Gardnella vaginitis.

It is an alteration of normal vaginal bacterial flora that results in the loss of hydrogen peroxide producing lactobacilli and an overgrowth of predominantly anaerobic bacteria.

Anaerobic bacteria can be found in less than 1% of the flora of normal women. In women with Bacterial Vaginosis, however, the concentration of anaerobes, as well as Gardnerella vaginalis and Mycoplasma hominis, is 100 to 1,000 times higher than in normal women. Lactobacilli are usually absent.

Risk Factors

It is not known what triggers the disturbance of normal vaginal flora. It has been postulated that repeated alkalinization of the vagina, which occurs with frequent sexual intercourse or use of douches, plays a role. After normal hydrogen peroxide producing lactobacilli disappear, it is difficult to reestablish normal vaginal flora, and recurrence of Bacterial Vaginosis is common.

Diagnosis

It is diagnosed on the basis of the following findings :

· A fishy vaginal odor

· Vaginal discharge are present ( gray and thinly coat the vaginal walls).

· The pH of these secretions is higher than 4.5 (usually 4.7 to 5.7).

· Microscopy of the vaginal secretions reveals an increased number of clue cells, and leukocytes are conspicuously absent.

· The addition of KOH to the vaginal secretions releases a fishy, amine like odor.

· Culture of G. vaginalis is not recommended as a diagnostic tool because of its lack of specificity.

Complication

Women with Bacterial Vaginosis are at increased risk for :

· Pelvic inflammatory disease (PID)

· Post-abortal PID

· Postoperative cuff infections after hysterectomy

· Abnormal cervical cytology.

Pregnant women with Bacterial Vaginosis are at risk for :

· Premature rupture of the membranes (PROM)

· Preterm labor and delivery

· Chorioamnionitis

· Post-cesarean endometritis.

Treatment

The effective treatment are :

1. Metronidazole is the drug of choice for treatment of Bacterial Vaginalis.

This antibiotic with excellent activity against anaerobes but poor activity against lactobacilli.

Dose :

· Oral : 500 mg twice a day for 7 days.

· Gel : Metronidazolegel, 0.75%, one applicator (5 g) intravaginally once or twice daily for 5 days.

2. Clindamycin is effective regimen in treating Bacterial Vaginosis.

Dose :

· Oral : 300 mg twice daily for 7 days.

· Cream : Clindamycin 2% one applicator full (5 g) intravaginally at night before sleep for 7 days.

Treatment of the male sexual partner has not been shown to improve therapeutic response and therefore is not recommended

Anemia Aplastic

sharemedicalexperience@gmail.com — Thu, 18 Feb 2010 18:34:12 PST

Definition

Aplastic anemia is a disorder of hematopoiesis characterized by pancytopenia and a marked reduction or depletion of erythroid, granulocytic, and megakaryocytic cells in bone marrow.

In aplastic anemia, hematopoietic stem cells are unable to proliferate, differentiate, or give rise to mature blood cells and their precursors.

Etiology

1. Idiopatic : 50-65% cases.

2. Acquired :

· Drugs : antimetabolites, antimitotic agents, chloramphenicol, phenylbutazone, sulfonamides.

· Radiation

· Chemicals : benzene, solvents, insecticides.

· Viruses: non-A, non-B, non-C hepatitis, Epstein-Barr virus.

· Paroxysmal nocturnal hemoglobinuria.

· Miscellaneous: pregnancy, connective tissue disorders.

3. Hereditary :

· Fanconi anemia.

· Dyskeratosis congenital.

· Schwachman syndrome.

Clinical Manifestations

The most common initial symptoms of aplastic anemia are caused by anemia and thrombocytopenia:

· Progressive weakness

· Fatigue, headaches

· Dyspnea on exertion

· Petechia

· Ecchymoses

· Epistaxis

· Metrorrhagia

· Gum bleeding.

If the anemia is severe, the patient may be tachy-cardic and have cardiac murmurs associated with high-flow states. Hepatosplenomegaly and lymphadenopathy are notably absent.

Diagnostic Evaluation

The diagnosis of aplastic anemia should be considered if a pancytopenic patient :

· normochromic, normoc

ytic (or slightly macrocytic), and aregenerative anemia.

· Thrombocytopenia with normal-sized platelets.

· Neutropenia and no ab

normal cells in the leukocyte differential.

The absolute reticulocyte count is low because the anemia is secondary to reduced or absent red cell production.

Confirmation of the diagnosis requires morphologic and cytogenetic evaluation of the bone marrow (numerous spicules with empty fatty spaces and a few hematopoietic cells).

Differential Diagnosis

· hypocellular myelodysplastic syndrome.

· Hypocellular acute leukemia.

· Hairy cell leukemia.

