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Thread: Q & A : FMGE March 2009

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    Arrow Q & A : FMGE March 2009

    Q & A : FMGE March 2009

    Which vitamin is deficient in breast milk?

    - Vitamin A
    - Vitamin D
    - Vitamin E
    - Vitamin K
    The content of vitamin K in breast milk is very low. Hence, the causes of vitamin K deficiency in children are due to the lack of the vitamin in breast milk and also due to sterile intestines in the infant. Breast milk supplies only about 20% of the requirement.

    Any deficiency of vitamin K causes hemorrhagic disease in the newborns. There is spontaneous bleeding under the skin or elsewhere, due to this disease. Sometimes the bleeding might take place in the brain, and can cause death, ultimately.

    In children it might lead to certain abnormalities like flat nasal bridge, short noses and shortened fingers. In adults, deficiency of vitamin K is rare. It is mostly found in people, who suffer from mal absorption of fats from dietary sources.

    The bone protein osteocalcium, when undergoing carboxylation with calcium requires vitamin K. Hence, its deficiency results in diseases like osteopenia and osteoporosis.

    Osteoporosis is a disease in which the bones become weak and are liable to be broken. There might be a risk of hip fracture in older people.

    Being a vitamin that aids in blood clotting, the deficiency of vitamin K leads to excessive bleeding. The blood clotting protein prothrombin becomes less active with the deficiency in vitamin K. Excessive bleeding might also result in death.

    Vitamin K deficiency results in health problems related to excessive bleeding like heavy menstrual bleeding, bleeding in the stomach and intestine, nose bleeding and hemorrhaging. Bleeding in the genitourinary tract leads to blood in the urine.

    The deficiency also leads to excessive calcium in the urine called Hypercalciuria.

    People deficient in vitamin K have to be fed on food items rich in vitamin K. Green leafy vegetables, oils, olive oil, soybean oil, peas, beans, cow milk, spinach, cabbage and broccoli are some of the food items that contain vitamin K.

    In infants, deficiency of vitamin K is treated and prevented with injectables whereas for adults oral doses are recommended. The RDA for an adult is 70-80 mg/day and for infants it is 5 mg/day.

    Vitamin K is obtained both from plant food and animal food. Vitamin K can be obtained either from food, or through its synthesis in the intestines of our body. Vitamin K found in plant food is called phylloquinone. In animal food it is found as menaquinone. The bacteria in the intestine can also produce vitamin K.

    vitamin K deficiency might occur in people of all age group, but is more common in infants.

    Inadequacy of vitamin K in the food or the destruction of intestinal bacteria can result in its deficiency. Intake of certain antibiotics can destroy the bacteria that aids in the synthesis of vitamin K. consuming salicylates or aspirin blocks vitamin K.


    Phytonadione (AquaMEPHYTON, Mephyton, Konakion)

    Promotes liver synthesis of clotting factors. The oral form requires the presence of bile in the small intestine for absorption and is therefore not used in emergency situations. Metabolism occurs in the liver, and elimination occurs in bile and urine. Phytonadione has a more rapid and prolonged effect than does menadione (water soluble). Protect the injectable form from light at all times (it may be autoclaved).

    Hemorrhagic disease of newborn: 1-2 mg/d IM/SC; 0.5-1 mg within 1 h of birth for prophylaxis

    VK deficiency:
    2.5-5 mg/d PO
    1-2 mg IM/SC once

    •Newborns commonly are administered VK-1 injection to prevent bleeding problems.

    Hemorrhagic Disease of the Newborn (Vitamin K Deficiency)

    What is hemorrhagic disease of the newborn?

    Hemorrhagic disease of the newborn is a bleeding problem that occurs in a newborn during the first few days of life.

    What causes hemorrhagic disease of the newborn?

    Babies are normally born with low levels of vitamin K, an essential factor in blood clotting. A deficiency in vitamin K is the main cause of hemorrhagic disease of the newborn.

    Who is affected by hemorrhagic disease of the newborn?

    Vitamin K deficiency may result in bleeding in a very small percentage of babies.

    Babies at risk for developing hemorrhagic disease of the newborn include the following:

    •babies who do not receive preventative vitamin K in an injection at birth

    •exclusively breastfed babies (breast milk contains less vitamin K than cow's milk formula.)

    •babies whose mothers have seizure disorders and take anti-convulsant medications

    Why is hemorrhagic disease of the newborn a concern?

    Without the clotting factor, bleeding occurs, and severe bleeding or hemorrhage can result.

    What are the symptoms of hemorrhagic disease of the newborn?

    The following are the most common symptoms of hemorrhagic disease of the newborn.

    However, each baby may experience symptoms differently. Symptoms may include:

    •blood in the baby's bowel movements
    •blood in urine
    •oozing around the umbilical cord

    The symptoms of hemorrhagic disease of the newborn may resemble other conditions or medical problems. Always consult your baby's physician for a diagnosis.

    How is hemorrhagic disease of the newborn diagnosed?

    In addition to a complete medical history and physical examination, a diagnosis is based on the signs of bleeding and by laboratory tests for blood clotting times.

    Treatment for hemorrhagic disease of the newborn:

    Specific treatment for hemorrhagic disease of the newborn will be determined based on:

    •your baby's gestational age, overall health, and medical history

    •extent of the disease

    •your baby's tolerance for specific medications, procedures, or therapies

    •expectations for the course of the disease

    •your opinion or preference

    The American Academy of Pediatrics (AAP) recommends giving every newborn baby an injection of vitamin K after delivery to prevent this potentially life-threatening disease.

    If bleeding occurs, vitamin K is also given. Blood transfusions may also be needed if bleeding is severe.

    Vitamin K Deficiency

    Vitamin K (VK), an essential, lipid-soluble vitamin that plays a vital role in the production of coagulation proteins, is found in green, leafy vegetables and in oils, such as soybean, cottonseed, canola, and olive oils.1 VK is also synthesized by colonic bacteria. The 3 main types of VK are K-1, which is derived from plants; K-2, menaquinone, which is produced by the intestinal flora; and K-3, which is a synthetic, water-soluble form used for treatment.

    VK deficiency can occur in persons of any age. Infants are at higher risk for hemorrhagic disease of newborn, caused by a lack of VK reaching the fetus across the placenta, the low level of VK in breast milk, and low colonic bacterial synthesis. However, a large amount of VK given to a pregnant patient can lead to jaundice in a newborn. In adults, VK deficiency is uncommon due to the intake of a wide variety of vegetables and other foods; the recycling ability of VK, which helps to conserve the body's supply; and adequate gut flora to produce VK.


    Vitamin K (VK) acts as a cofactor; it is needed for the conversion of 10-12 glutamic acid residue on the NH2-terminal of the precursor coagulation proteins into the action form of gamma-carboxyglutamic acid (which occurs via VK-dependent gamma-glutamyl carboxylase). This essential reaction allows the VK-dependent proteins to bind to surface phospholipids through calcium ion channel – mediated binding, in order to start the normal antithrombotic process. The exact mechanism by which VK functions as cofactor with the carboxylase is not fully understood. In addition to the coagulation factors, bone matrix proteins, specifically osteocalcin, undergo similar gamma carboxylation with calcium that requires VK; therefore, osteoporosis is associated with VK deficiency.

