ESOPHAGEAL VERICES

INTRODUCTION: Bleeding or hemorrhage from esophageal varices is one of the major causes of death in patients with cirrhosis. Esophageal varices are dilated veins usually found in the submucosa of the lower esophagus; they may develop higher in the esophagus or extend into the stomach. The condition is nearly always caused by portal hypertension.

RISK FACTORS FOR HEMORRHAGE: Risk factors for hemorrhage include muscular strain from heavy lifting; straining at stool; sneezing, coughing, or vomiting; esophagitis or irritation of vessels (rough food or irritating fluids); reflux of stomach contents (especially alcohol); and salicylates or any drug that erodes the esophageal mucosa.

CLINICAL MANIFESTATIONS: Hematemesis, melena, or general deterioration in mental or physical status; often a history of alcohol abuse. Signs and symptoms of shock including a cool clammy skin, hypotension, tachycardia and may be present.

ASSESSMENT AND DIAGNOSTIC METHODS: Endoscopy, barium swallow, ultrasonography, CT, and angiography.

Neurologic and portal hypertension assessment: Liver function tests including serum aminotransferases, bilirubin, alkaline phosphatase, and serum proteins. Splenoportography, hepatoportography, and celiac angiography.

MEDICAL MANAGEMENT: Aggressive medical care includes evaluation of extent of bleeding and continuous monitoring of vital signs when hematemesis and melena are present. Signs of potential hypovolemia are noted; blood volume is monitored with a central venous catheter or pulmonary artery catheter. Oxygen is administered to prevent hypoxia and to maintain adequate blood oxygenation, and IV fluids and volume expanders are administered to restore fluid volume and replace electrolytes. Transfusion of blood components may also be required. Nonsurgical treatment is preferred because of the high mortality associated with emergency surgery to control bleeding from esophageal varices and because of the poor physical condition of most of these patients.

Nonsurgical measures include: Pharmacologic therapy: vasopressin, vasopressin with nitroglycerin, somatostatin and octreotide, beta-blocking agents, and nitrates. Balloon tamponade, saline lavage, and endoscopic sclerotherapy. Esophageal banding therapy and variceal band ligation.

RELATED;

1.  NOSE BLEEDING

2.  PEPTIC ULCER DISEASE

3.  ULCERATIVE COLITIS

REFERENCES

HEPATIC FAILURE

 

INTRODUCTION:  hepatic failure is the clinical syndrome of sudden and severely impaired liver function in a previously healthy person. It is characterized by the development of first symptoms or jaundice within 8 weeks of the onset of disease. Three categories are frequently cited: hyperacute, acute, and subacute. The hepatic lesion is potentially reversible, and survival rates are approximately 20% to 50%, depending greatly on the cause of liver failure. Those who do not survive die of massive hepatocellular injury and necrosis.

CAUSES OF LIVER FAILURE:  Viral hepatitis a common cause; other causes include toxic drugs and chemicals, metabolic disturbances, and structural changes.

CLINICAL MANIFESTATIONS:  Jaundice and profound anorexia.  Often accompanied by coagulation defects, renal failure and electrolyte disturbances, cardiovascular abnormalities, infection, hypoglycemia, encephalopathy, and cerebral edema.

MANAGEMENT:  Liver transplantation (treatment of choice).  Blood or plasma exchanges. Liver support systems, such as hepatocytes within synthetic fiber columns, extracorporeal liver assist devices, and bioartificial liver, until transplantation is possible.

 

RELATED;

1.  JAUNDICE

2. REAL FAILURE

3. HYPOGLYCEMIA

4. EDEMA

5.  ANATOMY AND PHYSIOLOGY OF THE HUMAN LIVER

6.  FUNCTIONS OF THE LIVER

REFERENCES

GLAUCOMA

 

INTRODUCTION:  The presence of aqueous humor in the anterior cavity of the eye creates a pressure called intraocular pressure. An increase in this pressure is an important risk factor for glaucoma, which is now defined as a group of disorders that damage the optic nerve and cause loss of vision.  Other risk factors include high blood pressure and diabetes.

PATHOPHYSIOLOGY:  In the most common form of glaucoma, aqueous humor is not reabsorbed properly into the canal of Schlemm. Increased pressure in the anterior cavity is transmitted to the lens, the vitreous humor, and the retina and optic nerve. As pressure on the retina increases, halos may be seen around bright lights, and peripheral vision is lost. Frequently, however, there are no symptoms.

SIGNS AND SYMPTOMS:  A person with glaucoma may not notice the shrinking visual field in one eye before vision loss is far advanced. This happens because the brain will suppress a faulty image from one eye that it cannot easily integrate with the normal image of the other eye. When both eyes are affected, the person may not become aware of the gradual loss of peripheral vision, because close work such as reading does not require the edges of the visual fields.

