Bacillus anthracis as a Bioweapon

Anthrax may be the prototypic disease of bioterrorism. Although rarely, if ever, spread from person to person, the illness embodies the other major features of a disease introduced through terrorism. U.S. and British government scientists studied anthrax as a potential biologic weapon beginning approximately at the time of World War II (WWII). Offensive bioweapons activity including bioweapons research on microbes and toxins in the United States ceased in 1969 as a result of two executive orders by President Richard M. Nixon. The 1972 Biological and Toxin Weapons Convention Treaty outlawed research of this type worldwide. Clearly, the Soviet Union was in direct violation of this treaty until at least the Union dissolved in the late 1980s. It is well documented that during this post-treaty period, the Soviets produced and stored tons of anthrax spores for potential use as a bioweapon. At present there is suspicion that research on anthrax as an agent of bioterrorism is ongoing by several nations and extremist groups. 

Microbiology and Clinical Features

Anthrax is caused by B. anthracis, a gram-positive, nonmotile, spore-forming rod that is found in soil and predominantly causes disease in herbivores such as cattle, goats, and sheep. Anthrax spores can remain viable for decades. The remarkable stability of these spores makes them an ideal bioweapon, and their destruction in decontamination activities can be a challenge. Naturally occurring human infection is generally the result of contact with anthrax- infected animals or animal products such as goat hair. While an LD50 of 10,000 spores is a generally accepted number it has also been suggested that as few as one to three spores may be adequate to cause disease in some settings. Advanced technology is likely to be necessary to generate spores of the optimal size (1–5μm) to travel to the alveolar spaces as a bioweapon. The three major clinical forms of anthrax are gastrointestinal, cutaneous, and inhalational.

Treatement

Anthrax can be successfully treated if the disease is promptly recognized and appropriate therapy is initiated early. While penicillin, ciprofloxacin, and doxycycline are the currently licensed antibiotics for this indication, clindamycin and rifampin also have in vitro activity against the organism and have been used as part of treatment regimens. Until sensitivity results are known, suspected cases are best managed with a combination of broadly active agents. Patients with inhalational anthrax are not contagious and do not require special isolation procedures.

Vaccination and Prevention

The first successful vaccine for anthrax was developed for animals by Louis Pasteur in 1881. At present, the single vaccine licensed for human use is a product produced from the cell-free culture supernatant of an attenuated, nonencapsulated strain of B. anthracis (Stern strain), referred to as anthrax vaccine adsorbed (AVA). Clinical trials for safety in humans and efficacy in animals are currently under way to evaluate the role of recombinant protective antigen (one of the major components, along with lethal factor and edema factor, of B. anthracis toxins) as an alternative to AVA. In a postexposure setting in non-human primates a 2-week course of AVA + ciprofloxacin was found to be superior to ciprofloxacin alone in preventing the development of clinical disease and death. While the current recommendation for postexposure prophylaxis is 60 days of antibiotics, it would seem prudent to include immunization with anthrax  vaccine if available. Given the potential for B. anthracis to be engineeredto express penicillin resistance, the empirical regimen of choice in this setting is either ciprofloxacin or doxycycline. Continue

Postpartum hemorrhage

Postpartum hemorrhage

Postpartum hemorrhage is excessive bleeding ( more than 500 ml )following delivery. Blood loss during the first 24 hours after delivery is early post-partum hemorrhage. Blood lost 24 hours and 6 weeks after delivery is called late post-partum hemorrhage. The incidence of blood loss following vaginal delivery is 5-8%.Postpartum hemorrhage is the most common cause of excessive blood loss in pregnancy. In developing countries hemorrhage is the leading cause of maternal death. Prenatal Risk Factors are: Most of hemorrhage is not dependent on these factors: pre-eclampsia, previous postpartum hemorrhage , multiple gestation , previous ceserian section , multiparity.

Intrapartum risk factors are: prolonged 3rd stage ( more than 30 min), medio-lateral episiotomy, midline episiotomy, arrest of descent, lacerations, augmented labor, forceps delivery.

Other risk factors are: Coagulpathies hemorrhage or blood transfusion during a previous pregnancy,grandmultiparity,polyhydramnios,large infant,general anesthesia.

Abdominal or pelvic bleeding can be hidden.Physicians underestimate blood loss by 50%. Slow steady bleeding can be fatal.