    If a healthy person is subject to a complete dietary absence of VK, his/her VK reserve is adequate for 1 week. Because diet is the main source of VK, an adult's daily requirement has been estimated at 100-200 mcg/d. About 80-85% of VK is absorbed mainly in the terminal ileum into the lymphatic system; therefore, bile salts and normal fat absorption, as well as normal villi of the ileum, are necessary for the effective uptake of VK.

    The characteristics of VK deficiency vary according to the age of onset. In infants, it causes hemorrhagic disease of newborn, resulting especially in intracranial and retroperitoneal bleeding, which can occur at 1-7 days postpartum. The low transmission of VK across the placenta, liver prematurity with the prothrombin synthesis, lack of VK in breast milk, and the sterile gut in neonates account for VK deficiency in infants. Late hemorrhagic disease of newborn can occur as late as 3 months postpartum.

    In adults, low dietary intake of VK due to chronic illness, malnutrition, alcoholism, multiple abdominal surgeries, long-term parenteral nutrition, malabsorption, cholestatic disease, parenchymal liver disease, cystic fibrosis, inflammatory bowel disease, and drugs (eg, antibiotics [cephalosporin], Coumadin, salicylates, anticonvulsants, certain sulfa drugs) are some of the common causes of VK deficiency. Because 2 main sources of VK exist, neither dietary deficiency nor gut sterilization produces significant coagulopathy in a healthy person.
    Last edited by trimurtulu; 04-03-2009 at 09:06 AM.

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    Fracture of hyoid bone indicative of :

    - Hanging
    - Suffocation
    - Throttling
    - choking

    Hyoid bone
    The hyoid bone (lingual bone) (Latin os hyoideum) is a horseshoe shaped bone situated in the anterior midline of the neck between the chin and the thyroid cartilage. At rest, it lies at the level of the base of the mandible in the front and the third cervical vertebra behind.

    It is the only bone in the human skeleton not articulated to any other bone. It is kept suspended in position by muscles and ligaments. The hyoid bone provides attachment to the muscles of the floor of the mouth and the tongue above, the larynx below, and the epiglottis and pharynx behind.

    The hyoid bone (Lingual Bone) (lat. Os hyoideum) is a in the neck and is the only bone in the human skeleton not articulated to any other bone. It is supported by the muscle of the neck and in turn supports the root of the tounge.

    The hyoid bone is shaped like a horse shoe and is suspended from the tips of the styloid process of the temporal bones by the stylohyoid ligaments.

    Though the hyoid bone is present in many mammals, its descent in living creatures is unique to Homo sapiens, allowing for the production of a wide range of sounds that other animals cannot produce. It allows a wider range of tongue, pharyngeal and laryngeal movements by bracing these structures alongside each other in order to produce variation.

    The discovery of a modern-looking hyoid bone of a Neanderthal man in the Kebara Cave in Israel led its discoverers to argue that the Neanderthals had a descended larynx, and thus human-like speech capabilities. However, other researchers have claimed that the morphology of the hyoid is not indicative of the larynx's position.

    Fracture and Applied Anatomy
    Due to its position, the hyoid bone is not susceptible to easy fracture. In a suspected case of murder, a fractured hyoid strongly indicates throttling or strangulation. However this is not the case in children and adolescents where hyoid bone is still flexible as ossification is yet to be completed.

    The most common cause of hyoid bone fractures today is motor vehicle trauma . (In the past, strangulation and hanging caused a majority of cases . While fractures of the craniofacial skeleton and cervical spine are relatively common, fractures of the hyoid bone are quite rare, accounting for 0.002% of all fractures . Hyoid bone fractures often occur with concomitant mandible fractures, thyroid cartilage fractures, and cricoid cartilage fractures. The low number of hyoid injuries is believed to be due to the protective effect of the mandibular position and the free-floating nature of the hyoid bone, with its mobility in all directions . Fewer than 30 cases of hyoid bone fractures have been reported in the literature.

    The diagnosis of hyoid bone fracture is difficult. Usually, the finding is made by CT scan of the head and neck. Plain radiographs may reveal hyoid bone fractures; however, the detailed anatomy of the hyoid bone is often obstructed by the patient’s mandible or soft tissue.

    Fractures typically occur through one of two mechanisms:

    (a) They may result from direct blows to the hyoid. This typically occurs when the neck is extended, exposed, and unprotected by the mandible.

    (b) The hyoid bone can be fractured as an avulsion injury secondary to sudden neck hyperextension or forced swallowing. Both mechanisms may occur during motor vehicle accidents, whether the patient is restrained or unrestrained. The patient may present with ecchymosis of the neck, edema, crepitus, or stridor . Patients may complain of anterior neck pain, decreased
    range of motion, dysphonia (nasal or raspy sound), dyspnea, dysphagia (typically of solid foods), persistent cough, painful coughing, pain
    with nose blowing, or gagging . In more severe injuries, patients may complain of respiratory distress or hemoptysis

    The hyoid bone

    1. Greater horns

    2. Lesser horns

    3. Body

    This image shows the human hyoid bone, which helps to support the tongue and serves as an attachment point for several muscles that help to elevate the larynx during swallowing and speech. The hyoid bone is unique in that it is the only bone of the body that does not articulate with any other bone. Instead, it is suspended above the larynx where it is anchored by ligaments to the styloid processes of the temporal bones of the skull.

    A small, U-shaped bone situated centrally in the upper part of the neck, beneath the mandible but above the larynx near the level of the third cervical vertebra.

    The hyoid is (uniquely in the vertebrate skeleton) not joined to any other bone but is suspended by the stylohyoid ligaments from the styloid process of each temporal bone at the base of the skull. It is formed from three separate parts – the body, and the left and right greater and lesser cornu (horns) – which fuse in early adulthood. The function of the hyoid is to provide an anchor point for the muscles of the tongue and for those in the upper part of the front of the neck.

    The hyoid bone can be felt by pressing one's finger into the crease where the chin becomes the neck.



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    Gullian- barre most commonly involves which nerve?

    - Facial nerve
    - Optic nerve
    - Occulomotor nerve
    - Trochlear nerve


    Guillain-Barre Syndrome

    Guillain-Barré (ghee-yan bah-ray) syndrome (GBS) is a disorder in which the body’s immune system attacks part of the peripheral nervous system. The peripheral nervous system includes the cranial nerves (except the optic [eye] nerve), the spinal nerves, and the autonomic nervous system that governs involuntary actions. The central nervous system is the spinal cord and brain.

    GBS includes several subtypes, the most common of which is a multifocal demyelinating disorder of the peripheral nerves referred to as an acute inflammatory demyelinating polyneuropathy (AIDP). Some cases of GBS are associated with a primarily motor axonal process (acute motor axonal neuropathy; AMAN) with axonal degeneration (axons are long, thin extensions of the nerve cells and carry nerve signals) and sparing of the myelin (the myelin is an electrically insulating phospholipid layer that surrounds the axons of many neurons). Other cases appear to involve both sensory and motor axons and such cases are termed acute motor and sensory axonal neuropathy (AMSAN). More than 90% of patients with GBS in Europe and North America have AIDP. AMAN occurs in less than 10% of persons with GBS in the western hemisphere but in more than 40% of those affected in China and Japan. The incidence of AMSAN is very low (less than 10% of that of AMAN). Miller Fisher syndrome (MFS) is another GBS variant that occurs in about 5% of people affected by GBS. It is characterized by opthalmoplegia (eye muscle weakness), areflexia (absence of reflexes), ataxia (the inability to coordinate voluntary muscular movements such as walking), and, in some cases, facial and bulbar palsy (affecting vital functions, like breathing, and swallowing or speech).