PREVENTION AND TREATMENT: Glaucoma may often be controlled with medications that constrict the pupil and flatten the iris, thus opening up access to the canal of Schlemm. If these or other medications are not effective, laser surgery may be used to create a larger drainage canal.  Anyone over the age of 40 should have a test for glaucoma; anyone with a family history of glaucoma should have this test annually, as should those with diabetes or high blood pressure. If diagnosed early, glaucoma is treatable, and blindness can usually be prevented.

 

RELATED;

1.  BLOOD PRESSURE AND HYPERTENSION

2. DIABETES MELLITUS

3. MEDICAL CONDITIONS

4. REFERENCES

MEGALOBLASTIC ANEMIA

 

INTRODUCTION: In the anemias caused by deficiencies of vitamin B12 or folic acid, identical bone marrow and peripheral blood changes occur because both vitamins are essential for normal DNA synthesis. DNA,the genetic material

PATHOPHYSIOLOGY:

Folic Acid Deficiency: Folic acid is stored as compounds referred to as folates. The folate stores in the body are much smaller than those of vitamin B12, and they are quickly depleted when the dietary intake of folate is deficient (within 4 months). Folate deficiency occurs in people who rarely eat uncooked vegetables. Alcohol increases folic acid requirements; folic acid requirements are also increased in patients with chronic hemolytic anemias and in women who are pregnant. Some patients with malabsorptive diseases of the small bowel may not absorb folic acid normally.

Vitamin B12 Deficiency: A deficiency of vitamin B12 can occur in several ways. Inadequate dietary intake is rare but can develop in strict vegetarians who consume no meat or dairy products. Faulty absorption from the GI tract is more common, as with conditions such as Crohn’s disease or after ileal resection or gastrectomy. Another cause is the absence of intrinsic factor. A deficiency may also occur if disease involving the ileum or pancreas impairs absorption. The body normally has large stores of vitamin B12, so years may pass before the deficiency results in anemia.

Clinical Manifestations: Symptoms of folic acid and vitamin B12 deficiencies are similar, and the two anemias may coexist. Symptoms are progressive, although the course of illness may be marked by spontaneous partial remissions and exacerbations. Gradual development of signs of anemia (weakness, listlessness, and fatigue). Possible development of a smooth, sore, red tongue and mild diarrhea (pernicious anemia). Mild jaundice, vitiligo, and premature graying. Confusion may occur; more often, paresthesias in the extremities and difficulty keeping balance; loss of position sense. Lack of neurologic manifestations with folic acid deficiency alone. Without treatment, patients die, usually as a result of heart failure secondary to anemia.

ASSESSMENT AND DIAGNOSTIC FINDINGS: Schilling test (primary diagnostic tool): Complete blood cell count (Hgb value as low as 4 to 5 g/dL, WBC count 2,000 to 3,000 mm3 , platelet count fewer than 50,000 mm3 ; very high MCV, usually exceeding 110 m3 ). Serum levels of folate and vitamin B12 (folic acid deficiency and deficient vitamin B12)

MEDICAL MANAGEMENT: Folic Acid Deficiency: Increase intake of folic acid in patient’s diet and administer 1 mg folic acid daily. Administer IM folic acid for malabsorption syndromes. Prescribe additional supplements as necessary, because the amount in multivitamins may be inadequate to fully replace deficient body stores. Prescribe folic acid for patients with alcoholism as long as they continue to consume alcohol.

MEDICAL MANAGEMENT: Vitamin B12 Deficiency: Provide vitamin B12 replacement: Vegetarians can prevent or treat deficiency with oral supplements with vitamins or fortified soy milk; when the deficiency is due to the more common defect in absorption or the absence of intrinsic factor, replacement is by monthly IM injections of vitamin B12. A small amount of an oral dose of vitamin B12 can be absorbed by passive diffusion, even in the absence of intrinsic factor, but large doses (2 mg/day) are required if vitamin B12 is to be replaced orally. To prevent recurrence of pernicious anemia, vitamin B12 therapy must be continued for life.

RELATED;

1.  CONDITIONS OF ANEMIA  

2.  COMPOSITION OF BLOOD

3.  MEDICAL CONDITIONS

REFERENCES

PARKINSON’S DISEASE

 

INTRODUCTION: Parkinson’s disease is a slowly progressive degenerative neurologic disorder affecting the brain centers that are responsible for control and regulation of movement. The degenerative or idiopathic form of Parkinson’s disease is the most common; there is also a secondary form with a known or suspected cause. The cause of the disease is mostly unknown but research suggests several causative factors (eg, genetics, atherosclerosis, viral infections, head trauma). The disease usually first appears in the fifth decade of life and is the fourth most common neurodegenerative disease.