Anemia and excessive blood loss may predispose to subsequent puerperal infection. Postpartum hypotension may lead to partial or total necrosis of the anterior pituitary gland and cause postpartum panhypopituitarism. In excessive hemorrhage, sterility will result from hysterectomy.

Management:
Patients should have their blood typed and crssmatched immediately
The blood should be reserved in blood bank for 24 hours after delivery
A large bore IV catheter should be kept. Severely anemic patients should be transfused as soon as cross-matched blood is rarely

Following delivery the uterus is massaged in a circular or back and forth motion untill myometrium becomes firm and well contracted.

Gentle traction is maintained on the umblical cord until seperation of the plasenta occurs.
Uterotonic agents should be administered (oxytocin 10-20 units per liter of isotonic saline)
If bleeding is excessive before placental seperation, manual removal of the placenta is indicated. The vagina and cervix should be inspected. The episiotomy should be repaired after massage has produced a firm, contracted uterus. Continue

Pediatric dysrhythmias

Pediatric dysrhythmias

Pediatric dysrhythmias is vital to be aware of arrhythmias that occur in otherwise healthy children

Supraventricular tachycardia
Rapid, regular, usually narrow QRS rhythm, originating above the ventricles. Most common abnormal tachycardia seen in pediatric practice. Most common arrhythmia requiring treatment in pediatric population.

Sinus arrhythmia
Heart rate increases during inspiration, decreases during expiration, Normal in children

Sinus pause
The pacemakes ceases its activity for a relatively short period. If the duration is longer and results in an escape rhythm this is called sinus arrest. Increased vagal tone,hypoxia, digitalis, sick sinus syndrome. Treatment is rarely indicated except Digoxin toxicity and sick sinus syndrome

Sick sinus syndrome
Sinus node is abnormally slow and various arrhythmias are produced. Sinus bradycardia, sinus node exit block, sinus arrest with junctional escape, SVT, ectopic atrial or nodal rhythm and bradytachyarrhythmia may ocur. Cardiac surgery involving atria (Senning, Mustard), arteritis, myocarditis, or idiopathic. Profound bradycardia after tachyarrhythmia may cause syncope or even death.

Premature atrial contraction
QRS complex appears earlier than normal P wave is different than the P wave seen during sinus rhythm. Compansatory pause is incomplete. Occasionally P is not followed by QRS (non-conducted PAC) Healthy children and newborns

Wandering atrial pacemaker
Gradual changes in the shape of P waves and PR intervals, QRS complexes are normal
Benign arrhythmia, no treatment is indicated

Atrial tachycardia
Difficult to differentiate from nodal tachycardia ( All are called SVT)

Atrial flutter
Rhythm originates in an ectopic focus within the atria, rate is about 300 bpm causing saw teeth appearance ( F waves) Conduction to ventricles is with 2:1, 3:1, 4:1 AV block.

Atrial fibrillation
Atrial rate is between 350-600 bpm (f waves) QRS complexes are irregularly irregular
Structural heart disease, dilated atria, myocarditis, digitalis toxicity, previous intraatrial surgery.

Ventricular tachycardia
Regular wide complex tachycardia. Atrioventricular dissociation ocur. It is a life threatening arryhthmia. Continue

Food Allergy

Food Allergy

Nearly one in five individuals avoid foods because of a perceived “food allergy.” However, true food allergy, defined as an adverse immune response to food protein, affects 6-8 % of children and 2-4% of adults. Most food allergy is acquired in the first 1 to 2 years of life. Allergic reactions to food dyes and preservatives is very uncommon. In addition to food allergy, adverse reactions to foods may occur for reasons including intolerance (a non immune response), toxic and pharmacologic reasons. Spoiled dark meat fish may induce a toxic allergic –type reaction due to release of histamine like compounds. Sudden allergic reactions that may be immediately life-threatening are typically associated with the production of IgE antibodies. These specific antibodies arm tissue mast cells and blood basophils. When the protein cross links IgE antibodies on the surfaces of these cells, signal transduction results in release of preformed mediators (e.g., histamine) that mediate reactions.