    GBS can affect anybody. It can strike at any age; men may be more likely to develop GBS than women. Although this syndrome is rare (affecting about one to two persons in 100,000) it is the most common cause of acute neuromuscular paralysis in the world.

    Where does Guillain-Barré Syndrome come from?
    GBS often occurs a few days or weeks after a person has had symptoms of a respiratory or gastrointestinal viral or bacterial infection; in fact, two-thirds of affected individuals have had a preceding infection. Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, and Mycoplasma pneumoniae are commonly identified antecedent pathogens, although C. jejuni is the most common pathogen that elicits GBS. Occasionally surgery or vaccinations will trigger the syndrome. GBS is not contagious. It has been reported that GBS occurs more in men than in women and more often in the elderly. Seasonality has not been reported in developed countries like the United States (Church Potter & Kaneene, 2003).

    No one yet knows why GBS strikes some people and not others. Nor does anyone know exactly what sets the disease in motion. What scientists do know is that the body’s immune system begins to attack the body itself, causing what is known as an autoimmune disease. Usually the cells of the immune system attack only foreign material and invading organisms.

    In GBS, the immune system starts to destroy the myelin sheath that surrounds the axons of many peripheral nerves, or even the axons themselves. The myelin sheath surrounding the axon speeds up the transmission of nerve signals and allows the transmission of signals over long distances. In diseases in which these myelin sheaths are injured or degraded, the nerves cannot transmit signals efficiently. That is why the muscles begin to lose their ability to respond to commands from the brain that must be carried through the nerve network. The brain also receives fewer sensory signals from the rest of the body, resulting in an inability to feel textures, heat, pain, and other sensations. Alternately, the brain may receive inappropriate signals that result in tingling, “crawling-skin,” or painful sensations. Because the signals to and from the arms and legs must travel the longest distances, they are most vulnerable to interruption. Therefore, muscle weakness and tingling sensations usually first appear in the hands and feet and progress upwards.


    An acquired demyelinating disorder of the peripheral nervous system characterized by progressive motor weakness and areflexia.

    •incidence: 0.6-1.9/100,000 (adult & childhood cases)
    •age of onset:
    ◦patients are <20 years of age in 30% of cases
    ■2/3rds of these are in children <8 years of age
    ■rare in children <2 years of age
    •risk factors:
    ◦M > F (3:2)
    ◦season: fall and winter

    •50-70% of cases occur within 4 weeks of an antecedent illness (usually an upper respiratory tract infection or GI infection by CMV or EBV) -> autoimmune response towards peripheral nerves (via cell- and humorally-mediated immune mechanisms) -> focal areas of inflammation and demyelination of motor (+/- sensory) nerves - also may occur after hepatitis, immunizations, insect stings, surgery, viral exanthems, and other illnesses
    •Campylobacter jejuni and Mycoplasma pneumoniae have been implicated

    •widespread areas of focal inflammation and demyelination
    1. Sites of Attack◦most common
    ■proximal nerve roots at junction of dorsal & ventral nerve roots at the site of dural attachment
    ◦less common
    ■lumbar and brachial plexuses
    ■peripheral and cranial nerves
    ◦rarely affected
    ■dorsal root or ganglia
    ■sympathetic chain

    2. Inflammatory Response
    ◦inflammatory cells: macrophages and lymphocytes
    ◦these cells attack the myelin sheath of Schwann cells leaving the Schwann cells and axons undisturbed
    ■surrounding axons may be secondarily injured in areas of intense inflammation causing chromotolysis and neurono-phagia of the anterior horn cells
    ■inflammation at sites of dural attachment may cause breakdown of the blood-brain barrier resulting in transudation of plasma proteins into the CSF
    ■insertion of macrophages beneath the lamellae of the myelin sheath stripping away long sections -> focal demyelination
    ■-> conduction block

    1. Neurological Manifestations

    1. Progressive Motor Weakness
    ■usually ascends from legs to arms and may involve truncal and finally bulbar musculature (rarely descends)
    ■may present as a disturbance of gait or acute ataxia
    ■symmetrical with weakness greater distally than proximally
    ■may lead to transient quadriplegia
    ■respiratory paralysis in 18%
    ■cranial nerve palsies in 30-40%:
    ■7th - facial diplegia most common
    ■9&10 - dysphagia 2nd most common
    ■all may be involved rarely except the olfactory nerve
    ■if extraocular muscle involvement think of Miller-Fisher syndrome

    2. Reflexes
    ■symmetric areflexia or marked hyporeflexia
    ■may be mildly asymmetric initially
    ■may rarely precede motor weakness or may be a late finding

    3. Sensation
    ■loss of position and vibratory sensation
    ■occasionaly pain or parethesias
    ■insidious symptoms may precede motor weakness

    4. Autonomic Dysfunction
    ■bowel and bladder dysfunction
    ■transient and not seen at onset
    ■cardiovascular instability:
    ■hypertension, orthostatic hypotension, tachyarrhythmias

    1. Cerebral Spinal Fluid◦dissociation of elevated protein with lack of cellular response is highly suggestive of Guillain-Barre syndrome
    ◦elevated protein
    ■may be undetectable in 1st week of illness
    ■often peaks at 3-4 weeks
    ■proteins similar to those in plasma as well as Ig's and oligoclonal bands
    ◦slight pleocytosis (<10 cells/ul)

    2. Electrodiagnostic
    1. Nerve Conduction Velocity
    ■may be reduced to 60% of normal
    ■detected in 50% during first 2 weeks
    ■" 85% during 3rd week
    ■due to segmental demyelination -> conduction block
    ■may involve motor and sensory nerves
    ■distal > proximal initially (in 1st week)

    2. Somatosensory Evoked Responses
    ■altered reflecting proximal root involvement

    3. EMG
    ■no changes except decreased recruitment pattern

    1. For Guillain-Barre Syndrome
    1. Plasmapheresis
    ■may be beneficial in children with rapid deterioration or in those needing intubation
    2. Supportive
    1. Multidisciplinary Approach
    ■in an ICU setting
    ■Peaditrician, Intensivist, Neurologist, OT, PT, Psychology
    ■moniter neuromuscular, respiratory, cardiovascular status
    2. Intubation
    ■indications for
    ■respiratory distress/failure
    ■cardiovascular instability
    ■decrease in vital capacity to 50% of normal
    ■progression to dysphagia, shoulder or facial paresis may indicate need for intubation
    ■usual duration: 2-8 weeks with consideration of tracheostomy with lack of improvement after 2 weeks

    3. Prognosis
    1. Natural History
    ■usually a benign clinical course with recovery with 2-3 weeks with recovery of muscle function inversely related to onset of symptoms (i.e., bulbar -> arms -> legs)
    ■complete recovery:
    ■50% within 6 months
    ■60-70% within 12 months

    2. Complications
    ■10% with permanent deficits
    ■7% will relapse

    ■3-4% mortality
    ■chronic forms of Guillain-Barre:
    ■Chronic Relapsing Polyradiculoneuropathy
    ■Chronic Unremitting Polyradiculoneuropathy

    3. Poor Prognostic Indicators
    ■extensive denervation on EMG
    ■increased duration of time from maximal deficit to onset

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    Smallest pelvic diameter in obstetric examination:

    A. Diagonal conjugate
    B. True conjugate
    C. Obstetric conjugate
    D. And smth else


    The passageway

    The passageway, or birth canal, is composed of the rigid bony pelvis and the soft tissues of the cervix, vagina, and introitus.


