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  • Pharyngitis

    Pharyngitis:  Inflammation of the pharynx, referred
    to also as sore throat.

    Pharyngitis can be acute or chronic inflammation.  Commonly among
    adults who live or work in dusty or very dry environments, use their voices
    excessively, use tobacco or alcohol habitually, or suffer from chronic
    sinusitis, persistent coughs, or allergies.

    Acute pharyngitis may precede the common cold or other communicable
    diseases.  Chronic pharyngitis is commonly an extension of nasopharyngeal
    obstruction or inflammation.  Uncomplicated pharyngitis usually subsides
    in 3 to 10 days.

    Cause;  In children, it is often caused by streptococcal bacteria. 
    In 90% of cases, pharyngitis occurs as the result of a virus.

    Symptoms:

    Sore throat

    Difficulty swallowing (swallowing saliva is usually more painful than
    swallowing food)

    Sensation of a lump in the throat

    Have the urge to swallow constantly

    Redden, inflamed posterior pharyngeal wall

    Mild fever

    Headache

    Muscle and joint pain – especially in bacterial pharyngitis

    Treatment:

    Treatment is usually symptomatic – consisting mainly of rest, warm saline
    gargles, throat lozenges containing a mild anesthetic, plenty of fluids,
    and analgesics as prescribed by your doctor.

    Bacterial pharyngitis requires antibiotic therapy – usually penicillin
    or another broad spectrum antibiotic if the patients is allergic to penicillin.

  • Patent Ductus Arteriosus

    Patent: open, unobstructed

    Ductus: fetal blood vessel which joins the aorta and
    pulmonary artery

    Arteriosus:  pertaining to artery

    Patent Ductus Arteriosus:  (PDA)  This
    abnormal opening between the pulmonary artery and the aorta allows left
    to right shunting of blood from the aorta to the pulmonary artery. 
    This results in recirculation of arterial blood through the lungs.

    In the early stages, PDA may produce no clinical effects, but in time
    it can precipitate pulmonary vascular disease, causing symptoms to appear
    by age 40.  The patients with a small shunt or who undergo effective
    surgical repair have a good chance of recovery.  But PDA may advance
    to intractable CHF, which may be fatal.

    Most prevalent in premature infants, PDA often accompanies rubella syndrome. 
    It may be associated with other congenital defects, such as coarctation
    of the aorta, ventricular septal defect, and pulmonary and aortic stenoses.

    Cause:  Results from failure of the fetal ductus arteriosus
    (a fetal blood vessel that connects the pulmonary artery to the descending
    aorta) to close within days to weeks after birth.

    Symptoms:

    For infants, especially premature ones with a large PDA usually develop
    respiratory distress with signs of CHF. 

    Frequent respiratory infections

    Slow motor development

    Failure to thrive.

    Most children with PDA have only cardiac symptoms.  Others may
    exhibit signs of heart disease, such as physical underdevelopment and fatigability.

    By age 40, adults with untreated PDA may develop fatigability and dyspnea
    on exertion.  Cyanosis appears in the final stages of illness.

    Murmur (called Gibson murmur)  This continuous murmur is best heard
    at the base of the heart, at the second left intercostal space under the
    left clavicle in most children with PDA.

    May have bounding peripheral arterial pulses (Corrigan’s pulse), may
    have widened pulse pressure.

    Cardiomegaly

    Tachycardia

    Dilated ascending aorta

    Treatment:

    For infants with PDA that has no symptoms (asymptomatic) the patient
    may not require immediate treatment.

    Those with CHF require fluid restriction, diuretic, and digitalis to
    minimize or control symptoms.  If theses measure does not control
    CHF, the patient requires surgery to ligate the ductus.  The doctor
    may delay surgical correction until age 1 if the patient has only mild
    symptoms.

    Before surgery, children with PDA require antibiotics to protect against
    infective endocarditis.

    Other forms of therapy include cardiac catheterization to deposit a
    plug in the ductus to stop shunting, or administration of indomethacin
    I.V. (a prostaglandin inhibitor that provides an alternative to surgery
    in premature infants) to induce ductus spasm and closure.

  • Parkinson’s Disease

    Parkinson’s Disease: 
    This slowly progressive, degenerative neurologic disorder. This disorder
    is one of the most common crippling disorder in the US.  Deterioration
    progresses for an average of 10 years, at which time secondary disorders
    occurs such as pneumonia, aspiration or some other infection which can
    lead to death.  Parkinson’s disease affects men more often than women.