Treatment

· Immunosuppressive Therapy

The treatment of choice for aplastic patients who lack a histocompatible sibling or are older than 40 years is ATG (40 mg/kg/day for 4 days) alone or in combination with cyclosporine (10 mg/kg/day divided into two doses, with dose adjustments as needed to maintain levels of 200 to 400 μg/mL for 3 to 6 months and then tapered over a period of 3 months).

· Allogeneic Hematopoietic Stem Cell Transplantation

The curative treatment for anemia aplastic is hematopoietic stem cell transplantation from an HLA-compatible sibling.

· Supportive Therapy

Red cell and platelet transfusions.

Prognosis

· The pancytopenia of aplastic anemia is progressive and life-threatening.

· The prognosis at diagnosis is closely correlated with the severity of neutropenia.

· The risk for infection (mainly bacterial and fungal) and associated mortality is high in patients with very severe aplastic anemia.

TRIAGE

sharemedicalexperience@gmail.com — Wed, 17 Feb 2010 00:26:57 PST

Definition

The term triage, derived from the French word meaning “to sort,” in its military application involves prioritizing victims into categories based on their severity of injury, likelihood of survival, and urgency of care.

The goal of civilian prehospital triage is to identify high-risk injured patients who would benefit from the resources available in a trauma center.

Goal

The ideal tool to accomplish these two divergent tasks does not exist. Assessment must be made quickly, often under difficult conditions with limited resources, and current schemes are of limited accuracy.

Although it is easy to identify patients with severe injuries based on abnormal physiology, a more difficult problem is identification of high-risk patients whose initial physiologic status is normal.

Perhaps the most useful currently available system is that advocated by the Committee on Trauma of the American College of Surgeons, which assesses four components simultaneously:

1. Physiologic response

2. Injury anatomy

3. Injury biomechanics

4. Comorbid factors.

The goal of a trauma system is to prevent unnecessary death, and thus a certain degree of over-triage is acceptable and even desirable.

Under-triage, however, is always to be avoided because the benefits of trauma center care are withheld from a patient who is thus misclassified. Many studies have tried to determine and adjust the optimal ratio of under- and over-triage. Conventional wisdom suggests that a 50% over-triage rate may be required to minimize under-triage.

Triage can take on differing forms as the situation demands. As medical care resources become limited, alternative triage schemes may be used so that the greatest number of patients may be treated.

Such schemes may be seen in situations of multiple or mass casualties. In these cases the “most good is applied to the greatest number of patients.” This is different from our present triage scheme, whereby the most seriously injured patient receives the majority of the medical care while the less seriously injured wait for care.

Classification

The military uses a triage scheme in which patients are classified for transport as immediate, delayed, or expectant.

The method of triage widely used by municipalities is the START triage scheme, which stands for simple triage and rapid treatment. This is accomplished by color tagging of patients.

· The color red is first priority and signifies a critical patient.

· Yellow (urgent) is second priority.

· Green (minor) is a third-priority patient.

· Black represents expectant or dead patients.

The initial triage assessment components include the ability of the patient to :

· Ambulate

· Respiratory function

· Systemic perfusion

· Level of consciousness.

Patients are classified into transport categories on the basis of these assessments.

Breast Cyst

sharemedicalexperience@gmail.com — Wed, 17 Feb 2010 00:21:36 PST

Definition

Cysts within the breast are fluid-filled, epithelium-lined cavities that may vary in size from microscopic to large, palpable masses containing as much as 20 to 30 mL of fluid.

Clinical Manifestation

· A palpable cyst develops in at least 1 in every 14 women, and 50% of cysts are multiple or recurrent. The pathogenesis of cyst formation is not well understood. However, cysts appear to arise from destruction and dilation of lobules and terminal ductules.

· Cysts are influenced by ovarian hormones, a fact that explains their variation with the menstrual cycle. Most cysts occur in women older than 35. The incidence of cyst development steadily increases until menopause and sharply declines thereafter. New cyst formation in older women is generally associated with exogenous hormone replacement.

Laboratory Findings

· A palpable mass can be confirmed to be a cyst by aspiration or ultrasound. Cyst fluid can be straw colored, opaque, or dark green and may contain flecks of debris. Given the low risk for malignancy within a cyst, if the palpable mass disappears completely after aspiration and the cyst contents are not grossly bloody, the fluid need not be sent for cytologic analysis.

· If the cyst recurs multiple times (more than two times is a reasonable rule), cytology is justified.

· Microscopic studies have shown that fibrosis at or near the lobule, combined with continued secretion, results in unfolding of the lobule and expansion of an epithelium-lined cavity containing fluid.

Treatment

· Aspiration

· Surgery

Surgical removal of a cyst is usually indicated if the cytologic findings are suspicious or the cyst recurs multiple times.

