Introduction to Kyphosis

Kyphosis, also known as roundback, is an anteroposterior curving of the spine that causes a bowing of the back, commonly at the thoracic, but sometimes at the thoracolumbar or sacral, level.
Normally, the spine displays some convexity, but excessive thoracic kyphosis is pathologic. Kyphosis occurs in children and adults.

Causes
Congenital kyphosis is rare but usually severe, with resultant cosmetic deformity and reduced pulmonary function.
Adolescent kyphosis
Also called Scheuermann’s disease, juvenile kyphosis, and vertebral epiphysitis, adolescent kyphosis is the most common form of this disorder. It may result from growth retardation or a vascular disturbance in the vertebral epiphysis (usually at the thoracic level) during periods of rapid growth or from congenital deficiency in the thickness of the vertebral plates.
Other causes include infection, inflammation, aseptic necrosis, and disk degeneration. The subsequent stress of weight bearing on the compromised vertebrae may result in the thoracic hump commonly seen in adolescents with kyphosis. Symptomatic adolescent kyphosis is more prevalent in girls than in boys and usually occurs between ages 12 and 16.
Adult kyphosis
Also known as adult roundback, adult kyphosis may result from degeneration of intervertebral disks, atrophy, or osteoporotic collapse of the vertebrae that’s associated with aging; from an endocrine disorder, such as hyperparathyroidism or Cushing’s disease; or from prolonged steroid Continue reading “Introduction to Kyphosis”

Understanding Bone marrow Transplantation

In bone marrow transplantation, usually 500 to 700 ml of marrow is aspirated from the pelvic bones of a human leukocyte antigen (HLA)–compatible donor (allogeneic) or of the recipient himself during periods of complete remission (autologous). The aspirated marrow is filtered and then infused into the recipient in an attempt to repopulate the patient’s marrow with normal cells.
This procedure has effected long-term, healthy survivals in about half of the patients with severe aplastic anemia. Bone marrow transplantation may also be effective in treating patients with acute leukemia, certain immunodeficiency diseases, and solid-tumor cancers.
Because bone marrow transplantation carries serious risks, it requires strict adherence to infection protection techniques and strict aseptic technique. It also requires that a primary caregiver provide consistent care and continuous monitoring of the patient’s status.
Before bone marrow infusion
  • Explain to the patient that the success rate depends on the stage of the disease and on finding an HLA-identical sibling match.
  • After bone marrow aspiration is completed under local anesthetic, apply pressure dressings to the donor’s aspiration sites. Observe the sites for bleeding. Relieve pain with an analgesic and ice packs as needed.
  • Assess the patient’s understanding of bone marrow transplantation. If necessary, correct any misconceptions about the procedure and provide additional information. Prepare the patient to expect an extended facility stay. Explain that chemotherapy and, possibly, radiation therapy are necessary to remove cells that may cause the body to reject the transplant.
  • Various treatment protocols are used. For example, I.V. cyclophosphamide may be used Continue reading “Understanding Bone marrow Transplantation”

Brief Summary of Inguinal hernia

A hernia occurs when all or part of a viscus protrudes from a normal location in the body. Most hernias are protrusions of part of the abdominal viscus through the abdominal wall. Although many kinds of abdominal hernias are possible, inguinal hernias are most common.
With an inguinal hernia, the large or small intestine, omentum, or bladder protrudes into the inguinal canal. Hernias can be reducible, incarcerated, or strangulated.

Causes

In males, during the 7th month of gestation, the testes normally descend into the scrotum, preceded by the peritoneal sac. If the sac closes improperly, it leaves an opening through which the intestine can slip. In either sex, a hernia can result from weak abdominal muscles or increased intra-abdominal pressure. An inguinal hernia may be indirect or direct.
Indirect inguinal hernia
An indirect inguinal hernia, the more common hernia, results from weakness in the fascial margin of the internal inguinal ring. This type of hernia enters the inguinal canal through the internal inguinal ring and emerges through the external inguinal ring. The hernia extends down the inguinal canal into the scrotum or labia.
An indirect inguinal hernia may develop at any age, is three times more common in males, and is Continue reading “Brief Summary of Inguinal hernia”