    Cause:  Uncertain.  Dopamine
    deficiency prevents affected brain cells from performing their normal inhibitory
    function within the central nervous system

    Symptoms:

    Insidious tremor that begins in the fingers (unilateral
    pill roll tremor), increases during stress or anxiety and decreases with
    purposeful movement and sleep

    Muscle rigidity causing resistance to passive
    muscle stretching, which may be uniform or jerky

    Difficulty walking (gait lacks normal parallel
    motion and may be retropulsive or propulsive)

    High-pitched monotone voice

    Drooling

    Masklike facial expression with poor blink reflex
    and wide-open eyes

    Walks with body bent forward (loss of positive
    control)

    Slurred speech

    Oculogyric crises (eyes are fixed upward, with
    involuntary tonic movements)

    Difficulty swallowing (dysphagia)

    Treatment:

    No cure at present

    Treatment seeks to relieve symptoms and keep the
    patient functional as long as possible.

    Drug therapy

    Physical therapy

    Stereotactic neurosurgery

  • Pancreatitis

    Pancreatitis:  Inflamation fo the pancreas. 
    May results from edema, necrosis, or hemorrhage.  In this disorder,
    the enzymes normally excreted by the pancreas attack and digest the surrounding
    pancreatic tissue. Pancreatitis occurs in acute and chronic forms. Prognosis
    is good when pancreatitis follows biliary tract disease but poor when it
    follows alcoholism.  mortality rises as high as 60% when pancreatits
    is associated with necrosis and hemorrhage.

    Cause:  Most commonly caused by biliary tract disease
    and alcoholism, pancreatitis also results from pancreatic carcinoma; certain
    drugs, such as glucocorticoids and chlorothiazide.  Less commonly,
    the disorderresults from metabolic and endocrine disorders, vascular disease,
    viral infections, or pregnancy.

    Symptoms:

    Epigastic pain

    Vomiting

    Extreme pain

    Abdominal rigidity

    Diminished bowel activity

    Extreme malaise

    Restlessness

    Mottled skin

    Tachycardia

    Low grade fever

    Cold, sweaty extremities

    Treatment:

    Maintain circulation and fluid volume

    Relieve pain

    Decreased pancreatic secretions.

    Antibiotic therapy

    I.V. replacement of electrolytes and proteins.

    Note:  If you expierence above symptoms see your doctor immediately,
    or go to the Emergency Room.

    Shock may occur (most common cause of death in early stage pancreatitis)

  • Osteoporosis

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    Osteoporosis: In this metabolic bone disorder, the rate of bone resorption accelerates while the rate of bone formation slows down, causing a loss of bone mass.

    Bones lose calcium and phosphate salts and , thus, become porous (penetrated by pores and open spaces), brittle, and abnormally vulnerable to fracture. Osteoporosis may be primary or secondary to an underlying disease. Often called senile or postmenopausal osteoporosis, primary osteoporosis most commonly develops in elderly, postmenopausal women.

    The cause of primarily osteoporosis remains unknown.  Secondary osteoporosis may result from prolonged therapy with steroids or heparin, or total immobilization or disuse of a bone (such case as hemiplegia).  It has also been link to alcoholism, malnutrition, malabsorption, scurvy, lactose intolerance, hyperthyroidism.  Risk factors include estrogen deficiency, poor dietary intake of calcium, declining gonadal adrenal function, and those who is lacking in mobility (sedentary life – style)

    Symptoms:

    Pain in lower back that radiates around the trunk
    Curving of the thoracic spine (kyphosis) – hump back in appearance
    Deformity
    Loss of height
    An elderly person often  becomes aware of the disorder when he bends to lift something, hears a snapping sound, then feels a sudden pain in the lower back.

    Treatment:

    Symptomatic treatment for preventive measures to decrease and or eliminate other fractures and to control pain., includes:  Physical therapy, estrogen therapy to decrease the rate of bone resorption, fluoride to stimulate bone formation, and calcium and vitamin D to support normal bone metabolism.

    Steroid therapy

    Patient may require a back brace to support the weakened vertebrae.

    Pain medication may be prescribed

    Proper diet of calcium and vitamin D, and gentle exercise

  • Nephrotic Syndrome

    Nephrotic Syndrome:  this disorder is characterized
    by marked proteinuria, hypoalbuminemia, hyperlipidemia, and edema. 
    Although nephrotic syndrome (NS) is not a disease itself, it results from
    a specific glomerular defect and indicates renal damage.

    Cause:  Primary (idiopathic) glomerulonephritis causes 75%
    of the cases (affecting adults and children).  Other causes include
    metabolic diseases such as diabetes mellitus; collagen vascular disorders,
    such as systemic lupus erythematosus and periarteritis nodosa; circulatory
    diseases, such as CHF, sickle cell anemia, and renal vein thrombosis; nephrotoxins,
    such as mercury, gold, and bismuth; allergic reactions, and infections,
    such as tuberculosis and enteritis.