Herpes Zoster

sharemedicalexperience@gmail.com — Tue, 16 Feb 2010 14:07:35 PST

Definition

Herpes zoster is the recidivans form of varicella-zoster virus infection. The primary infection varicella or chickenpox most commonly occurs as an acute childhood exanthem.

The virus establishes latent infection in sensory ganglia at the base of the brain and spinal column. As the cell-mediated immune response conferred at the time of primary infection wanes, the disease increases in incidence. Certain provoking factors and concomitant illness are associated with attacks.

Onset

Zoster attacks may occur in children and young adults, but are quite rare.
Severe or prolonged attacks, especially in young persons, should raise concern about concomitant illness and immune status.

Provoking Factors

Immunosuppression, whether iatrogenic or secondary to disease.
Hemorrhagic zoster lesions or zoster of unusual severity in a young host should raise suspicion of underlying disease such as lymphoma, hematologic malignancies, or HIV disease.
Physical trauma to infected sensory ganglia, and occasionally to peripheral nerves, can trigger attacks.
Radiation therapy of solid tumors and spinal manipulation are among the other common causes.

Clinical Manifestation

Most cases of herpes zoster present with pain that is variously described as shock-like or a continuous burning sensation with hyperalgesia. Other patients experience less intense but equally uncomfortable crawling or pruritic parasthesias, and find that even fabric touching the area is intolerable.
Within 2 or 3 days, and rarely as long as a week, skin lesions develop within the anatomic area of the involved nerve segment. These lesions, like those of herpes simplex virus (HSV), consist of tightly grouped vesicles on an erythematous, urticarial base. The lesions are usually more extensive than those of HSV and may be continuous or, more often, exhibit skip areas within the neurologic segment.
Mild constitutional symptoms of fatigue and lassitude may precede the skin lesions, but fever is rare.
Uncomplicated zoster in children usually is mild and often painless. It can run its entire course in 2 weeks or less, and normally clears without sequelae. In young adults, the average course is 2 to 3 weeks long, pain is mild to moderate, and sequelae are rare.

The following anatomic locations are most frequently involved:

· Thoracic dermatomes 53%

· Cervical dermatomes 20%

· Trigeminal nerve 15%

· Lumbosacral dermatomes 11%

Dermatologic Physical Exam

Primary Lesions

1. Erythematous urticarial plaque or plaques within a dermatome segment or contiguous dermatomes.

2. Grouped 3- to 5-mm vesicles that evolve and often umbilicate.

3. Pustules that replace vesicles as the lesions mature.

Secondary Lesions

1. Erosions as blisters and pustules rupture.

2. Crusting as pustules dry and shrink or due to secondary infection.

3. Hemorrhage into vesicles.

4. Necrosis and gangrene in severe lesions having an active vascular component.

5. Postinflammatory hyperpigmentation, common even in uncomplicated zoster.

6. Scarring, more common in older patients or in zoster that is associated with underlying systemic disease.

Distribution

Microdistribution: None.

Macrodistribution: Follows a dermatome segment or contiguous neural segments.

Laboraotry studies

Tzanck Smear

· A smear of material from a fresh ruptured blister base is placed on a glass slide and immediately stained with Giemsa or some similar stain.

· A positive smear will show herpesvirus effect by the presence of keratinocytes with balloon nuclei and multinucleated giant cells with similar changes.

· This test is rapid and inexpensive, and can be performed with equipment that is readily accessible.

· Sensitivity, in experienced hands, from a fresh vesicle approaches or exceeds 70%.

Biopsy

· Biopsy of a zoster lesion shows pathognomonic features, but is usually done only to investigate a lesion that is clinically atypical.

· Biopsy does not distinguish HZV from HSV- 1 or HSV-2, and adds nothing if the lesions are clinically diagnostic.

Complement Fixation Tests

· These titers rise rapidly following onset, and are useful in atypical infections.

Viral Culture

· Although culture is very specific and will distinguish HZV from HSV-1 and HSV-2, sensitivity is low (50% or less).

· Cultures may be used to confirm the diagnosis in unusual cases. In otherwise clinically typical cases, culture is unnecessary and the diagnosis can usually be confirmed by Tzanck smear or RIF test.

Rapid Immunofluorescence Test (RIF) for Herpes

· This test employs a monoclonal antibody system and exhibits a sensitivity of about 65%.

· In addition to speed, RIF can distinguish among HZV, HSV-1, and HSV-2.

· The specimen consists of a smear from a blister, and the test is practical and reproducible. Results are available in 1 hour or less after receiving the specimen.

Polymerase Chain Reaction (PCR)

· PCR testing performed from blister specimens shows a sensitivity of 97%, which is superior to culture.

· PCR is rapid and can distinguish HZV from HSV-1 and HSV-2.

· It is positive when performed from crusts and material from involuting lesions where culture, Tzanck, and RIF results are less reliable.