Any food can potentially trigger a food allergic response. major allergens: milk, egg, peanut, wheat, soy, tree nuts, fish and shellfish. Severe and life threatening food allergies are most typically associated with responses to peanut, nuts from trees, fish and shellfish. Milk, egg, wheat and soy allergies are more common in infants and children and these allergies often abate by late childhood. While not typically severe, allergic reactions to milk, egg, wheat soy and even fruits and vegetables may be severe in some persons. 85% of young children outgrow egg, milk, wheat and soy allergy by age 5 years; though peanut allergy tends to persist, 20% of young children with a peanut allergy will experience resolution of the allergy by age 5 years.

Food Allergy Evaluation

History: Details of diet, possible triggers, alternative diagnoses
Physical: To exclude other causes, Testing
Tests for IgE to suspected triggers
Skin prick tests by an allergist
Serum tests widely available (not affected by anti-histamines)
May require diet elimination/physician supervised oral food challenges. Continue

Menopause

Menopause

Menopause means loss of ovarian activity and loss of menses. Menopause is not a disease.It has some stages: perimenopause, menopause, postmenopause, climacterium. Premature Menopause is cessation of menstrual bleeding for more than a year before 40 yrs of age. The menstrual  cycle shortens  over time while  approaching  to menopause. Primary symptoms of menopause is cycle changes, oligoamenorrhea – amenorrhea, vasomotor , vaginal dryness. Secondary symptoms of menopause include: Urinary – stress/urge incontinence, frequency – burning ( cystitis), psychophysiologic changes, musculoskeletal pains , decrease concentration, decreased libido. Late postmenopausal problems are cardiovascular problems, osteoporotic fractures in large bones and  vertebral, breast disease incidence increases. Actions of Estrogen: Development of ovaries, tubes, uterus and vagina, secondary sexual characteristics, HPO axis interaction, proliferative changes in the endometrium, increases fat deposition and vascular profusion of skin.

Actions of Progesterone: Interacts with hypothalmus and pituitary to regulate menstrual cycle produces secretory changes in the endometrium, increases viscosity of cervical mucus , prepares breast for lactation during pregnancy.

Initial Work up of Menopause

mammography , blood chemistry:, urine analysis, blood pressure, pelvic Examination

Management Modalities: Estrogens…..oral,transdermal,nasal
Estrogen+Progesteron
Low dose combinations
Specific Estrogen Receptor Modulators
Biphosphonates
Calcium &vit D
Parathormone… Continue

Cholesterol Treatment

Cholesterol Treatment

Cholesterol is of two types high density lipid that is good and low density lipid that is bad. Excess levels of cholesterol build up plaque in the blood that causes blockages in the arteries. Blocked arteries may lead to a cardiac arrest or stroke.
One way to reduce cholesterol is oral medications combined with diet control. Some medications for cholesterol treatment are statin, bile acid sequestrants and niacin. Additionally a person can adopt some self care measures to reduce high levels of cholesterol.

Statins are effective and widely used to reduce the level of bad cholesterol. The possibility of side effects iabdominal region. Some persons may also complain about headaches, muscle pains and liver problem.

Zetia may sometimes be administered along with a statin to combat high cholesterol levels. The medicine works inside the digestive tract that reduces the cholesterol absorption.

Bile acid sequestrants may be administered along with a statin or by itself. The drug may cause bloating, gassiness, constipatio n or pain in the abdomen.
Niacin is a vitamin B that is useful to reduce LDL and triglycerides and also increases the HDL level. Experiencing hot flushes, nausea, indigestion, gas and diabetes are some side effects of this cholesterol treatment method.
Fibric acid are prescribed to reduce high triglyceride level and increase the low HDL levels. Though side effects are rare, some individuals may complain about feelings of nausea, gassiness and may also trigger formation of gall bladder stones. These drugs are typically combined with statins for higher effectiveness.
Self care methods like controlling the diet, weight and increasing physical activity are recommended. Eliminating food products known to have high levels of cholesterol is advisable. Substituting harmful foods with healthier options is effective to reduce excess levels of cholesterol.

Controlling the weight as obesity may lead to cardiac arrest is necessary. Physical inactivity is also a risk that can cause a heart attack. Regular exercise helps combat obesity and helps to control the cholesterol levels. Continue

Breat Cancer Stage 1 Treatment

Breat Cancer Stage 1 Treatment

Stage I of breast cancer is an early stage cancer that has not spread beyond the breast. There are numerous breast cancer stage I treatments available and the success rate of these is very high. Doctors do a follow-up check on the effectiveness of the treatment after five years and almost 90% of women do not have any recurrence of the cancer.