    Pregnancy, hereditary nephritis, multiple myeloma, and other neoplastic
    diseases may also cause NS.

    Symptoms:

    Mild to severe dependent edema of the ankles or sacrum, or periorbital
    edema, (especially in children). 

    Symptoms may lead to  ascites, pleural effusion, and swollen external
    genitalia.

    May show signs of  orthostatic hypotension, lethargy, anorexia,
    depression, and pallor.

    Treatment:

    The goal is to correct the underlying cause (if possible)

    Supportive treatment consists of protein replacement with a nutritional
    diet of 1.5 protein/kg of body weight and restricted sodium intake.

    Diuretics for edema

    Antibiotics for infection

    Possible corticosteroid therapy 

  • Neonatal Disorders

    Hyperbilirubinemia

    Hyperbilirubinemia:  Also known as – Neonatal
    Jaundice    :  This disorder is the result of hemolytic processes
    in the neonate and brings elevated serum bilirubin levels and mild jaundice
    (yellowness of the skin).  It can be physiologic (with jaundice the
    only symptom)  it is very common and tends to more common and more
    severe in certain ethnic groups whose mean peak of unconjugated bilirubin
    is approximately twice that of the rest of the population.  It can
    be pathologic (resulting from an underlying disease).  Physiologic
    jaundice is self limiting; prognosis for pathologic jaundice varies, depending
    on the cause.  Untreated, severe hyperbilirubinemia may result in
    kernicterus, a neurologic syndrome resulting from deposition of unconjugated
    bilirubin in the brain cells and characterized by severe neural symptoms. 
    Survivors may develop cerebral palsy, epilepsy, or mental retardation,
    or may have only minor sequelae, such as perceptual motor handicaps and
    learning disorders.

    Causes:  As erythrocytes break down at the end of their
    neonatal life cycle, hemoglobin separates into globin (protein) and heme
    (iron) fragments.  heme fragments form unconjugated  (indirect)
    bilirubin, which binds with albumin for transport to lliver cells to conjugate
    with glucuronide, forming direct bilirubin. Because unconjugated bilirubin
    is fat soluble and cannot be excreted in the urine or bile, it may escape
    to extravascular tissue, especially fatty tissue and the brain, resulting
    in hyperbilirubinemia.

    This pathophysiologic process may develop several ways.  Factors
    that disrupt conjugation and usurp albumin-binding sites include drugs
    such as aspirin, tranquilizers, and sulfonamides and conditions such as
    hypothermia, anoxia, hypoglycemia, and hypoalbuminemia..  Decreased
    hepatic function can result in reduced bilirubin conjugation.  increased
    erythrocyte production or breakdown can accompany hemolytic disorders,
    or Rh or ABO incompatibility.  Biliary obstruction or hepatitis may
    block normal bile flow.  maternal enzymes present in breast milk can
    inhibit the neonate’s glucuronyl transferase conjugation activity.

    Symptoms:

    The predominant sign of hyperbilirubinemia is jaundice, which does not
    become clinically apparent until serum bilirubin levels reach about 7 mg/100
    ml.  Physiologic jaundice develops 24 hours after delivery in 50%
    of term neonates (usually day 2 – day 3) and 48 hours after delivery in
    80% of premature neonates (usually 3 – 5 days).  It generally disappears
    by day 7 in term neonates and by day 9 or day 10 in premature neonates. 
    Throughout physiologic jaundice, serum unconjugated bilirubin does not
    exceed 12 mg/100 ml.  Pathologic jaundice may appear anytime after
    the first day of life and persists beyond 7 days with serum bilirubin levels
    greater than 12 mg/100 ml in a term neonate, 15 mg/100 ml in a premature
    neonate, or increasing more than 5 mg/100 ml in 24 hours.

    Treatment:

    Depending on the underlying cause, treatment may include phototherapy,
    exchange transfusions, albumin infusion, and possible drug therapy . 
    Phototherapy is the treatment of choice for physiologic jaundice and pathologic
    jaundice from erythroblastosis fetalis (after the initial exchange transfusion). 
    Phototherapy uses fluorescent light to decompose bilirubin in the skin
    by  oxidation and is usually discontinued after bilirubin levels fall
    below 10 mg/100 ml and continue after bilirubin levels fall below 10 mg/100
    ml and continue to decrease for 24 hours.