· The technology is expensive and not universally available at present.

Complications

Generalized zoster

In addition to the problems associated with the special forms reviewed above, one of the most serious complications is generalized herpes zoster. Many patients will develop a few scattered lesions that are out of the primary neurologic segment. When extensive lesions occur along with fever and systemic toxicity, however, it is an indication of general viremia.

Postherpetic neuralgia (PHN)

It is the most common complication of herpes zoster. The incidence peaks in patients in their sixth and seventh decades, probably due to more severe attacks and lowered capacity to regenerate after nerve injury.

Pain or altered nerve function persisting more than 30 days after the onset of skin lesions is considered PHN. Of those with persisting pain or altered sensation, a large number gradually improve and clear over several months. Lancinating pain, hyperalgesia, and crawling dysesthesias are most common.

Other rare complications:

Encephalitis
Myelitis
Cranial/peripheral nerve palsies
Delayed contralateral hemiparesis
Acute retinal necrosis

Therapy

· Analgetic : NSAID (e.g. mefenamic acid 500 mg, indometasin 25 mg three times a day or ibuprofen 400 mg three times a day)

· Phenol-zinc lotion for vesicular phase.

· Acyclovir 800 mg five times a day for one week on early phase. Or another anti viral (e.g famcyclovir, valacyclovir).

· Antibiotic : for secondary infection

Postherpetic neuralgia (PHN) :

· Fenol 3-5% cream 2-6 times a day.

· Amitriptilin 10-25 mg/night or gabapentin 100-300 mg/day.

Obesity in Children

sharemedicalexperience@gmail.com — Tue, 16 Feb 2010 13:04:30 PST

Defintion

The definition of obesity is individuals whose body mass index (BMI) (weight in kilograms divided by the square of the height in meters; kg/m²) exceeds the age-gender-specific 95th percentile.

Etiology

Multifactorial :

· Genetic background

· Environmental stimuli

· Developmental processes.

An important factor in maintenance of body weight is the relationship between body weight and total energy expenditure.

Clinical Manifestations

In children, obesity is most often associated with tall stature, slightly advanced bone age, and somewhat early puberty. In most patients with obesity, rapid growth in height precludes the diagnosis of hypothyroidism and hypercortisolism. By contrast, hypothyroidism and cortisol excess cause delayed skeletal development, short stature, and delayed puberty. Many obese youth also have acanthosis nigricans, a hypertrophic hyperpigmentation of the skin most commonly seen on the posterior neck and in skin creases. This condition is associated with insulin resistance and a higher risk of developing type 2 diabetes.

Laboratory Findings, Diagnosis, and Differential Diagnosis

· Obesity can be diagnosed in most cases by simple inspection of the patient. If needed, BMI can be plotted on BMI growth curves to identify those who are over the 95th percentile. Early identification of children at risk includes the demonstration of early adiposity rebound.

· The most important tests in the evaluation and follow-up of obese patients are those that evaluate cardiovascular disease risk and diabetes risk. These include plasma lipid profiles, fasting glucose and insulin levels, and hemoglobin A1C. It may also be necessary to perform studies to test for sleep apnea.

· Hypothyroidism and hypercortisolemia can be ruled out by demonstrating normal free thyroxine and thyroid-stimulating hormone levels and 24 hr urinary free cortisol or diurnal salivary cortisol levels.

· If patients have severe early-onset obesity, out of proportion to the family history, one of the single gene defects mentioned earlier may need to be considered.

Complication

Obesity-associated co-morbidities include significantly increased risks for :

· Diabetes Mellitus

· Cardiovascular disease

· Cancer

· Respiratory disease (asthma, sleep apnea)

· Infertility

· Degenerative joint disease

· Proteinuria

· Depression

· Anxiety

· Discrimination both in social life and in the workplace.

Prevention

· Increasing physical activity.

· Changing dietary habits.

Treatment

Behaviour

· Reduction of dietary calories and fat

Diets that are lower in carbohydrates may be useful in some individuals, but the basic goal should be reduction in energy intake and increase in energy expenditure.

· Increasing dietary fiber.

· Increase in physical activity (regular aerobic exercise, decrease in television viewing and computer games).

Medication

Anti-obesity drugs are not approved for prolonged use or for use in youth.

The major classes of drugs are :

· Reduce food intake (monoamine oxidase inhibitors, sympathomimetic drugs)

· Increase energy expenditure (ephedrine, caffeine)

· Inhibit fat absorption (orlistat).

Surgery

Surgical therapy to reduce the volume of the stomach may be successful in the long term in some patients. Procedures to bypass the absorptive surfaces of the intestine have been associated with many complications, the most predictable being nutritional deficiencies.