Special considerations in Ulcerative colitis

  • Accurately record intake and output, particularly the frequency and volume of stools.
  • Watch for signs of dehydration and electrolyte imbalances, specifically signs of hypokalemia (muscle weakness, paresthesia) and hypernatremia (fever, tachycardia, flushed skin, dry tongue).
  • Monitor hemoglobin and hematocrit, and transfuse if necessary.
  • Provide good mouth care for the patient who is allowed nothing by mouth.
  • After each bowel movement, thoroughly clean the skin around the rectum.
  • Administer medication. Watch for adverse effects of prolonged corticosteroid therapy (moonface, hirsutism, edema, gastric irritation). Be aware that such therapy may mask infection.
  • If the patient needs total parenteral nutrition, change dressings, assess for inflammation at the insertion site, and check blood glucose every 6 hours.
  • Take precautionary measures if the patient is prone to bleeding. Watch closely for signs of complications, such as a perforated colon and peritonitis (fever, severe abdominal pain, abdominal rigidity and tenderness, and cool, clammy skin), and toxic megacolon Continue reading “Special considerations in Ulcerative colitis”

Abruptio Placentae

With abruptio placentae, also called placental abruption, the placenta separates from the uterine wall prematurely, usually after the 20th week of gestation, producing hemorrhage. Abruptio placentae is most common in multigravidas—usually in women older than age 35—and is a common cause of bleeding during the second half of pregnancy. Fetal prognosis depends on gestational age and amount of blood lost; maternal prognosis is good if hemorrhage can be controlled.

Causes
In many cases, the cause of abruptio placentae is unknown. Predisposing factors include cocaine use, trauma (such as a direct blow to the uterus resulting from abuse or accidental trauma), placental site bleeding from a needle puncture during amniocentesis, chronic or pregnancy-induced hypertension (which raises pressure on the maternal side of the placenta), multiparity of more than five, short umbilical cord, dietary deficiency, smoking, advanced maternal age, and pressure on the venae cavae from an enlarged uterus.
With abruptio placentae, blood vessels at the placental bed rupture spontaneously, owing to a lack of resiliency or to abnormal changes in uterine vasculature. Hypertension complicates the situation, as does an enlarged uterus, which can’t contract sufficiently to seal off the torn vessels. Consequently, bleeding continues unchecked, possibly shearing off the placenta partially or completely. If a peripheral portion of the placenta separates from the uterine wall, such bleeding is typically external or marginal (in about 80% of patients); if the central portion of the placenta becomes detached and the still-intact peripheral portions trap the blood, the bleeding is typically internal or concealed (in about 20% of patients). As blood enters the muscle fibers, the uterus is unable to completely relax, increasing uterine tone and irritability. If bleeding into the muscle fibers is profuse, the uterus turns blue or purple and the accumulated blood prevents its normal Continue reading “Abruptio Placentae”

Mallory-Weiss syndrome

Mild to massive and usually painless bleeding due to a tear in the mucosa or submucosa of the cardia or lower esophagus characterizes Mallory-Weiss syndrome. Such a tear, usually singular and longitudinal, results from prolonged or forceful vomiting. About 60% of these tears involve the cardia; 15%, the terminal esophagus; and 25%, the region across the esophagogastric junction. Mallory-Weiss syndrome is most common in men older than age 40, especially alcoholics.
Causes
The direct cause of a tear in Mallory-Weiss syndrome is forceful or prolonged vomiting, probably when the upper esophageal sphincter fails to relax during vomiting. This lack of sphincter coordination is more common after excessive intake of alcohol. Other factors and conditions that may also increase intra-abdominal pressure and predispose to esophageal tearing include coughing, straining during bowel movements, trauma, seizures, childbirth, hiatal hernia, esophagitis, gastritis, and atrophic gastric mucosa.
Signs and symptoms
Typically, Mallory-Weiss syndrome begins with the vomiting of blood or the passing of large amounts of blood rectally a few hours to several days after normal vomiting. This bleeding, which may be accompanied by epigastric or back pain, may range from mild to massive but is generally more profuse than in esophageal rupture.
In patients with Mallory-Weiss syndrome, the blood vessels are only partially severed, preventing Continue reading “Mallory-Weiss syndrome”

Introduction to Metabolic alkalosis

metabolic alkalosisA clinical state marked by decreased amounts of acid or increased amounts of base bicarbonate, metabolic alkalosis causes metabolic, respiratory, and renal responses, producing characteristic symptoms—most notably, hypoventilation. This condition always occurs secondary to an underlying cause. With early diagnosis and prompt treatment, the prognosis is good; however, untreated metabolic alkalosis may lead to coma and death.