    An exchange transfusion replaces the neonate’s blood with fresh blood
    (less than 48 hours old), removing some of the unconjugated bilirubin in
    serum.  Possible indications for exchange transfusions include hydrops
    fetalis, polycythemia, erythroblastosis fetalis, marked reticulocytosis,
    drug toxicity, and jaundice that develops within the first 6 hours after
    birth.

    For excessive bilirubin levels, treatment may include albumin administration,
    which provides additional albumin for binding unconjugated bilirubin. 
    This may be done 1 to 2 hours before exchange or as a substitute for a
    portion of the plasma in the transfused blood.

     

    Erythroblastosis Fetalis

    Erythroblastosis Fetalis:   Hemolytic
    anemia of the fetus or newborn due to transplacental transmission of maternally
    formed antibody against the fetus erythrocytes, usually secondary to an
    incompatibility between the mother’s Rh blood group and that of her offspring.

    A hemolytic disease of the fetus and newborn, this disorder stems from
    an incompatibility of fetal and maternal blood, resulting in maternal antibody
    activity against fetal RBC’s.

    Intrauterine transfusions can save 40% of fetuses with erythroblastosis. 
    However, in severe, untreated erythroblastosis fetalis, prognosis is poor,
    especially if kernicterus (a condition with severe neural symptoms associated
    with high bilirubin in the blood) develops.

    Causes:  Although more than 60 RBC antigens can stimulate
    antibody formation, erythroblastosis fetalis usually results from Rh isoimmunization
    – a condition that develops in approximately 7% of all pregnancies in the
    US.  Before the development of Rh (D) immune globulin (human), this
    condition was a major cause of kernicterus and neonatal death.

    During her first pregnancy, an Rh-negative female becomes sensitized
    by exposure to Rh-positive fetal blood antigens inherited from the father.
    A female may also become sensitized from receiving blood transfusions with
    alien Rh antigens, causing agglutinins to develop; from inadequate doses
    of Rh(D); or from failure to receive Rh (D) after significant fetal maternal
    leakage from abruptio placentae.  Subsequent pregnancy with an Rh-positive
    fetus provokes increasing amounts of maternal agglutinating antibodies
    to cross the placental barrier, attach to Rh-positive cells in the fetus,
    and cause hemolysis and anemia.  To compensate for this, the fetus
    steps up the production of RBC’s, and erythroblast, (immature RBC’s) appear
    in the fetal circulation.  Extensive hemolysis results in the release
    of large amounts of unconjugated bilirubin, which the liver is unable to
    conjugate and excrete, causing hyperbilirubinemia and hemolytic anemia.

    Symptoms:

    Jaundice usually isn’t present at birth but may appear as soon as 30
    minutes later or within 24 hours.  The mildly affected neonate shows
    mild to moderate hepatosplenomegaly and pallor.  In severely affected
    neonates who survive birth, erythroblastosis fetalis usually produces pallor,
    edema, petechiae, hepatosplenomegaly, grunting respiration’s, crackles,
    poor muscle tone, neurologic unresponsiveness, possible heart murmurs,
    a bile stained umbilical cord, and yellow or meconium stained amniotic
    fluid.  Untreated neonates may develop kernicterus from hemolytic
    disease and show signs such as anemia, lethargy, poor sucking ability,
    retracted head, stiff extremities, squinting, a high pitched cry, and convulsions.

    Hydrops fetalis causes extreme hemolysis, fetal hypoxia, heart failure
    (with possible pericardial effusion and circulatory collapse), edema, peritoneal
    and pleural effusions, and green or brown tinged amniotic fluid (usually
    indication a stillbirth).

    Other symptoms of the neonate with hydrops fetalis include: enlarged
    placenta, marked pallor, hepatosplenomegaly, cardiomegaly, and ascites.

    Treatment:

    Treatment depends on the degree of maternal sensitization and the effects
    of hemolytic disease on the fetus or neonate.

    Intrauterine intraperitoneal transfusion is performed when amniotic
    fluid analysis suggests the fetus is severely affected, and delivery is
    inappropriate because of fetal immaturity.  A transabdominal puncture
    under fluoroscopy into the fetal peritoneal cavity allows infusion of group
    O, Rh-negative blood.

    Planned delivery, usually 2 to 4 weeks before term date, depends on
    maternal history, serologic tests, and amniocentesis; labor may be induced
    from the 34th to 38th week of gestation.  During labor, the fetus
    should be monitored electronically; capillary blood scalp sampling determines
    acid base balance.  Any indication of fetal distress necessitates
    immediate cesarean delivery.

    phenobarbital administered during the last 5 to 6 weeks of pregnancy
    may lower serum bilirubin levels in the neonate.  An exchange transfusion
    removes antibody coated RBC’s and prevents hyperbilirubinemia through removal
    of the neonate’s blood and replacements with fresh group O, Rh-negative
    blood.  Albumin infusion helps to bind bilirubin, reducing the chances
    of hyperbilirubinemia.  Phototherapy by exposure to ultraviolet light
    also reduces bilirubin levels.