    Assessment of the bony pelvis

    The purpose of the examination of the bony pelvis is to determine if the pelvic cavity is of adequate size to allow for the passage of a full-term fetus.

    This examination may be performed during the first prenatal evaluation and need not be repeated if the pelvis is of adequate size. However, if findings indicate that the pelvis is of borderline adequacy or if the examination could not be done because the woman was tense, the examination is repeated between 32 and 36 weeks’ gestation.

    In the third trimester of pregnancy, the examination may be more through and results more accurate because there is a relaxation of pelvic joints and ligaments, and the woman may be more accustomed to examination.

    Pelvic joints

    The four pelvic joints are:

    ·1 the symphysis pubis,

    ·2 the right and the left sacroiliac joints and

    ·3 the sacro-coccygeal joint.

    The joints of the pelvic bones are synchondroses (joints in which the surfaces are connected by plates of cartilage) that allow little movement in the nonpregnant state; the hormone during pregnancy, especially the ovarian hormone progesterone, cause considerable mobility to develop.

    Because the examiner does not have direct access to the bony structures and because the bones are covered with variable amounts of soft tissue, estimates are approximate.

    Precise bony pelvis measurements can be determined using computed tomography and ultrasound.

    The bony pelvis is separated by the brim or inlet into two parts:

    ·4 the false pelvis and

    ·5 the true pelvis

    The false pelvis is that part above the brim and is of no obstetric interest.

    The true pelvis is divided into three planes:

    ·6 the inlet or brim,

    ·7 the midpelvis or cavity, and

    ·8 the outlet:

    1. The pelvic inlet, or brim of the pelvis, is formed

    ·1 anteriorly by the upper margins of the pubic bone,

    ·2 laterally by the iliopectineal lines along the innominate bones, and

    ·3 posteriorly by the anterior, upper margin of the sacrum, the sacral promontory.
    1. The pelvic cavity, or midpelvis, is a curved passage having a short anterior wall and a much deeper concave posterior wall. It is bounded by

    ·1 the posterior aspect of the symphysis pubis,

    ·2 the ischium,

    ·3 a portion of the ilium, and

    ·4 the sacrum and coccyx.
    1. The pelvic outlet when viewed from below is ovoid, somewhat diamond shaped, bounded by

    ·1 the pubic arch anteriorly,

    ·2 the ischial tuberosities laterally, and

    ·3 the tip of the coccyx posteriorly

    In the latter part of pregnancy, the coccyx is movable (unless it had been broken in a fall while skiing, skating, etc. and had fused to the sacrum during healing).

    The pelvic canal varies in size and shape at various levels. The diameters at the plane of the pelvic inlet, midpelvis, and outlet and the axis of the birth canal determine whether vaginal delivery is possible and the manner by which the fetus may pass down the birth canal (mechanism of labour).

    Problems can be expected in women with rickets, osteomalacia, or paralysis of one or both extremities or following a motor vehicle accident in which the woman experienced a crushed pelvis.

    Obstetric measurements

    Plane of inlet (superior strait). The principal pelvic diameters of the plane of the inlet as follows:

    1. Anteroposterior diameters

    *A) The true conjugate, or conjugata vera (11 cm or more), is the distance from the upper margin of the symphysis to the sacral promontory. This dimension usually is a radiographic or ultrasonic measurement.

    *B) The diagonal conjugate (12.5 to 13 cm) is the distance from the lower border of symphysis pubis to the promontory of the sacrum. The diagonal conjugate is the only dimension of the inlet that can be obtained by vaginal examination. Its length is used to estimate the obstetric conjugate; it is 1.5 to 2 cm greater than the obstetric conjugate.

    *C) The obstetric conjugate is the distance between the inner surface of the symphysis pubis slightly below its upper border and the sacral promontory.

    The obstetric conjugate determines whether the presenting part can enter the true pelvis because it is the smallest diameter. Therefore this diameter is the most important measurement of inlet.
    The obstetric conjugate is estimated by subtracting 1.5 to 2 cm from the diagonal conjugate depending on the length and inclination of the symphysis pubis.

    2. The transverse diameter of the inlet (13.5 cm or more) is an important determinant in assessing the shape of the inlet.

    3. The oblique diameter (12.75 cm or larger) is directed from the sacroiliac joint on one side to the opposite iliopectineal prominence. The fetal head often enters the pelvis in the oblique diameter because the colon fills part of the left pelvis and the sacral promontory protrudes into the area of the transverse diameter.

    The plane or inclination of the pelvic inlet (brim) normally describes an angle of approximately 60 degrees with the horizontal when the woman is standing.

    Midplane of the pelvis

    The midplane of the pelvis normally contains the planes of greatest and shortest pelvic dimensions

    1) Anteroposteriorly the greatest dimension is from midsymphysis to the sacrum at the fused second and third vertebras. This measurement should be 12.75 cm or more.

    2) Extending from the middle of the posterior borders of the ischial bones are the ischial spines.

    · The distance between these spines (10.5 cm) represents the shortest transverse diameter of the true pelvic cavity.

    · The ischial spines are the bony attachments for the pelvic floor muscles and are at the same level as the vaginal vault. They can be reached during vaginal examination.

    · the ischial spines also serve as landmarks in the determining station, or the level to which the presenting part of the fetus has descended into the pelvic cavity

    Plane of pelvic outlet

    The outlet presents the smallest plane of the pelvic canal and is the easiest structure to evaluate. The significant diameters are as follows:

    1) The anteroposterior diameter (about 11.9 cm) extends from the lower margin of the symphysis to the sacrococcygeal joint rather than the tip of the coccyx. The mobility of the never-damaged coccyx, because of the relaxation of the sacrococcygeal joint, permits its backward displacement during labour

    2) The transverse or intertuberous diameter of the outlet is measured from the inner border of one ischial tuberosity to the other (about 10 to 11 cm)

    3) the posterior sagittal diameter (about 9 cm) of the outlet is projected from the tip of the sacrum to a point in space where the intertuberous diameter transects the anteroposterior projection.

    The subpubic angle, which indicates the type of pubic arch, together with the length of the pubic rami and the intertuberous diameter, is a great importance. Because the presenting part must pass beneath the pubic arch, a narrow subpubic angle will be less favorable than a rounded, wide arch. If the subpubic angle is narrow, the fetal head for example, is forced backward toward the coccyx, and the extension of the head may be difficult.

    Descent of the fetus through the birth canal follows an orderly process. Generally the fetal head (usually presenting first) enters the inlet to the true pelvis in transverse fashion. Descent continues in a slightly backward and downward direction to the ischial spines.

    An almost right-angled anterior turn occurs in the birth canal at the ischial spines. When the head turns to pass between the ischial spines. It contacts the forward-sloping pelvic floor musculature and sacrum and is generally directed forward and downward. The fetal head thus is guided into the direction of the pelvic outlet and the vagina.