Causes
Metabolic alkalosis results from loss of acid, retention of base, or renal mechanisms associated with decreased serum levels of potassium and chloride.
Loss of acid
Causes of critical acid loss include vomiting, nasogastric tube drainage or lavage without adequate electrolyte replacement, fistulas, and the use of steroids and certain diuretics (furosemide, thiazides, and ethacrynic acid).
Hyperadrenocorticism is another cause of severe acid loss. Cushing’s disease, primary hyperaldosteronism, and Bartter’s syndrome, for example, all lead to retention of sodium and Continue reading “Introduction to Metabolic alkalosis”

Introduction to Metabolic acidosis

A physiologic state of excess acid accumulation and deficient base bicarbonate, metabolic acidosis is produced by an underlying pathologic disorder. Symptoms result from the body’s attempts to correct the acidotic condition through compensatory mechanisms in the lungs, kidneys, and cells.
Metabolic acidosis is more prevalent among children, who are vulnerable to acid-base imbalance because their metabolic rates are faster and their ratios of water to total body weight are lower. Severe or untreated metabolic acidosis can be fatal.
Causes
Metabolic acidosis usually results from excessive burning of fats in the absence of usable carbohydrates. This can be caused by diabetic ketoacidosis, chronic alcoholism, malnutrition, or a low-carbohydrate, high-fat diet—all of which produce more keto acids than the metabolic process can handle.
Other causes include:
  • anaerobic carbohydrate metabolism: a decrease in tissue oxygenation or perfusion, as occurs with pump failure after myocardial infarction, or when pulmonary or hepatic disease, shock, or anemia forces a shift from aerobic to anaerobic metabolism, causing a corresponding rise in the lactic acid level
  • renal insufficiency and failure (renal acidosis): underexcretion of metabolized acids or the Continue reading “Introduction to Metabolic acidosis”

Summary of Idiopathic thrombocytopenic purpura

Idiopathic thrombocytopenic purpura (ITP), thrombocytopenia that results from immunologic platelet destruction, may be acute (postviral thrombocytopenia) or chronic (Werlhof’s disease, purpura hemorrhagica, essential thrombocytopenia, autoimmune thrombocytopenia). Acute ITP usually affects children between ages 2 and 6; chronic ITP mainly affects adults younger than age 50, especially women between ages 20 and 40.
Causes
ITP may be an autoimmune disorder because antibodies that reduce the life span of platelets have been found in nearly all patients. The spleen probably helps to remove platelets modified by the antibody. Acute ITP usually follows a viral infection, such as rubella and chickenpox, and can follow immunization with a live virus vaccine. Chronic ITP seldom follows infection and is commonly linked to immunologic disorders, such as systemic lupus erythematosus or human immunodeficiency virus infection. It’s also linked to drug reactions.

Signs and symptoms
Signs and symptoms of ITP common to all forms of thrombocytopenia include petechiae, ecchymoses, and mucosal bleeding from the mouth, nose, and GI tract. Generally, hemorrhage is a rare physical finding. Purpuric lesions may occur in vital organs, such as the lungs, kidneys, or brain, and may prove fatal.
With acute ITP, which is common in children, onset is usually sudden and without warning, causing easy bruising, epistaxis, and bleeding gums. Onset of chronic ITP is insidious.

Diagnosis
Platelet count less than 20,000/µl combined with prolonged bleeding time suggest ITP. Platelet size and morphologic appearance may be abnormal; anemia may be present if bleeding has Continue reading “Summary of Idiopathic thrombocytopenic purpura”

Introduction to Neurogenic bladder

Also known as neuromuscular dysfunction of the lower urinary tract, neurologic bladder dysfunction, and neuropathic bladder, neurogenic bladder refers to all types of bladder dysfunction caused by an interruption of normal bladder innervation. Subsequent complications include urinary incontinence, residual urine retention, urinary tract infection, calculi formation, and renal failure. A neurogenic bladder can be spastic (hypertonic, reflex, or automatic), flaccid (hypotonic, atonic, nonreflex, or autonomous), or uncoordinated (dyssynergic).
Causes
At one time, neurogenic bladder was thought to result primarily from spinal cord injury; now, it appears to stem from a host of underlying conditions:
  • cerebral disorders, such as cerebrovascular accident, brain tumor (meningioma and glioma), Parkinson’s disease, multiple sclerosis, and dementia
  • spinal cord disease or trauma, such as spinal stenosis (causing cord compression) or arachnoiditis (causing adhesions between the membranes covering the cord), cervical spondylosis, myelopathies from hereditary or nutritional deficiencies and, rarely, tabes dorsalis
  • disorders of peripheral innervation, including autonomic neuropathies resulting from endocrine disturbances such as diabetes mellitus (most common)
  • metabolic disturbances, such as hypothyroidism, porphyria, or uremia (infrequent)
  • acute infectious diseases such as Guillain-Barré syndrome
  • heavy metal toxicity
  • chronic alcoholism
  • collagen diseases such as systemic lupus erythematosus Continue reading “Introduction to Neurogenic bladder”