    Neonatal therapy for hydrops fetalis consists of maintaining ventilation
    by intubation, oxygenation, and mechanical assistance, when necessary;
    and removal of excess fluid to relieve severe ascites and respiratory distress. 
    Other appropriate measures include an exchange transfusion and maintenance
    of the neonate’s body temperature.

    Gamma globulin that contains anti-Rh-positive antibody (Rh (O) can provide
    passive immunization, which prevents maternal Rh isoimmunization in Rh-negative
    females.  However, it is ineffective if sensitization has already
    resulted from a previous pregnancy, abortion, or transfusion.

  • Nasal Polyps

    Nasal Polyps:  These benign and edematous
    growths are usually multiple, mobile, and bilateral.  Nasal distention
    and enlargement of the bony framework may be a result from nasal polyps
    that are large and numerous., and possibly occluding the airway. 
    Nasal polyps usually develop as a result of continuous pressure resulting
    from a chronic allergy that causes mucous membrane edema in the nose and
    sinuses.  They usually occur more commonly in adults.

    Symptoms:

    Nasal obstruction

    Anosmia ( absence of the sense of smell )

    A sensation of fullness in the face

    Nasal discharge

    SOB ( shortness of breath )

    Treatment:   

    Corticosteroids ( either by direct injection into the polyp or
    by local spray, to reduce the polyp temporarily.

    Treatment of the underlying cause may include:  antihistamines
    to
    control allergy and antibiotic therapy if infection is present. 
    Local application of an astringent shrinks hypertrophied tissue.

    Medical management alone is rarely effective, and for this reason,
    the treatment of choice is polypectomy (intranasal removal of the nasal
    polyp with a wire snare), usually performed under local anesthesia. 
    If continued recurrence, surgical opening of the ethmoidal and maxillary
    sinuses, and evacuation of diseased tissue may be done.

  • Rubella

    also called German measles and or
    Three
    day measles.

    Rubella is a contagious viral infection that is associated
    with a rash, inflamed eyes that may last one – to five days before the
    rash appears, fever, malaise, runny nose, and headache.  Rubella is
    cause by a virus that is transmitted through the air or by close contact. 
    An expecting mother who has this disease can transmit it to the fetus,
    and it can be very serious because it can cause defects to their unborn
    child.  If the women is infected with Rubella in her first trimester,
    congenital rubella syndrome can occur, and defects are rare if the expecting
    mom contracted rubella after her 20th week of pregnancy. A person can transmit
    rubella from 7 days before rash appears and until 1 week after the rash
    disappears.

    Symptoms:

    Red rash

    Low grade fever

    Headache

    Malaise

    Runny nose

    Inflammation of the eyes

    Or the patient may experience no symptoms at all.

    Treatment: There is no specific treatment for Rubella. Other
    than-

    See your Doctor.

    Rest.

    Acetaminophen may be given to relieve fever and for the discomfort.

    Fluids.

    Prevention:

    Children should get complete immunization shots (MMR )

    Women of childbearing age, should get screen by rubella serology, and
    if immunity is not present, immunization can be given providing that conception
    can be prevented for at least 3 months after getting vaccination. * Vaccination
    should not be given to pregnant women at any time.

  • Restless Leg Syndrome

    Restless Leg Syndrome:    Is a
    neurological disorder. Patients who suffers from this disorder feel a tingling
    or a crawling sensation deep in the legs, sometimes patients complain of
    pain and a burning sensation and have the need to move their legs to relieve
    the discomfort.  The symptoms is usually worst at night and can lead
    to insomnia. It may also be brought on by excessive use of caffeine products,
    it has also been link to folic acid and iron deficiencies.

    Symptoms:

    Tingling sensation deep in the legs

    Pain

    May experience a burning and or crawling sensation in the legs

    Often feels it at night

    Insomnia and or disturbance of sleep pattern

    Treatment:

    Relieving Pain, Your doctor may prescribe anywhere from simple over
    the counter medication to something stronger.

    Your doctor may prescribe medication used to treat Parkinson’s disease.

    With all medication use as prescribed by your doctor

     * Call your doctor if you experience the above symptoms so
    your doctor can evaluate you and give you the proper course of treatment. 
    The symptoms above resembles those of Deep vein thrombosis, and or any
    other neurological disorders, Kidney disease, Parkinson’s and many others.
    It is important to be diagnosis and treated properly by your Physician