Surgery to remove fat (liposuction), if used alone, is not a long-term solution. However, it may be a useful cosmetic adjunct in patients who are successful with diet and exercise, with or without surgical gastroplasty.

Poison

sharemedicalexperience@gmail.com — Tue, 16 Feb 2010 02:09:19 PST

Definition

•Any substance that causes injury or illness or death of a living organism

•Anything that harms or destroys

•Advantages:

–Stealth

–Separation from criminal to victim

–Difficulty identifying criminal who administered

–May be disguised as a natural cause of death

Who uses poison?

•Chemicals may be hard to come by:

–Only professionals who have access

–Doctors, Pharmacists, etc

•Accidental poisoning

–Mistakes of prescription medication

–Accidental ingestion of household chemicals

•Suicide

–Example: Normal medications taken in excess

Accidental Poisons

•Some chemicals are too easily detected to be used for murder

•These are usually found in accidental deaths

•Household Chemicals:

–Strong acids (ex. Battery Acid)

–Strong bases (ex. Drano)

•However some criminals still use acids to try to destroy evidence/body

Accidental Poisons

•Disinfectants

–Lysol

•Gardening Supplies

–Slug killing chemicals

•Carbon Monoxide

–By-product of incomplete combustion

–Replaces the oxygen in the blood

–Causing person to fall unconscious

Suicides

•Many suicides use prescription medications taken in excess

•Especially drugs that will knock person unconscious so that they don’t have too much pain:

–Choral hydrate

–ASA –used for anesthesiology

•CO piped in from a car exhaust

–Causes the person to fall unconscious

Identifying CO Poisoning

•Carbon Monoxide poisoning easily recognized

•Carboxy-hemoglobin in blood turns:

–Skin

–Internal organs

•Bright cherry red

•Evidence lasts even months after death

•If body is not found –cause of death can still be determined

Murderers’Poisons

Murderer wants the following:

•Poison to be lethal

•To happen at time or place that is separate from criminal activity

–Can have an alibi

•Produce symptoms that suggest a natural cause of death

•Not be traceable to the specific murderer

Natural Poisons

Hemlock

•Conium maculatum –known as Hemlock

•Symptoms look like suffocation

•Socrates’suicide

Aconitine

•Extracted from Monkshood

•Paralyzes the body’s organs

•Heart failure or lung failure

Atropine

•Extracted from nightshade

•Headaches to hallucinations

•Eventually coma

•Heart or respiratory failure

•Dilates the eyes:

–This is evidence of atropine poisoning

–Also used in very small doses for some eye treatments

Strychnine

•Extracted from Strychnos nux-vomica

•Extremely bitter tasting

•Violent muscle contractions

•Jaw paralysis renders victim speechless

–Muscles draw back into “grin”

•Death caused by paralysis of lungs

•Was mistaken for tetanus or epilepsy

Chemical Poisons

Thallium

•Metal salt

–Dissolves into water invisibly and tastelessly

•Symptoms look the same as:

–Muscle weakness, the flu or just old age

•Death by internal organ damage over time

•Victim’s hair will fall out

Antimony

•Elemental metal

•Symptoms look same as:

–Stomach sicknesses/infections

•Stomach pain, loss of appetite, painful cramps and diarrhea

•Eventually convulsions and heart failure

Cyanide

•Organic chemical:

–Carbon and Nitrogen

•Works the same as carbon monoxide

–Starving the blood of oxygen

•Works in a matter of minutes

–Much faster than CO

•Distinct almond smell and very bitter taste

Arsenic

•Elemental metal

•Symptoms similar to:

–Extreme food poisoning

–Cholera or Dysentery

•Headaches, confusion, convulsions

•Traces are evident in all body parts

–Even years after poison was administered

Medicinal Drugs

Morphine

•Derived from Opium

•Depresses the CNS –blocks pain

•Overdose may lead to respiratory failure

Heroin

•Also derived from Opium

•Overdose will lead to the heart stopping

Also –Codeine, Demerol, Vicoden

Depressants

Alcohol

•Relaxation, euphoria, drowsiness

•Alcohol Poisoning

–Confusion, Seizures, even death

•More commonly:

–Choke on vomit while passed out/asleep

Barbiturates/Tranquilizers

•Same symptoms and problems

Stimulants

Cocaine

•Stimulating the CNS

•Feelings of confidence, energy, excitement

•Give way to dread, paranoia and fatigue

•Death from heart failure

Amphetamines

•Same symptoms and problems

Forensic Tests

•Begin with a sample of victim’s blood, urine or tissue

•Screening tests:

–Check rapidly for wide variety of drugs or poisons

•Identify exact substance:

–Gas or liquid chromatography

–Immune based assays

–Mass spectrometry

Gas Chromatography (GC)

•Liquid sample is injected into machine and vaporized into a gas

•Sample travels through a column at different speeds depending on its size and chemical composition