    Classification of pelvis

    The four basic types of pelvis are as follows:

    1. Gynecoid (the classic female type)

    2. Anthropoid

    3. Platypelloid (the flat pelvis)

    4. Android (resembling the male pelvis)

    The gynecoid pelvis is the most favorable for normal delivery.

    Engagement usually is in the transverse or oblique diameter, descent is rapid, rotation occurs in the midpelvis, and delivery of the vertex in an occiput anterior position (OA)

    often occurs spontaneously.

    Implications for Nursing Care

    The examination of the bony pelvis can be uncomfortable for the gravida

    It should be done after the internal examination of the soft pelvic organs.

    The preparation of the woman includes

    · an explanation of the procedure,

    · a request for her to empty her bladder,

    · coaching her for relaxation,

    · and maintaining eye contact with her whenever possible.
    Whenever the woman is in a supine position for a procedure,

    · place a pillow under her head and

    · ask her to flex her knees.

    · Drape her as necessary.
    If she shows signs of supine hypotension or the vagal nerve is occurring. e.g.

    · she becomes pale,

    · breathless,

    · and faint

    · and her skin becomes clammy), turn her onto her left side to relive the signs and symptoms.
    Soft tissues

    The soft tissues of the passage include the distensible lower uterine segment, cervix and vaginal canal.

    Before labour begins, the uterus is composed of the uterine body (corpus) and cervix.

    After labour has begun, the uterine contractions cause the uterine body to differentiate into a thick and muscular upper segment and a thin-walled passive muscular tube, the lower segment.

    A physiologic retraction ring separates the two. The lower uterine segment gradually distends to accommodate the intrauterine contents as the walls of the upper segment become thicker and its content is reduced.

    The downward pressure caused by contraction of the fundus is transmitted to the cervix, and its effaces and dilates sufficiently to allow descent of the presenting part into the vagina.

    Actually, the cervix is drawn upward and over the presenting part as the vertex or breech descends.

    The vagina in turn distends to permit passage of the fetus into the external world.
    Last edited by trimurtulu; 04-03-2009 at 04:09 PM.

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    Largest fetal head diameter:?

    A. Occipitofrontal

    B. Suboccipitofrontal

    The occipito-frontal diameter range was wider due to a poorly defined occipital bone and this also translated to the head circumference differences.

    Fetal presentation

    Fetal presentation means the part of the fetus that is "presenting" at the cervix:

    • Cephalic presentation means head first. This is the normal presentation. (Occurs 97 %)

    • Breech presentation means the fetal butt is coming out first.

    • Transverse lie means the fetus is oriented from one side of the mother to the other and neither the head nor the butt is coming out first.

    • Compound presentation means that a fetal hand is coming out with the fetal head.

    • Shoulder presentation means that the fetal shoulder is trying to come out first.

    Fetal "presentation" is different from fetal "position." Fetal position refers to the orientation of the fetus within the birth canal (eg, looking toward the mother's pubic bone (OP), or look toward the mother's coccyx (OA), etc.)


    Fetal Presentation

    I.Presentation: Breech (Head is not presenting part)
    A.Occurs in 25% of pregnancies at 30 weeks
    B.Abnormal after 32 weeks
    C.Fetal Malpresentation
    II.Presentation: Cephalic (Head is presenting part)

    A.Normal Presentation: Vertex
    1.Normal Attitude: Fetus is in full flexion
    2.Every fetal joint is flexed
    3.Smallest fetal head diameter: Suboccipitobregmatic
    B.Abnormal presentations: Extended Attitude
    a.Abnormal Attitude: Fetal head is extended
    b.Results in largest head diameter: Occipitomental
    c.Increases diameter 3 cm (24%) over flexed head
    d.May results in Failure to Progress
    2.Face Presentation

    3.Brow Presentation

    4.Shoulder Presentation

    C.Abnormal Presentation: Asynclitism
    a.Lateral flexion of head
    b.Sagittal Suture not in midline of vaginal canal
    a.Mild asynclitism is normal
    b.Extreme asynclitism interferes with delivery
    1. i.May result in Failure to Progress
    2. ii.Interferes with forceps application


    Full Details:




    Last edited by trimurtulu; 04-03-2009 at 06:28 PM.

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    In case of a corneal ulcer perforation, the best treatment option would be: -

    A. Tissue adhesive glue

    B. Flap graft from conjunctiva

    cyanoacrylate adhesive tissue

    The use of cyanoacrylate tissue adhesive in cases with corneal perforation greater than 3 mm is very encouraging.

    The use of cyanoacrylate tissue adhesive offers to the clinician a safe technique for healing corneal wounds that avoids tectonic penetrating keratoplasty with its associated complications.

    A running 10.0 nylon suture can be used to create a reticulum over the space of the corneal perforation upon which the glue was applied.

    Choroidal detachment following corneal ulcer perforation is common and is more likely in larger corneal perforations. Preoperative B-scan should be considered in cases of large corneal perforations requiring therapeutic keratoplasty to document choroidal detachment, which if large may require drainage.

    Cyanoacrylate glue is an effective and safe method for sealing small corneal perforations. A vigil must be maintained for infection while the glue and bandage contact lens are in situ.


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    Which is true regarding vaccination for an HIV positive newborn?

    A. Only killed vaccines to be given
    B. Both live and killed vaccines
    C. Regular vaccination scheduled to be followed
    D. No vaccination to be given

    Infants and children infected with HIV should receive, on schedule, all the routinely recommended Killed (inactivated) vaccines.

    The Main Types of Vaccines

    The safety and effectiveness of a vaccine depends on how it is made and what it contains. There are four main ways to develop vaccines:

    Live attenuated vaccines contain bacteria or viruses that have been altered so they can't cause disease.

    Killed vaccines contain killed bacteria or inactivated viruses.

    Toxoid vaccines contain toxins (or poisons) produced by the germ that have been made harmless.

    Component vaccines contain parts of the whole bacteria or viruses.

    Live attenuated vaccines

    Live attenuated vaccines usually are created from the naturally occurring germ itself. The germs used in these vaccines still can infect people, but they rarely cause serious disease. Viruses are weakened (or attenuated) by growing them over and over again in a laboratory under nourishing conditions called cell culture.

    The process of growing a virus repeatedly-also known as passing--serves to lessen the disease-causing ability of the virus. Vaccines are made from viruses whose disease-causing ability has deteriorated from multiple passages.

    Examples of live attenuated vaccines include:

    Measles vaccine (as found in the MMR vaccine)

    Mumps vaccine (MMR vaccine)

    Rubella (German measles) vaccine ( MMR vaccine)

    Oral polio vaccine (OPV)

    Varicella (chickenpox) vaccine[quote]

    Inactivated (killed) vaccines

    Inactivated (killed) vaccines cannot cause an infection, but they still can stimulate a protective immune response. Viruses are inactivated with chemicals such as formaldehyde.

    Examples of inactivated (killed) vaccines:

    Inactivated polio vaccine (IPV), which is the shot form of the polio vaccine

    Inactivated influenza vaccine.

    Toxoid vaccines

    Toxoid vaccines are made by treating toxins (or poisons) produced by germs with heat or chemicals, such as formalin, to destroy their ability to cause illness. Even though toxoids do not cause disease, they stimulate the body to produce protective immunity just like the germs' natural toxins.