A combination of treatments is used to treat stage I breast cancer. A brief discussion on the various treatments is provided below.

Surgery is a common treatment for breast cancer stage I treatment. A lumpectomy is performed to remove the tumor and a minute amount of the tissue surrounding the tumor. Another surgery option is mastectomy where the surgeon removes the entire breast affected with the tumor. Under both the surgeries, the physician is needed to remove a lymph node. A surgical treatment treats the cause of the surgery. Other adjuvant treatments are provided to ensure that the tumor does not recur.

Chemotherapy uses medications to assault the cancerous cells. The treatment is provided after a surgery to eliminate the possibility of the recurrence of the tumor. Generally women who have large tumors removed with a surgical procedure are advised to take chemotherapy sessions.

Radiation therapy is provided to women after a lumpectomy. The radiations kill any cancerous cells that may have been missed during the surgery.

Hormone therapy is provided to women whose cancer is linked to the estrogen levels in the body. Medications are given that disallows the cancerous cells to receive the necessary hormone required for their growth. Non-menopausal women may opt to take out their ovaries to eliminate the production of estrogen within their bodies.

Biological therapy is the latest treatment for stage I breast cancer. Herceptin, a drug is administered in women who have metastatic cancer. The medicine prohibits the growth of the cancer due to the HER-2 protein and is used to complement the effects of chemotherapy. Continue

Acne – Myths And Truths

Acne – Myths And Truths

Acne is a skin condition that affects a large population of teenagers and young adults in their early twenties. There are also myths surrounding this skin disorder. The following discussion will help individuals know the real truth about acne.

Myth 1: Acne is caused by dirt. The fact is dirt is not a cause of this skin condition. Washing the face very frequently with soap removes the oiliness of the skin that results in more production of the oil, which may worsen the condition.

Myth 2: French fries and candies cause acne. This skin disorder is not a result of any food that an individual consumes. The growth of a pimple takes about three weeks and is not affected by what foods are consumed.

Myth 3: Acne is common only in teenagers. Though it is more common for teenagers to be affected by this skin disorder, many adult men and women can also have this skin problem that can last for many years. Hormones and genetically related reasons cause acne that can be triggered by stress, which may be a cause for adult pimples.

Myth 4: Spot treatments work best to cure acne. Since a pimple takes two or three weeks to emerge, spot treatments are ineffective to cure the root cause of pimples. Another option to spot treatment is a twice daily skin care routine that prevents break out of pimples.

Myth 5: Acne is nothing to worry about. Though true to an extent, the condition may affect an individual’s mental, physical and emotional health. Moreover prolonged pimple break outs can cause permanent scarring of the skin.

Myth 6: Exposure to the sun is good for acne. The truth is that too much skin exposure to the sun may worsen the condition as skin cells shed more and this is a major cause of acne.

Myth 7: Acne can be cured. There is no treatment for pimples. The cause of pimples is related to hormones and genetics effects that last over a prolonged period. However by adhering to a daily skin care routine, individuals can control the acne.. Continue

Cholesterol

Cholesterol

Cholesterol is not bad for the health but is required for the smooth functioning of the human body. A part of the cholesterol required is within the body while the balance is received from the foods that a person consumes.

Cholesterol is classified as good and bad. It is important that an individual understands the difference between the two. An excess of one or the deficiency of another creates an imbalance that could be harmful to the heart and may cause a cardiac arrest or stroke.

The liver and body cells contribute approximately seventy five percent of the cholesterol required. The balance twenty five percent is contributed by the foods consumed by the individual. Only food products from animals contain cholesterol.
Cholesterol does not dissolve in the blood and is transported through the lipoproteins to and from the body cells. Low density lipoprotein is the bad cholesterol and high density lipoprotein is known as good cholesterol. These two lipids along with triglyceride and Lp(a) cholesterol contribute to the body’s total cholesterol count, which can be tested through a blood test.

Bad cholesterol circulates in the blood vessels and may build up inside the artery walls that supply blood to the heart and the brain. LDL when combined with some other elements causes plaque that narrows the arteries and decreases their functioning. This is medically termed as atherosclerosis, a clot that forms in a narrow artery may result in a cardiac arrest.