PATHOPHYSIOLOGY: Parkinson’s disease is associated with decreased levels of dopamine resulting from destruction of pigmented neuronal cells in the substantia nigra in the basal ganglia region of the brain. Dopamine  The loss of dopamine stores in this area of the brain results in more excitatory neurotransmitters than inhibitory neurotransmitters, leading to an imbalance that affects voluntary movement. Cellular degeneration causes impairment of the extrapyramidal tracts that control semiautomatic functions and coordinated movements; motor cells of the motor cortex and the pyramidal tracts are not affected.

CLINICAL MANIFESTATIONS: The cardinal signs of Parkinson’s disease are tremor, rigidity, bradykinesia (abnormally slow movements), and postural instability. Resting tremors: a slow, unilateral turning of the forearm and hand and a pill-rolling motion of the thumb against the fingers; tremor at rest and increasing with concentration and anxiety. Resistance to passive limb movement characterizes muscle rigidity; passive movement may cause the limb to move in jerky increments (lead-pipe or cog-wheel movements); stiffness of the arms, legs, face, and posture are common; involuntary stiffness of passive extremity increases when another extremity is engaged in voluntary active movement. Impaired movement: Bradykinesia includes difficulty in initiating, maintaining, and performing motor activities. Loss of postural reflexes, shuffling gait, loss of balance (difficulty pivoting); postural and gait problems place the patient at increased risk for falls.

OTHER CHARACTERISTICS: Autonomic symptoms that include excessive and uncontrolled sweating, paroxysmal flushing, orthostatic hypotension, gastric and urinary retention, constipation, and sexual dysfunction. Psychiatric changes may include depression, dementia, delirium, and hallucinations; psychiatric manifestations may include personality changes, psychosis, and acute confusion. Auditory and visual hallucinations may occur. Hypokinesia (abnormally diminished movement) is common. As dexterity declines, micrographia (small handwriting) develops. Masklike facial expression. Dysphonia (soft, slurred, low-pitched, and less audible speech).

ASSESSMENT AND DIAGNOSTIC METHODS: Patient’s history and presence of two of the four cardinal manifestations: tremor, rigidity, bradykinesia, and postural changes. Positron emission tomography (PET) and single photon emission computed tomography (SPECT) scanning have been helpful in understanding the disease and advancing treatment. Medical history, presenting symptoms, neurologic examination, and response to pharmacologic management are carefully evaluated when making the diagnosis.

MEDICAL MANAGEMENT: Goal of treatment is to control symptoms and maintain functional independence; no approach prevents disease progression.

PHARMACOLOGIC THERAPY: Levodopa is the most effective agent and the mainstay of treatment. Anticholinergic agents to control tremor and rigidity. Amantadine hydrochloride (Symmetrel), an antiviral agent, to reduce rigidity, tremor, and bradykinesia. Dopamine agonists (eg, pergolide, bromocriptine mesylate), ropinirole, and pramipexole are used to postpone the initiation of carbidopa and levodopa therapy. Monoamine oxidase inhibitors (MAOIs) to inhibit dopamine breakdown. Catechol-O-methyltransferase (COMT) inhibitors to reduce motor fluctuation. Antidepressant drugs. Antihistamine drugs to allay tremors.

RELATED;

1.  STROKE

2.  MEDICAL CONDITIONS

REFERENCES

WOUND HEALING BY FIRST INTENTION (PRIMARY UNION)

 

INTRODUCTION: Wounds are some of the most common disruptions on the human skin and the leading ports of entry for microbes into the body.  Whether a wound is following a surgical operation, burns or an accidental injury if it is not catered for, it may cause infections from the external environment.  In our discussion here, we are looking at the process through which a surgical and clean wound will take to heal.

This type of healing occurs when there is no contamination of the wound, and the edges of the wound are approximated, thus closing the wound. The best example of this situation is the surgical incision where contamination of the wound is minimized and the wound is closed by suturing, once the wound is sutured, the incision space fills with blood, which contains fibrin and blood cells and which subsequently clots, the surface of this clot becomes dehydrated and forms a scab.

Within 24 hours, neutrophils appear at the edges of the incision and the epithelium at the edges of the incision begins to proliferate, it migrates under the scab and forms a thin continuous epithelial layer.

By 72 hours, macrophages are usually the most numerous inflammatory cells and granulation tissue starts to develop, collagen fibers are present but do not bridge the incision site, the epithelial cells continue to proliferate under the scab and the epidermal covering over the incision becomes thicker.

By day 5, the incision space is filled with granulation tissue and collagen fibers begin to bridge the incision, the epidermis returns to its normal thickness and keratinized architecture.

During the second week, there is continued accumulation of collagen fibers and proliferation of fibroblasts, inflammatory cells, edema disappears, and the process of blanching begins.

By the end of one month, a connective tissue scar is devoid of inflammatory cells and is covered by an intact epidermis.