    Examples of toxoid vaccines:

    Diphtheria toxoid vaccine (may be given alone or as one of the components in the DTP, DTaP, or dT vaccines)

    Tetanus toxoid vaccine (may be given alone or as part of DTP, DTaP, or dT)

    Component vaccines

    Some vaccines are made by using only parts of the viruses or bacteria. These vaccines cannot cause disease, but they can stimulate the body to produce an immune response that protects against infection with the whole germ. Four of the newest vaccines are made this way.

    Examples of component vaccines:

    • Haemophilus influenzae type b (Hib) vaccine
    • Hepatitis B (Hep B) vaccine
    • Hepatitis A (Hep A) vaccine
    • Pneumoccocal conjugate vaccine


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    Carpal tunnel syndrome


    Carpal tunnel syndrome is due to involvement of which nerve?



    Carpal tunnel release

    During carpal tunnel release, the transverse carpal tunnel ligament is severed to relieve pressure on the median nerve. The surgery may be done by making one incision on the palm side of the wrist, or by making several small incisions

    Although it might seem that carpal tunnel syndrome is a condition born from long hours spent working on a computer keyboard, carpal tunnel syndrome actually has numerous causes.

    Bound by bones and ligaments, the carpal tunnel is a narrow passageway — about as big around as your thumb — located on the palm side of your wrist. This tunnel protects a main nerve to your hand and nine tendons that bend your fingers. Pressure placed on the nerve produces the numbness, pain and, eventually, hand weakness that characterize carpal tunnel syndrome.
    Fortunately, for most people who develop carpal tunnel syndrome, proper treatment usually can relieve the pain and numbness and restore normal use of their wrists and hands.

    Carpal tunnel syndrome typically starts gradually with a vague aching in your wrist that can extend to your hand or forearm. Other common carpal tunnel syndrome symptoms include:

    • Tingling or numbness in your fingers or hand, especially your thumb and index, middle or ring fingers, but not your little finger. This sensation often occurs while holding a steering wheel, phone or newspaper or upon awakening. Many people "shake out" their hands to try to relieve their symptoms. As the disorder progresses, the numb feeling may become constant.

    • Pain radiating or extending from your wrist up your arm to your shoulder or down into your palm or fingers, especially after forceful or repetitive use. This usually occurs on the palm side of your forearm.

    • A sense of weakness in your hands and a tendency to drop objects.


    The cause of carpal tunnel syndrome is pressure on the median nerve. The median nerve is a mixed nerve, meaning it has a sensory function and also provides nerve signals to move your muscles (motor function). The median nerve provides sensation to your thumb, index finger, middle finger and the middle-finger side of the ring finger.

    Pressure on the nerve can stem from anything that reduces the space for it in the carpal tunnel. Possible causes include:

    Other health conditions. Some examples include rheumatoid arthritis, certain hormonal disorders — such as diabetes, thyroid disorders and menopause — fluid retention due to pregnancy, or deposits of amyloid, an abnormal protein produced by cells in your bone marrow.

    Repetitive use or injury. Repetitive flexing and extending of the tendons in the hands and wrists, particularly when done forcefully and for prolonged periods without rest, also can increase pressure within the carpal tunnel. Injury to your wrist can cause swelling that exerts pressure on the median nerve.

    Physical characteristics. It may be that your carpal tunnel is more narrow than average.

    Carpal Tunnel Syndrome - Test Your Knowledge

    The wrist is surrounded by a band of tissue. Between the band of tissue and the wrist bone is the carpal tunnel.

    How much do you know about carpal tunnel syndrome?

    Q: Symptoms of carpal tunnel syndrome which occur in the hand include:

    A. pain
    B. numbness
    C. tingling, burning, or itchiness
    D. weakness
    E. All of the above
    F. None of the above

    Q: Carpal tunnel syndrome results from:

    A. pressure on or compression of the median nerve in the wrist.
    B.cracking your knuckles
    C. falling asleep on your arm.

    Q: Symptoms of carpal tunnel syndrome do not usually affect the:

    index finger.
    little finge

    Q: Diagnostic tests for carpal tunnel syndrome may include:

    Tinel's sign.
    Phalen's maneuver.
    Nerve conduction velocity study.
    All of the above
    None of the above

    Q: Tinel's sign is performed by:

    tapping over the nerve to elicit a tingling sensation.
    bending the wrist forward to provoke a tingling sensation.

    Q: Phalen's maneuver is performed by:

    moving the wrist from side to side.
    bending the wrist forward to provoke a tingling sensation.

    Q: Which statement is true? With carpal tunnel, fingers:

    may feel swollen even if they are not visibly swollen.
    never are swollen.

    Q: A similar condition to carpal tunnel syndrome which occurs in the ankle is known as:

    ankle arthritis.
    tarsal tunnel syndrome.
    ankle fusion.

    Q: Conditions which can lead to carpal tunnel syndrome include:

    fluid retention from pregnancy or menopause.
    injury or trauma.
    All of the above
    None of the above

    Q: Certain rare diseases can cause deposits of abnormal substances in and around the carpal tunnel leading to carpal tunnel syndrome symptoms. Which is not one of those conditions?

    multiple myeloma

    Q: Though carpal tunnel symptoms can occur anytime, carpal tunnel symptoms usually are more bothersome during the:


    Q: Carpal tunnel syndrome is:

    always chronic and persistent.
    temporary condition in some cases.

    Q: Treatment options for carpal tunnel syndrome can include:

    medications including NSAIDS and corticosteroids.
    modifying activities and rest.
    surgery (carpal tunnel release).
    All of the above
    None of the above

    Q: Though the mechanism is unknown it has been reported that this vitamin can help relieve symptoms associated with carpal tunnel syndrome. What vitamin is it?

    Vitamin B6
    Vitamin B12
    Vitamin C

    Q: Other symptoms which may be associated with carpal tunnel syndrome include:

    shooting pains through arm.
    waking at night, needing to shake out the feeling in your hand.
    loss of grip strength.
    muscles at base of thumb atrophy.
    All of the above
    None of the above

    Q: According to NINDS (National Institute of Neurological Disorder and Stroke), there is little clinical data which proves or confirms that repetitive movements of the hand and wrist cause carpal tunnel syndrome. True or False?


    Q: It is three times more likely for:

    men to develop carpal tunnel syndrome than women.
    women to develop carpal tunnel syndrome than men.

    Q: Which statement is true about carpal tunnel syndrome? Carpal tunnel:

    usually occurs only in adults.
    usually affects dominant hand first.
    leaves some people unable to distinguish by touch between hot and cold.
    may occur in people who have a smaller than average carpal tunnel.
    All of the above
    None of the above

    Q: A Clinical study revealed that heavy computer use (defined as up to 7 hours per day):

    did increase risk of developing carpal tunnel syndrome.
    did not increase risk of developing carpal tunnel syndrome.

    Great Tips for Easing the Pain of Carpal Tunnel Syndrome
    #1: Lie down on your back and prop up your arm with pillows

    #2: Avoid using your hand too much. Try to use the other hand more often

    #3: Find a new way to use your hand by using a different or smaller tool.

    #4: Take regular breaks from repeated hand movements.

    #5: Avoid bending your wrists down for long periods.

    #6: Take some Ibuprofen to help ease the discomfort of carpal tunnel syndrome.

    #7: Wear a splint or a brace on your wrist, especially at night.

    #8: Put ice on your wrist as often as you can

    #9: Massaging the area and doing stretching exercises of the wrist may help too.