•How long it takes to travel through column is noted:

–Each component is identified

•Exact chemical can be identified by its different components

Liquid Chromatography (HPLC)

•Liquid sample is placed onto a gel or film

•Solvents are added to see how different components of sample will move through gel/film with different solvents

•Examine each component’s banding pattern on gel/film:

–Each component is identified

•Exact chemical can be identified by its different components

Immuno-assays

•Using an antibody that is raised against that specific drug/chemical compound

•Raise antibodies in an animal model

–Administering drug/compound to animal

•Then add antibodies to test sample:

–Either of pure drug

–Or of blood, urine or tissue

•If antibodies react then drug is present

•VERY specific test

Mass Spectrometry

•Every compound has a very specific pattern on a Mass Spec

•Put compound into Mass Spec

•Bombard with stream of electrons

•Component will break up and produce a very specific pattern of light

•Every known drug/poison/atom/chemical has a known mass spec pattern

Drug Identification

•If drugs are found at the scene

•Can be tested and identified quickly

•Glass tubes with treated crystals that will react to specific illegal drugs

•Add a small sample of the drug in question and watch for specific reaction/color change in the tube

•Sort of similar to a breathalyzer for alcohol

–Only done on the drug not the person

Migraine

sharemedicalexperience@gmail.com — Mon, 15 Feb 2010 15:35:20 PST

Definition

Migraine is a periodic headache often accompanied by nausea and sensitivity to light and noise (photophobia and phonophobia).

A typical attack consists of a prodromal phase of warning (premonitory) symptoms, followed by an aura, the actual headache phase, and a resolution phase.

Attack characteristics often change over time. Attacks often tend to occur in the morning or evening but may occur at any time. They typically last 4–72 hours.

Symptoms and Signs

Prodromal phase

The migraine attack may be preceded by a period of variable prodromal phenomena lasting a few hours to two days.
Most patients complain of sensitivity to smells and noise, irritability, restlessness, drowsiness, fatigue, lack of concentration, depression, and polyuria.
In children, the chief complaints are abdominal pain and dizziness.

Aura

This is the period preceding the focal cerebral symptoms of the actual migraine headache.
Some patients experience attacks without an aura (common migraine), while others have attacks with an aura (classic migraine) that develops over 5–20 minutes and usually lasts less than one hour, but may persist as long as one week (prolonged aura).

Auras typically involve :

Visual disturbances, which can range from undulating lines (resembling hot air rising), lightning flashes, circles, sparks or flashing lights (photopsia), or zig-zag lines (fortification figures, teichopsia, scintillating scotoma). The visual images, which may be white or colored, cause gaps in the visual field and usually have scintillating margins.
Unilateral paresthesiae (tingling or cold sensations) may occur.
Emotional changes (anxiety, restlessness, panic, euphoria, grief, aversion) of variable intensity are relatively common.

Headache phase

Most patients (ca. 60%) complain of pulsating, throbbing, or continuous pain on one side of the head (hemicrania).
Others have pain in the entire head, particularly behind the eyes (“as if the eye were being pushed out”), in the nuchal region, or in the temples.
Migraine headache worsens on physical exertion and is often accompanied by anorexia, malaise, nausea, and vomiting.

Resolution phase

This phase is characterized by listlessness, lack of concentration, and increased pain sensitivity in the head.

Pathogenesis

During the interval between attacks, various disturbances (genetically determined) may be observed, e. g., cerebral hypomagnesemia, elevated concentration of excitatory amino acids (glutamate, aspartate), and increased reactivity of cranial blood vessels. The cumulative effect of

these disturbances is a heightened sensitivity to nociceptive stimuli (migraine pain threshold).

Impulses from the cortex, thalamus, and hypothalamus activate the so-called migraine center responsible for the generation of migraine attacks, putatively located in the brain stem.

The migraine center triggers cortical spreading depression (suppression of brain activity across the cortex) accompanied by oligemia, resulting in an aura. Trigeminovascular input from meningeal vessels is relayed to the brain stem, via projecting fibers to the thalamus and then, by the parasympathetic efferent pathway, back to the meningeal vessels (trigeminal autonomic reflex circuit). Perivascular trigeminal C-fiber endings (trigeminovascular system) are stimulated

to release vasoactive neuropeptides such as substrate P, neurokinin A, and calcitonin gene-regulated polypeptide (CGRP), causing a (sterile) neurogenic inflammatory response. Vasoconstriction and vascular hyperesthesia with subsequent vasodilatation spread via trigeminal axon reflexes. The perception of pain is mediated by the pathway from the trigeminal nerve to the nucleus caudalis, thalamus (p. 94) and cortex. Trigeminal impulses also reach autonomic centers.