RELATED;

1. WOUND HEALING BY SECONDARY INTENTION  

2. COMPLICATIONS OF WOUND HEALING  

3. CHRONIC INFLAMMATION

4.  BURNS

REFERENCES

SPINAL CORD INJURIES

 

INTRODUCTION: Spinal cord injuries (SCIs) are a major health problem. Most SCIs result from motor vehicle crashes. Other causes include falls, violence especially primarily from gunshot wounds, and recreational sporting activities. Half of the victims are between 16 and 30 years of age; most are males. Another risk factor is substance abuse (alcohol and drugs). There is a high frequency of associated injuries and medical complications. The vertebrae most frequently involved in SCIs are the fifth, sixth, and seventh cervical vertebrae (C5–C7), the 12th thoracic vertebra (T12), and the first lumbar vertebra (L1). These vertebrae are the most susceptible because there is a greater range of mobility in the vertebral column in these areas. 

Damage to the spinal cord ranges from transient concussion (patient recovers fully), to contusion, laceration, and compression of the cord substance (either alone or in combination), to complete transection of the cord (paralysis below the level of injury). Injury can be categorized as primary (usually permanent) or secondary (nerve fibers swell and disintegrate as a result of ischemia, hypoxia, edema, and hemorrhagic lesions). Whereas a primary injury is permanent, a secondary injury may be reversible if treated within 4 to 6 hours of the initial injury. The type of injury refers to the extent of injury to the spinal cord itself. Incomplete spinal cord lesions are classified according to the area of spinal cord damage: central, lateral, anterior, or peripheral. A complete SCI can result in paraplegia (paralysis of the lower body) or tetraplegia (formerly quadriplegia— paralysis of all four extremities).

CLINICAL MANIFESTATIONS: The consequences of SCI depend on the type and level of injury of the cord.

Neurologic Level: The neurologic level refers to the lowest level at which sensory and motor functions are normal. Signs and symptoms include the following: Total sensory and motor paralysis below the neurologic level. Loss of bladder and bowel control (usually with urinary retention and bladder distention). Loss of sweating and vasomotor tone. Marked reduction of BP from loss of peripheral vascular resistance. If conscious, patient reports acute pain in back or neck; patient may speak of fear that the neck or back is broken.

Respiratory Problems: Related to compromised respiratory function; severity depends on level of injury. Acute respiratory failure is the leading cause of death in high cervical cord injury.

ASSESSMENT AND DIAGNOSTIC METHODS: Detailed neurologic examination, x-ray examinations (lateral cervical spine x-rays), computed tomography (CT), magnetic resonance imaging (MRI), and ECG (bradycardia and asystole are common in acute spinal injuries) are common assessment and diagnostic methods.

COMPLICATIONS: Spinal shock, a serious complication of SCI, is a sudden depression of reflex activity in the spinal cord (areflexia) below the level of injury. The muscles innervated by the part of the cord segment situated below the level of the lesion become completely paralyzed and flaccid, and the reflexes are absent. BP and heart rate fall as vital organs are affected. Parts of the body below the level of the cord lesion are paralyzed and without sensation.

EMERGENCY MANAGEMENT: Immediate patient management at the accident scene is crucial. Improper handling can cause further damage and loss of neurologic function. Consider any victim of a motor vehicle crash, a diving or contact sports injury, a fall, or any direct trauma to the head and neck as having an SCI until ruled out. Initial care includes rapid assessment, immobilization, extrication, stabilization or control of life-threatening injuries, and transportation to an appropriate medical facility. Maintain patient in an extended position (not sitting); no body part should be twisted or turned. The standard of care is referral to a regional spinal injury center or trauma center for treatment in first 24 hours.

MEDICAL MANAGEMENT: Acute Phase Goals of management are to prevent further SCI and to observe for symptoms of progressive neurologic deficits. The patient is resuscitated as necessary, and oxygenation and cardiovascular stability are maintained. High-dose corticosteroids (methylprednisolone) may be administered to counteract spinal cord edema. Oxygen is administered to maintain a high arterial PaO2. Extreme care is taken to avoid flexing or extending the neck if endotracheal intubation is necessary. Diaphragm pacing (electrical stimulation of the phrenic nerve) may be considered for patients with high cervical spine injuries. SCI requires immobilization, reduction of dislocations, and stabilization of the vertebral column. The cervical fracture is reduced and the cervical spine aligned with a form of skeletal traction (using skeletal tongs or calipers or the halo-vest technique). Weights are hung freely so as not to interfere with the traction. Early surgery reduces the need for traction. The goals of surgical treatment are to preserve neurologic function by removing pressure from the spinal cord and to provide stability.

MANAGEMENT OF COMPLICATIONS:

Spinal and Neurogenic Shock: Intestinal decompression is used to treat bowel distention and paralytic ileus caused by depression of reflexes. This loss of sympathetic innervation causes a variety of other clinical manifestations, including neurogenic shock signaled by decreased cardiac output, venous pooling in the extremities, and peripheral vasodilation. Patient who does not perspire on paralyzed portion of body requires close observation for early detection of an abrupt onset of fever. Body defenses are maintained and supported until the spinal shock abates and the system has recovered from the traumatic insult (up to 4 months).