    Full Details:






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    To confirm diagnosis of rabies on post-mortem:

    A. Find negri bordies in saliva
    B. Find negri bodies in corneal scraping -
    C. Anti-rabies antibodies in blood(?)

    Rabies diagnosis in animals

    The direct fluorescent antibody test (dFA) is the test most frequently used to diagnose rabies. This test requires brain tissue from animals suspected of being rabid. The test can only be performed post-mortem (after the animal is dead).

    Rabies diagnosis in humans
    Several tests are necessary to diagnose rabies ante-mortem (before death) in humans; no single test is sufficient. Tests are performed on samples of saliva, serum, spinal fluid, and skin biopsies of hair follicles at the nape of the neck. Saliva can be tested by virus isolation or reverse transcription followed by polymerase chain reaction (RT-PCR). Serum and spinal fluid are tested for antibodies to rabies virus. Skin biopsy specimens are examined for rabies antigen in the cutaneous nerves at the base of hair follicles.

    The importance of routine rabies tests
    Rapid and accurate laboratory diagnosis of rabies in humans and other animals are essential for timely administration of postexposure prophylaxis. Within a few hours, a diagnostic laboratory can determine whether or not an animal is rabid and inform the responsible medical personnel. The laboratory results may save a patient from unnecessary physical and psychological trauma, and financial burdens, if the animal is not rabid.

    In addition, laboratory identification of positive rabies cases may aid in defining current epidemiologic patterns of disease and provide appropriate information for the development of rabies control programs.

    Laboratory tests for rabies
    The standard test for rabies testing is dFA. This test has been thoroughly evaluated for more than 40 years, and is recognized as the most rapid and reliable of all the tests available for routine use. All rabies laboratories in the United States perform this test (post-mortem) on animals suspected of having rabies.

    Other tests for diagnosis and research, such as electron microscopy (EM), histologic examination, immunohistochemistry (IHC), RT-PCR, and isolation in cell culture are useful tools for studying the virus structure, histopathology, molecular typing, and virulence of rabies viruses.

    Direct fluorescent antibody test (dFA)
    The dFA test is based on the observation that animals infected by rabies virus have rabies virus proteins (antigen) present in their tissues. Because rabies is present in nervous tissue (and not blood like many other viruses), the ideal tissue to test for rabies antigen is brain. The most important part of a dFA test is flouresecently-labelled anti-rabies antibody. When labelled antibody is incubated with rabies-suspect brain tissue, it will bind to rabies antigen. Unbound antibody can be washed away and areas where antigen is present can be visualized as fluorescent-apple-green areas using a fluorescence microscope. If rabies virus is absent there will be no staining.

    Antigen detection by dFA
    The rabies antibody used for the dFA test is primarily directed against the nucleoprotein (antigen) of the virus (see The Virus section on viral structure). Rabies virus replicates in the cytoplasm of cells, and infected cells may contain large round or oval inclusions containing collections of nucleoprotein (N) or smaller collections of antigen that appear as dust-like fluorescent particles if stained by the dFA procedure.

    General histopathology
    Histologic examination of biopsy or autopsy tissues is occasionally useful in diagnosing unsuspected cases of rabies that have not been tested by routine methods. When brain tissue from rabies virus-infected animals are stained with a histologic stain, such as hematoxylin and eosin, evidence of encephalomyelitis may be recognized by a trained microscopist. This method is nonspecific and not considered diagnostic for rabies.

    Before current diagnostic methods were available, rabies diagnosis was made using this method and the clinical case history. In fact, most of the significant histopathologic features (changes in tissue caused by disease) of rabies infection were described in the last quarter of the 19th century. After Louis Pasteur's successful experiments with rabies vaccination, scientists were motivated to identify the pathologic lesions of rabies virus.

    Histopathologic evidence of rabies encephalomyelitis (inflammation) in brain tissue and meninges includes the following:

    • Mononuclear infiltration
    • Perivascular cuffing of lymphocytes or polymorphonuclear cells
    • Lymphocytic foci
    • Babes nodules consisting of glial cells
    • Negri bodies

    Perivascular cuffing or inflammation around a blood vessel. Perivascular inflammatory cell infiltrates in hematoxylin & eosin stained brain tissue.

    Negri bodies
    In 1903, most of the histopathologic signs of rabies were recognized, but rabies inclusions had not yet been detected. At this time, Dr. Adelchi Negri reported the identification of what he believed to be the etiologic agent of rabies, the Negri body. In his report, he described Negri bodies as round or oval inclusions within the cytoplasm of nerve cells of animals infected with rabies. Negri bodies may vary in size from 0.25 to 27 µm. They are found most frequently in the pyramidal cells of Ammon's horn, and the Purkinje cells of the cerebellum. They are also found in the cells of the medulla and various other ganglia. Negri bodies can also be found in the neurons of the salivary glands, tongue, or other organs. Staining with Mann's, giemsa, or Sellers stains can permit differentiation of rabies inclusions from other intracellular inclusions. With these stains, Negri bodies appear magenta in color and have small (0.2 µm to 0.5 µm), dark-blue interior basophilic granules.

    The presence of Negri bodies is variable. Histologic staining for Negri bodies is neither as sensitive nor as specific as other tests. Some experimentally-infected cases of rabies display Negri bodies in brain tissue; others do not. Histologic examination of tissues from clinically rabid animals show Negri bodies in about 50% of the samples; in contrast, the dFA test shows rabies antigen in nearly 100% of the samples. In other cases, non-rabid tissues have shown inclusions indistinquishable from Negri bodies. Because of these problems, the presence of Negri bodies should not be considered diagnostic for rabies.


    Full Details:



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    Drugs used in Hodgkin lymphoma:


    Chemotherapy drugs for Hodgkin's lymphoma and their side effects

    Drugs that doctors use to treat Hodgkin's lymphoma
    There are many, many different combinations of drugs used to treat Hodgkin’s lymphoma. These combinations are sometimes called chemotherapy regimes or regimens.

    Doctors often shorten the names of these combinations by using the first letter of each drug. The most commonly used combination for Hodgkin's lymphoma is ABVD, which contains the drugs Adriamycin (doxorubicin), bleomycin, vinblastine and dacarbazine.

    There has been a trial looking into Hodgkin's treatment that is comparing ABVD with a shorter more intensive chemotherapy course called Stanford V. This contains the drugs mustine, doxorubicin, vinblastine, vincristine, bleomycin, etoposide and steroids. With this combination, you have chemotherapy weekly over 12 weeks. This trial has now stopped recruiting patients.

    There are many other combinations of chemotherapy drugs that doctors use to treat Hodgkin's lymphoma, including ChlvPP. Your specialist will pick the drug combination which best suits your situation and test results.

    Side effects
    All chemotherapy drugs have side effects. Drugs affect people in different ways. Not everyone has the same side effects with the same drug - some people have very few at all. It is not possible to tell how you will react until you have had that particular drug. It is important to remember that these effects are temporary. They will go away when your treatment is finished. All the drugs have different side effects. Ask your doctor or nurse which are most common with the chemotherapy drugs you will be having.

    There are some side effects that are quite common with many chemotherapy drugs. These are

    A fall in the number of blood cells
    Feeling and being sick
    Sore mouth and mouth ulcers
    Hair loss or thinning
    Feeling tired and run down
    Chemotherapy drugs
    Doxorubicin (also called Adriamycin)
    Etoposide (also called VP16)
    Vincristine (also called Oncovin)

    Some of these drugs can cause a lot of damage if they leak into the tissues. This is less likely these days with the use of central lines.