Treatment

Good patient–physician communication is essential for the diagnosis and treatment of headache. The most important clues to differential diagnosis are derived from the case history. The medication history must be obtained, and psychological factors must also be considered headache is often associated with anxiety, e. g., fear of a brain tumor, of a mental illness, or of not having one’s complaints taken seriously.

Acute Migraine

General measures

Rest, ice packs

Pharmacotherapy

Antiemetic (metoclopramide or domperidone)
Aspirin or acetaminophen
Triptans (if ineffective)

Prophylaxis

General measures

Behavioral therapy

Pharmacotherapy

1st line: Beta-blockers (e. g., metoprolol, propranolol);
2nd line: flunarizine or valproate;
3rd line: methysergide or pizotifen

Appendicitis

sharemedicalexperience@gmail.com — Mon, 15 Feb 2010 12:45:41 PST

Pathophysiology

Obstruction of the lumen is the major cause of acute appendicitis. This may be due to fecalith or appendicolith, lymphoid hyperplasia, vegetable matter or seeds, parasites, or a neoplasm. The lumen of the appendix is small and this configuration may predispose to closed-loop obstruction. Obstruction of the lumen contributes to bacterial overgrowth, and continued secretion of mucus leads to intraluminal distention and increased wall pressure. Luminal distention produces the visceral pain sensation experienced by the patient as periumbilical pain. Subsequent impairment of lymphatic and venous drainage leads to mucosal ischemia. These findings in combination promote a localized inflammatory process that may progress to gangrene and perforation. Inflammation of the adjacent peritoneum gives rise to localized pain in the right lower quadrant. Although there is considerable variability, perforation typically occurs after at least 48 hours from the onset of symptoms and is accompanied by an abscess cavity walled-off by the small intestine and omentum. Rarely, free perforation of the appendix into the peritoneal cavity occurs that may be accompanied by peritonitis and septic shock and can be complicated by the subsequent formation of multiple intraperitoneal abscesses.

Diagnosis
History

The typical presentation begins with periumbilical pain (due to activation of visceral afferent neurons) followed by anorexia and nausea. The pain then localizes to the right lower quadrant as the inflammatory process progresses to involve the parietal peritoneum overlying the appendix. This classic pattern of migratory pain is the most reliable symptom of acute appendicitis.
Fever ensues, followed by the development of leukocytosis. These clinical features may vary.
Although most patients with appendicitis develop an adynamic ileus and absent bowel movements on the day of presentation, occasional patients may have diarrhea. Others may present with small bowel obstruction related to contiguous regional inflammation.

Physical Examination

Patients with acute appendicitis typically look ill and are lying still in bed.

Low-grade fever is common (∼38°C).

The exact location of the tenderness is directly over the appendix, which is most commonly at McBurney's point (located one third of the distance along a line drawn from the anterior superior iliac spine to the umbilicus).

Peritoneal irritation can be elicited on physical examination by the findings of voluntary and involuntary guarding, percussion, or rebound tenderness. Any movement, including coughing (Dunphy's sign), may cause increased pain.

Other findings may include pain in the right lower quadrant during palpation of the left lower quadrant (Rovsing's sign), pain on internal rotation of the hip (obturator sign, suggesting a pelvic appendix), and pain on extension of the right hip (iliopsoas sign, typical of a retrocecal appendix).

Rectal and pelvic examinations are most likely to be negative. However, if the appendix is located within the pelvis, tenderness on abdominal examination may be minimal, whereas anterior tenderness may be elicited during rectal examination as the pelvic peritoneum is manipulated. Pelvic examination with cervical motion may also produce tenderness in this setting.

If the appendix perforates :

Abdominal pain becomes intense and more diffuse, and abdominal muscular spasm increases, producing rigidity.

The heart rate rises, with an elevation of temperature above 39°C.

The patient may appear ill and require a brief period of fluid resuscitation and antibiotics before the induction of anesthesia.

Occasionally, pain may improve somewhat after rupture of the appendix, although a true pain-free interval is uncommon.

Laboratory Studies

The white blood cell count is elevated with more than 75% neutrophils in most patients. A completely normal leukocyte count and differential is found in about 10% of patients with acute appendicitis.

A high white blood cell count (>20,000/mL) suggests complicated appendicitis with either gangrene or perforation. A

Urinalysis can also be helpful in excluding pyelonephritis or nephrolithiasis.

Other blood tests are generally not helpful and are not indicated in the patient with suspected appendicitis.

Radiography
Barium Enema

Failure of the appendix to fill during a barium enema has been associated with appendicitis, but this finding lacks both sensitivity and specificity because up to 20% of normal appendices do not fill.

Ultrasonography

Ultrasonography has a sensitivity of about 85% and a specificity of more than 90% for the diagnosis of acute appendicitis.
Ultrasonography has the advantages of being a noninvasive modality requiring no patient preparation that also avoids exposure to ionizing radiation.