RELATED;

1. THE CENTRAL NERVOUS SYSTEM  

2. THE ENTERIC NERVOUS SYSTEM  

3. ACTIVATION OF A NERVE IMPULSE

4.  BACK PAIN

REFERENCES

CARDIOGENIC SHOCK

INTRODUCTION: Cardiogenic shock occurs when the heart’s ability to contract and to pump blood is impaired and the supply of oxygen is inadequate for the heart and tissues. The causes of cardiogenic shock are known as either coronary or non-coronary. Coronary cardiogenic shock is more common than non-coronary cardiogenic shock and is seen most often in patients with acute myocardial infarction. Non-coronary causes of cardiogenic shock are related to conditions that stress the myocardium (eg, severe hypoxemia, acidosis, hypoglycemia, hypocalcemia, and tension pneumothorax) and conditions that result in ineffective myocardial function (eg, cardiomyopathies, valvular damage, cardiac tamponade, dysrhythmias).

CLINICAL MANIFESTATIONS: Classic signs include low blood pressure (BP), rapid and weak pulse. Dysrhythmias are common. Angina pain may be experienced. Hemodynamic instability. Complaints of fatigue.

MEDICAL MANAGEMENT: Goals of medical treatment include limiting further myocardial damage, preserving the healthy myocardium, and improving cardiac function. It is necessary first to treat the oxygenation needs of the heart muscle, increasing oxygen supply to the heart muscle while reducing oxygen demands. First-line treatment includes administering supplemental oxygen, controlling chest pain, administering fluids, and administering vasoactive medications (eg, dobutamine, nitroglycerin, dopamine) and antiarrhythmic medications. Hemodynamic monitoring and laboratory marker monitoring are performed. 

Mechanical cardiac support may be necessary. Coronary cardiogenic shock may be treated with thrombolytic therapy, a percutaneous coronary intervention, coronary artery bypass graft surgery, and/or intra-aortic balloon pump therapy. Noncoronary cardiogenic shock may be treated with cardiac valve replacement, correction of dysrhythmia, correction of acidosis and electrolyte disturbances, or treatment of the tension pneumothorax.

RELATED;

1. OTHER TYPES OF SHOCK  

2.  HYPERTENTION.  

3.  CONGESTIVE CARDIAC FAILURE

4.  MEDICAL CONDITIONS

REFERENCES

PANCREATITIS

 

INTRODUCTION: Pancreatitis (inflammation of the pancreas) is a serious disorder that can range in severity from a relatively mild, selflimiting disorder to a rapidly fatal disease that does not respond to any treatment. Acute pancreatitis is commonly described as an autodigestion of the pancreas by the exocrine enzymes it produces, principally trypsin. [Readabout biochemistry of enzymes]

Eighty percent of patients with acute pancreatitis have biliary tract disease or a history of long-term alcohol abuse. Other less common causes of pancreatitis include bacterial or viral infection, with pancreatitis occasionally developing as a complication of mumps virus.  Many disease processes and conditions have been associated with an increased incidence of pancreatitis, including surgery on or near the pancreas, medications, hypercalcemia, and hyperlipidemia. Up to 10% of cases are idiopathic, and there is a small incidence of hereditary pancreatitis. Mortality is high because of shock, anoxia, hypotension, or fluid and electrolyte imbalances. [Readabout shock]

Attacks of acute pancreatitis may result in complete recovery, may recur without permanent damage, or may progress to chronic pancreatitis.

CLINICAL MANIFESTATIONS: Severe abdominal pain is the major symptom. Pain in the midepigastrium may be accompanied by abdominal distention; a poorly defined, palpable abdominal mass; decreased peristalsis; and vomiting that fails to relieve the pain or nausea. Pain is frequently acute in onset (24 to 48 hours after a heavy meal or alcohol ingestion); may be more severe after meals and unrelieved by antacids. Patient appears acutely ill, Abdominal guarding; rigid or boardlike abdomen (generally an ominous sign, usually indicating peritonitis). Ecchymosis in the flank or around the umbilicus, which may indicate severe hemorrhagic pancreatitis. Nausea and vomiting, fever, jaundice, mental confusion, agitation. Hypotension related to hypovolemia and shock. May develop tachycardia, cyanosis, and cold, clammy skin. Acute renal failure common. Respiratory distress and hypoxia. May develop diffuse pulmonary infiltrates, dyspnea, tachypnea, and abnormal blood gas values. Myocardial depression, hypocalcemia, hyperglycemia, and disseminated intravascular coagulation (DIC).