Good cholesterol comprises 1/3rd to 1/4th part of the total blood cholesterol. HDL is known to prevent against the possibility of heart attack. The good cholesterol is shown to transport the cholesterol from the arteries to the liver. Additionally HDL also prevents the accumulation of plaque within the artery walls thus eliminating blockage.

The other two types of cholesterol, triglycerides and Lp(a) cholesterol.

Triglycerides levels can increase by smoking, alcohol consumption and no exercise. Lp (a) is a variation of the LDL and is related to genetics. These two types of cholesterol are still being studied to know their benefits and disadvantages. Continue

Paraneoplastic Syndromes

Paraneoplastic Syndromes

In addition to local tissue invasion and metastasis, neoplastic cells can produce a variety of peptides that that can stimulate hormonal, hematologic, dermatologic, or neurologic responses. Paraneoplastic syndromes refer to the disorders that accompany benign or malignant tumors but are not directly related to mass effects or invasion. Tumors of neuroendocrine origin, such as small cell lung carcinoma (SCLC) and carcinoids, produce a wide array of peptide hormones and are common causes of paraneoplastic syndromes. However, almost every type of malignancy has the potential to produce hormones or cytokines, or to induce immunologic responses. Careful studies of the prevalence of paraneoplastic syndromes indicate that they are more common than is generally appreciated. The signs, symptoms, and metabolic alterations associated with paraneoplastic disorders may be overlooked in the context of a malignancy and its treatment. Consequently, atypical clinical manifestations in a patient with cancer should prompt consideration of a paraneoplastic syndrome. The most common endocrinologic and hematologic syndromes associated with underlying neoplasia will be discussed here.

Epidemiology

These syndromes may be the first sign of a malignancy and may affect up to 15% of patients with cancer. However, if patients with cachexia are excluded, the incidence probably drops to only a few percent.
Paraneoplastic syndromes are important clinically for a number of reasons. First, they may be the initial presenting sign or symptom of an underlying malignancy. Up to two thirds of paraneoplastic syndromes arise before an associated malignancy is diagnosed. In some cases, the paraneoplastic syndrome may be associated with relatively small tumors; recognition of these associations may lead to earlier diagnosis and better therapy. Second, one of the hallmarks in defining a paraneoplastic syndrome is that the course of the syndrome generally parallels the course of the tumor. Therefore, effective treatment of the underlying malignancy is often accompanied by improvement or resolution of the syndrome. Conversely, recurrence of the cancer may be heralded by return of systemic symptoms. One exception is the neurologic paraneoplastic syndromes, in which damage to structures within the nervous system may not be reversible. Third, the clinical manifestations of the paraneoplastic syndrome (or the toxic effects of electrolyte disturbances) may constitute a more urgent hazard to life or have a greater impact on quality of life than the underlying cancer.

Pathobiology

Paraneoplastic syndromes may be caused by a variety of mechanisms; the endocrine and neurologic syndromes are the best understood. Possible etiologies include (1) secretion of proteins that are not associated with the normal tissue equivalent of the cancer (e.g., ectopic endocrine syndromes, local destruction of tissues by tumor-secreted cytokines), (2) antibodies that are directed against aberrantly expressed antigens on the tumor cell that cross-react with antigens that are normally expressed on other tissues (e.g., neurologic syndromes), and (3) effects related to unknown mechanisms, such as unidentified tumor products or circulating immune complexes stimulated by the tumor (e.g., osteoarthropathy associated with bronchogenic carcinoma) Clinical findings may resemble those of primary metabolic, hematologic, dermatologic, or neuromuscular disorders or be specific to a cancer-related syndrome. Even such nonspecific symptoms as fever and weight loss are truly paraneoplastic and are due to the production of specific factors (e.g., tumor necrosis factor) by tumor cells or by normal cells in response to the tumor.

Diagnosis

In a patient who presents with symptoms or signs of a paraneoplastic syndrome, the screening evaluation should focus on the most common associated malignancies. If the initial evaluation is unrevealing, a repeated evaluation should be considered after several months. If the relationship between the syndrome and malignancy is less clear or less frequently observed, the evaluation should be focused on the patient’s individual risks and symptoms… Continue

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