CT-Scan

Computed tomography (CT) is commonly used in the evaluation of adult patients with suspected acute appendicitis. CT Scan has a sensitivity of about 90% and a specificity of 80% to 90% for the diagnosis of acute appendicitis among patients with abdominal pain.

Classic findings include a distended appendix greater than 7 mm in diameter and circumferential wall thickening, which may give the appearance of a halo or target.

As inflammation progresses, one may see periappendiceal fat stranding, edema, peritoneal fluid, phlegmon, or a periappendiceal abscess.

Differential Diagnoses

Infants : pyloric stenosis.
Preschool-aged children : Intussusception, Meckel's diverticulitis, and acute gastroenteritis.
School-aged children : Gastroenteritis, inflammatory bowel disease, constipation
Adults : pyelonephritis, colitis, and diverticulitis.
Women : pelvic inflammatory disease (PID), tubo-ovarian abscess, ruptured ovarian cyst or ovarian torsion, and ectopic pregnancy.

Treatment
Most patients with acute appendicitis are managed by prompt surgical removal of the appendix. A brief period of resuscitation is usually sufficient to ensure the safe induction of general anesthesia. Preoperative antibiotics cover aerobic and anaerobic colonic flora. For patients with nonperforated appendicitis, a single preoperative dose of antibiotics reduces postoperative wound infections and intra-abdominal abscess formation. Postoperative oral antibiotics do not further reduce the incidence of infectious complications in these patients. For patients with perforated or gangrenous appendicitis, we continue postoperative intravenous antibiotics until the patient is afebrile.

Open appendectomy
Open appendectomy is usually easily performed through a transverse right lower quadrant incision (Davis-Rockey) or an oblique incision (McArthur-McBurney).

Laparoscopic appendectomy
Laparoscopic appendectomy offers the advantage of diagnostic laparoscopy combined with the potential for shorter recovery and incisions that are less conspicuous.

Dysmenorrhea

sharemedicalexperience@gmail.com — Fri, 12 Feb 2010 21:21:14 PST

Definition

Dysmenorrhea is a common gynecologic disorder affecting as many as 50% of menstruating women.

Primary dysmenorrhea refers to menstrual pain without pelvic pathology, usually appears within 1 to 2 years of menarche, when ovulatory cycles are established. The disorder affects younger women but may persist into the 40s.

Secondary dysmenorrhea is defined as painful menses associated with underlying pathology, usually develops years after menarche and can occur with anovulatory cycles.

Symptoms

The pain of primary dysmenorrhea usually begins a few hours before or just after the onset of a menstrual period and may last 48 to 72 hours with suprapubic cramping, and may be accompanied by lumbosacral backache, radiating down the anterior thigh.

Nausea, vomiting, diarrhea, and rarely syncopal episodes.

Signs

The vital signs are normal. The suprapubic region may be tender to palpation. Bowel sounds are normal, and there is no upper abdominal tenderness and no abdominal rebound tenderness. Bimanual examination at the time of the dysmenorrheic episode often reveals uterine tenderness; however, severe pain does not occur with movement of the cervix or palpation of the adnexal structures. The pelvic organs are normal in primary dysmenorrhea

Diagnosis

To diagnose primary dysmenorrhea, it is necessary to rule out underlying pelvic pathology and confirm the cyclic nature of the pain. The differential diagnosis of secondary dysmenorrhea includes primary dysmenorrhea and noncyclic pelvic pain. Whereas the diagnosis of primary dysmenorrhea is based on history and presence of a normal pelvic examination,

The diagnosis of secondary dysmenorrhea may require review of a pain diary and an ultrasound examination or laparoscopy or hysteroscopy or both. During the pelvic examination, the size, shape, and mobility of the uterus; the size and tenderness of adnexal structures; and the nodularity or fibrosis of uterosacral ligaments or rectovaginal septum should be assessed. Cervical studies for gonorrhea and chlamydia and, if relevant, a complete blood count with an ESR, are helpful to rule out subacute salpingo-oophoritis. If no abnormalities are found, a tentative diagnosis of primary dysmenorrhea can be established.

Treatment

· Prostaglandin synthase inhibitors, or NSAIDs, are effective for the treatment of primary dysmenorrhea The medication may be contraindicated in patients with gastrointestinal ulcers or bronchospastic hypersensitivity to aspirin. Side effects are usually mild and include nausea, dyspepsia, diarrhea, and occasionally fatigue.

· Acupuncture or transcutaneous electrical nerve stimulation (TENS), may also be useful.

· Spinal manipulation.

In clinical trials, however, it has not been found to be effective. Methods used only rarely to treat primary dysmenorrhea include surgical laparoscopic uterine nerve ablation and presacral neurectomy.