ASSESSMENT AND DIAGNOSTIC FINDINGS: Diagnosis is based on history of abdominal pain, the presence of known risk factors, physical examination findings, and diagnostic findings (increased urine amylase level and white blood cell [WBC] count; hypocalcemia; transient hyperglycemia; glucosuria and increased serum bilirubin levels in some patients). X-rays of abdomen and chest, ultrasound, and contrast-enhanced computed tomography (CT) scan may be performed. Hematocrit and hemoglobin levels are used to monitor the patient for bleeding. Serum amylase and lipase levels are most indicative (elevated within 24 hours; amylase returns to normal within 48 to 72 hours; lipase remains elevated for longer period). Peritoneal fluid is evaluated for increase in pancreatic enzymes.

MEDICAL MANAGEMENT:

Acute Phase: During the acute phase, management is symptomatic and directed toward preventing or treating complications. Oral intake is withheld to inhibit pancreatic stimulation and secretion of pancreatic enzymes. Parenteral nutrition (PN) is administered to the debilitated patient. Nasogastric suction is used to relieve nausea and vomiting and to decrease painful abdominal distention and paralytic ileus. Histamine-2 (H2) receptor antagonists (cimetidine, ranitidine) or, sometimes, proton pump inhibitors are given to decrease hydrochloric acid secretion.  Adequate pain medication, such as morphine, is administered. Antiemetic agents may be prescribed to prevent vomiting. Correction of fluid, blood loss, and low albumin levels is necessary. Antibiotics are administered if infection is present. Insulin is necessary if significant hyperglycemia occurs. Aggressive respiratory care is provided for pulmonary infiltrates, effusion, and atelectasis. Biliary drainage (drains and stents) results in decreased pain and increased weight gain.  Surgical intervention may be performed for diagnosis, drainage, resection, or debridement.

MEDICAL MANAGEMENT:

Postacute Phase. Antacids are given when the acute episode begins to resolve. Oral feedings low in fat and protein are initiated gradually. Caffeine and alcohol are eliminated. Medications (eg, thiazide diuretics, glucocorticoids, or oral contraceptives) are discontinued.

RELATED;

1. INSULIN  

2. GLUCAGON

3.  THE ENDOCRINE PANCREAS

REFERENCES

ANAPHYLAXIS

 

INTRODUCTION: Anaphylaxis is a clinical response to an immediate (type I hypersensitivity) immunologic reaction between a specific antigen and an antibody. The reaction results from a rapid release of IgE-mediated chemicals, which can induce a severe, life-threatening allergic reaction. Substances that most commonly cause anaphylaxis include foods, medications, insect stings, and latex. Immunoglobulins

Foods that are common causes of anaphylaxis include peanuts, tree nuts, shellfish, fish, milk, eggs, soy, and wheat. Many medications have been implicated in anaphylaxis. Those that are most frequently reported include antibiotics (eg, penicillin), radiocontrast agents, IV anesthetics, aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), and opioids. Penicillins: Anaesthetic medication: Opioid analgesics  Closely related to anaphylaxis is a nonallergenic anaphylaxis (anaphylactoid) reaction.

Clinical Manifestations: Anaphylactic reactions produce a clinical syndrome that affects multiple organ systems. Reactions may be categorized as mild, moderate, or severe. The severity depends on the degree of allergy and the dose of allergen.  Mild Symptoms include peripheral tingling, a warm sensation, fullness in the mouth and throat, nasal congestion, periorbital swelling, pruritus, sneezing, and tearing eyes. Symptoms begin within 2 hours of exposure. Moderate Symptoms include flushing, warmth, anxiety, and itching in addition to any of the milder symptoms. More serious reactions include bronchospasm and edema of the airways or larynx with dyspnea, cough, and wheezing. The onset of symptoms is the same as for a mild reaction.

Severe: Severe systemic reactions have an abrupt onset with the same signs and symptoms described previously. Symptoms progress rapidly to bronchospasm, laryngeal edema, severe dyspnea, cyanosis, and hypotension.  Dysphagia, abdominal cramping, vomiting, diarrhea, and seizures can also occur.  Cardiac arrest and coma may follow.

Assessment and Diagnostic Methods: Diagnostic evaluation of the patient with allergic disorders commonly includes blood tests (complete blood cell count [CBC] with differential, high total serum IgE levels), smears of body secretions, skin tests, and the radioallergosorbent test (RAST).

Prevention: Prevention by avoidance of allergens is of utmost importance. If avoidance of exposure to allergens is impossible, the patient should be instructed to carry and administer epinephrine to prevent an anaphylactic reaction in the event of exposure to the allergen.  Health care providers should always obtain a careful history of any sensitivities before administering medications. Venom immunotherapy may be given to people who are allergic to insect venom. Insulin-allergic patients with diabetes or penicillin-sensitive patients may require desensitization.