    If you are having medication to control side effects and it isn't working, do tell your doctor or chemotherapy nurse. There are lots of different anti sickness and anti diarrhoea medicines, for example. Another one may work better for you.

    Possible long term side effects
    Chemotherapy can have long term effects on your health. These most certainly do not happen to everyone. The commonest is infertility. Your doctor will try to choose drugs that are less likely to cause infertility if you are young and have not yet had children. Other long term effects are much less common, but include heart disease, damage to the lungs and risk of getting another cancer in the future.

    Unfortunately some chemotherapy used to treat Hodgkin's lymphoma can cause damage to your ovaries or testicles. This can mean that you can't have children (infertility). It is difficult for doctors to say definitely whether this will happen to you. It depends on

    • The chemotherapy drugs you are having
    • Your total dose of the drugs
    • Your age if you are a woman

    It may be possible for men and teenage boys to store sperm before they start their chemotherapy. This is called sperm banking. Ask your doctor if you think you would like to do this.

    For women, chemotherapy can cause an early menopause. Doctors can treat this with hormone replacement therapy. There is a lot of research looking into ways of trying to preserve the fertility of young women given chemotherapy, such as freezing bits of ovarian tissue and replacing them after treatment. But this research is still at a very early stage. It is now possible to freeze unfertilised eggs, but the difficulty is that it can take a few weeks to harvest the eggs and your doctor may be keen to get on with giving you your treatment. There is more about ways women can keep their fertility in the section on fertility and chemotherapy in CancerHelp UK.

    Look in the section on sex and fertility in living with Hodgkin's lymphoma for more about coping with these effects of chemotherapy.

    Second cancers
    Your treatment might increase the risk of you getting another type of cancer in the future. This is a small risk, but it is there. Both chemotherapy drugs and radiotherapy work by damaging cells. They damage and kill the Hodgkin’s lymphoma cells, but can damage healthy cells as well. The damage can lead to other cells becoming cancerous years after your treatment.

    If you have had chemotherapy to treat Hodgkin's lymphoma, you have a small increased risk of getting leukaemia in the future. Research that followed people treated as children has found that this risk peaks about 5 years after treatment and then drops away over the next 10 years. So 15 years after your treatment, your leukaemia risk is no longer increased.

    Doctors don't know whether this increased risk of cancer in the future is only because of treatment. People who get lymphoma have a slightly increased risk of getting cancer anyway. The lymphoma is an immediate risk to your health. Your doctors have to balance this against the long term risks of another cancer if you are cured.

    You probably agree that the most important thing is to treat your Hodgkin’s lymphoma. Your doctor will want you to come back to the hospital for check ups for many years so that they can keep an eye on you and watch out for any signs of a second cancer.

    Heart disease
    Some drugs used to treat Hodgkin’s lymphoma can cause heart problems. This is also true of radiotherapy to the middle of the chest. You may be at a slightly increased risk of heart attack or other heart problems in the future. As with the risk of second cancers, your doctors will be trying their best to treat your lymphoma effectively while trying to keep down these other long term risks as much as they can.

    Lung damage
    Some chemotherapy drugs, particularly bleomycin, can cause inflammation of the lungs. This usually shows up at the time you are treated. It is called pneumonitis (new-mon-itis). If you get this side effect, your doctors will probably stop giving you bleomycin straight away. Usually once you stop having the bleomycin, the lung inflammation goes away. In rare cases, the lung damage does not get better and causes breathlessness.


    What ABVD is?
    ABVD is the name of a chemotherapy treatment used for Hodgkin’s lymphoma. It is made up of the drugs

    A – Adriamycin (now called doxorubicin)
    B – Bleomycin
    V – Vinblastine
    D – Dacarbazine (DTIC)

    How you have treatment
    You have ABVD drugs into your bloodstream (intravenously). You can have them through a thin, short tube (a cannula) put into a vein in your arm each time you have treatment. Or you may have them through a central line or a PICC line. These are long, plastic tubes that give the drugs directly into a large vein in your chest. You have the tube put in just before your course of treatment starts and it stays in place as long as you need it.

    You usually have ABVD chemotherapy as cycles of treatment. Each cycle of treatment lasts 4 weeks. Depending on your needs, you may have from 4 to 6 cycles, taking 4 to 6 months in total.

    You have each cycle of treatment in the following way. On the first day you have all 4 drugs mentioned above as injections or drips into your cannula, central line or PICC line. You then have a 2 week break. Then you have another dose of the same 4 drugs followed by another 2 week break. This completes one cycle of treatment and you then start another treatment cycle.

    ABVD may have a harmful effect on a developing baby and it is not advisable to become pregnant or father a child if you are having this treatment. You should talk about contraception with your doctor before treatment starts.

    Women may stop having periods (amenorrhoea). This may only be temporary.


    Hodgkin's Lymphoma

    Chemotherapy uses drugs to kill cancer cells. The drugs are called cytotoxic medications. Chemotherapy is referred to as body-wide, or systemic, therapy because the drugs travel throughout the entire body.

    Cytotoxic drugs may be taken by mouth or given by injection. Treatment may be administered at a medical center, doctor's office, or even a patient's home. Some patients receiving chemotherapy may need to remain in the hospital for several days so the effects of the drug can be monitored.

    Patients may receive 4 - 8 cycles of chemotherapy, depending on the stage. A cycle is usually 28 days and consists of several doses of drug administration followed by a period of rest.

    Specific Drugs and Drug Combinations Used in Hodgkin's Disease
    The standard chemotherapy regimens for Hodgkin’s disease are ABVD and Stanford V.

    ABVD consists of a 4-drug combination:

    • Doxorubicin (Adriamycin)
    • Bleomycin
    • Vinblastine
    • Dacarbazine

    Stanford V consists of a 7-drug combination:

    • Doxorubicin (Adriamycin)
    • Mechlorethamine (nitrogen mustard)
    • Vincristine
    • Vinblastine
    • Bleomycin
    • Etoposide
    • Prednisone

    BEACOPP (bleomycin, etoposide, Adriamycin, cyclophosphamide, vincristine, procarbazine, and prednisone) is a chemotherapy regimen reserved for high-risk patients. This regimen is proving to be extremely effective, particularly in advanced stages, with studies reporting remission rates of over 95% in patients with advanced Hodgkin's. However, this regimen also increases the risk for developing secondary cancers such as leukemia. Patients who are treated with BEACOPP should receive long-term follow-up care to monitor for side effects from this therapy.

    Combinations of Chemotherapy and Radiation(Combined Modality) Regimens.

    Chemotherapy (usually ABVD) plus radiation, referred to as combined modality, is a common treatment approach for patients with more advanced-stage disease and for those who have early-stage bulky (large mass) disease.

    Chemotherapy with low-dose radiation is being used in children with excellent results, even for late stage cancer. In one study, 82% of the children were still disease free at 5 years. Some chemotherapy drugs or high doses of radiation may be more deleterious to a boy's future fertility than to a girl's. A gender-specific combined regimen for pediatric Hodgkin's reduces the amount of radiation given to boys and also substitutes etoposide for procarbazine in the chemotherapy mixture (procarbazine, vincristine, prednisone, and doxorubicin).



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