Medical Management: Respiratory and cardiovascular functions are evaluated and cardiopulmonary resuscitation (CPR) is initiated in cases of cardiac arrest. Oxygen is administered in high concentration during CPR or when the patient is cyanotic, dyspneic, or wheezing. Patients with mild reactions need to be educated about the risk for recurrences. Patients with severe reactions need to be observed for 12 to 14 hours.

Pharmacologic Therapy: Epinephrine, antihistamines, and corticosteroids may be given to prevent recurrences of the reaction and to relieve urticaria and angioedema. Corticosteroids.  IV fluids (eg, normal saline solution), volume expanders, and vasopressor agents are administered to maintain blood pressure and normal hemodynamic status; glucagon may be administered. Plasmavolume expanders  Aminophylline and corticosteroids may also be administered to improve airway patency and function.

RELATED;

1. ASTHMA  

2.  ALLERGIC RHINITIS

3.  IMMUNOLOGY

4.  LACTOSE INTOLERANCE

REFERENCES

ANGINA PECTORIS

 

INTRODUCTION: Angina pectoris is a clinical syndrome characterized by paroxysms of pain or a feeling of pressure in the anterior chest. The cause is insufficient coronary blood flow, resulting in an inadequate supply of oxygen to meet the myocardial demand. Angina is usually a result of atherosclerotic heart disease and is associated with a significant obstruction of a major coronary artery. Factors affecting anginal pain are physical exertion, exposure to cold, eating a heavy meal, or stress or any emotion-provoking situation that increases blood pressure, heart rate, and myocardial workload. Unstable angina is not associated with the above and may occur at rest.

CLINICAL MANIFESTATIONS: Pain varies from a feeling of indigestion to a choking or heavy sensation in the upper chest ranging from discomfort to agonizing pain. The patient with diabetes mellitus may not experience severe pain with angina. Angina is accompanied by severe apprehension and a feeling of impending death. The pain is usually retrosternal, deep in the chest behind the upper or middle third of the sternum. Discomfort is poorly localized and may radiate to the neck, jaw, shoulders, and inner aspect of the upper arms (usually the left arm). A feeling of weakness or numbness in the arms, wrists, and hands, as well as shortness of breath, pallor, diaphoresis, dizziness or lightheadedness, and nausea and vomiting, may accompany the pain. Anxiety may occur with angina. An important characteristic of anginal pain is that it subsides when the precipitating cause is removed or with nitroglycerin.

ASSESSMENT AND DIAGNOSTIC METHODS: Evaluation of clinical manifestations of pain and patient history. Electrocardiogram changes (12-lead ECG), stress testing, blood tests. Echocardiogram, nuclear scan, or invasive procedures such as cardiac catheterization and coronary angiography.

MEDICAL MANAGEMENT: The objectives of the medical management of angina are to decrease the oxygen demand of the myocardium and to increase the oxygen supply. Medically, these objectives are met through pharmacologic therapy and control of risk factors. Alternatively, reperfusion procedures may be used to restore the blood supply to the myocardium. These include PCI procedures (eg, percutaneous transluminal coronary angioplasty [PTCA], intracoronary stents, and atherectomy) and coronary artery bypass graft (CABG).

PHARMACOLOGIC THERAPY: Nitrates, the mainstay of therapy (nitroglycerin). Beta-adrenergic blockers (metoprolol and atenolol). Calcium channel blockers/calcium ion antagonists (amlodipine and diltiazem). Antiplatelet and anticoagulant medications (aspirin, clopidogrel, heparin, glycoprotein [GP] IIb/IIIa agents [abciximab, tirofiban, eptifibatide]). Oxygen therapy.

RELATED;

1. ARTERIOSCLEROSIS  

2. BETA BLOCKERS  

3. CHAMBERS AND CIRCULATION THROUGH THE HEART

REFERENCES

BACK PAIN

 

INTRODUCTION: Most low back pain is caused by one of many musculoskeletal problems, including acute lumbosacral strain, unstable lumbosacral ligaments and weak muscles, osteoarthritis of the spine, spinal stenosis, intervertebral disk problems, and unequal leg length. Obesity, postural problems, structural problems, stress, overstretching of the spinal supports, and occasionally depression may also result in back pain. Back pain due to musculoskeletal disorders usually is aggravated by activity, whereas pain due to other conditions is not. Older patients may experience back pain associated with osteoporotic vertebral fractures, osteoarthritis of the spine, spinal stenosis, and spondylolisthesis, among other conditions.

CLINICAL MANIFESTATIONS: Acute or chronic back pain (lasting more than 3 months without improvement) and fatigue. Pain that radiates down the leg (radiculopathy, sciatica); presence of this symptom suggests nerve root involvement. Gait, spinal mobility, reflexes, leg length, leg motor strength, and sensory perception may be affected. Paravertebral muscle spasm (greatly increased muscle tone of back postural muscles) occurs with loss of normal lumbar curve and possible spinal deformity.

ASSESSMENT AND DIAGNOSTIC METHODS: Health history and physical examination (back examination, neurologic testing). Spinal x-ray. Bone scan and blood studies. Computed tomography (CT) scan. Magnetic resonance imaging (MRI). Electromyogram and nerve conduction studies. Myelogram, Ultrasound.

MEDICAL MANAGEMENT: Most back pain is self-limited and resolves within 4 weeks with analgesics, rest, and relaxation. Management focuses on relief of pain and discomfort, activity modification, and patient education. Bed rest is recommended for 1 to 2 days, for a maximum of 4 days and only if pain is severe. Other effective nonpharmacologic interventions include the application of superficial heat and spinal manipulation. Cognitive-behavioral therapy (eg, biofeedback), exercise regimens, spinal manipulation, physical therapy, acupuncture, massage, and yoga are all effective nonpharmacologic interventions for treating chronic low back pain but not acute low back pain. Most patients need to alter their activity patterns to avoid aggravating the pain. They should avoid twisting, bending, lifting, and reaching, all of which stress the back. A gradual return to activities and a program of low-stress aerobic exercise are recommended.

PHARMACOLOGIC THERAPY: Acute low back pain: nonprescription analgesics (eg, acetaminophen), nonsteroidal anti-inflammatory drugs (NSAIDs) (eg, ibuprofen), and prescription muscle relaxants (eg, cyclobenzaprine). Chronic low back pain: tricyclic antidepressants (eg, amitriptyline). Others: opioids (eg, morphine), tramadol (Ultram), benzodiazepines (eg, diazepam [Valium]), and gabapentin (Neurontin).

RELATED;

1. CHRONIC PAIN  

2. INFLAMMATION  

3. OSTEOPOROSIS

4.  MEDICAL CONDITIONS

REFERENCES

MENINGITIS

 

INTRODUCTION:  Meningitis is an inflammation of the lining around the brain and spinal cord caused by bacteria or viruses. Meningitis is classified as septic or aseptic. The aseptic form may be viral or secondary to lymphoma, leukemia, or human immunodeficiency virus (HIV). The septic form is caused by bacteria such as Streptococcus pneumoniae and Neisseria meningitidis.

PATHOPHYSIOLOGY:  The causative organism enters the bloodstream, crosses the blood brain barrier, and triggers an inflammatory reaction in the meninges.  The blood brain barrier  Independent of the causative agent, inflammation of the subarachnoid and piamater occurs. Increased intracranial pressure (ICP) results. Meningeal infections generally originate in one of two ways: either through the bloodstream from other infections (cellulitis) or by direct extension (after a traumatic injury to the facial bones). Bacterial or meningococcal meningitis also occurs as an opportunistic infection in patients with acquired immunodeficiency syndrome (AIDS) and as a complication of Lyme disease. Bacterial meningitis is the most significant form. The common bacterial pathogens are; N. meningitidis (meningococcal meningitis) and S. pneumoniae, accounting for 80% of cases of meningitis in adults. Haemophilus influenzae was once a common cause of meningitis in children, but, because of vaccination, infection with this organism is now rare in developed countries. Streptococcus:

CLINICAL MANIFESTATIONS:  Headache and fever are frequently the initial symptoms; fever tends to remain high throughout the course of the illness; the headache is usually either steady or throbbing and very severe as a result of meningeal irritation.  Meningeal irritation results in a number of other wellrecognized signs common to all types of meningitis:  Nuchal rigidity (stiff neck) is an early sign.  Positive Kernig’s sign: When lying with thigh flexed on abdomen, patient cannot completely extend leg.  Positive Brudzinski’s sign: Flexing patient’s neck produces flexion of the knees and hips; passive flexion of lower extremity of one side produces similar movement for opposite extremity.  Photophobia (extreme sensitivity to light) is common.  Rash (N. meningitidis): ranges from petechial rash with purpuric lesions to large areas of ecchymosis.  Disorientation and memory impairment; behavioral manifestations are also common. As the illness progresses, lethargy, unresponsiveness, and coma may develop.  Seizures can occur and are the result of areas of irritability in the brain; ICP increases secondary to diffuse brain swelling or hydrocephalus; initial signs of increased ICP include decreased level of consciousness and focal motor deficits.  An acute fulminant infection occurs in about 10% of patients with meningococcal meningitis, producing signs of overwhelming septicemia: an abrupt onset of high fever, extensive purpuric lesions (over the face and extremities), shock, and signs of disseminated intravascular coagulation (DIC); death may occur within a few hours after onset of the infection.

ASSESSMENT AND DIAGNOSTIC FINDINGS: Computed tomography (CT) scan or magnetic resonance imaging (MRI) scan to detect a shift in brain contents (which may lead to herniation) prior to a lumbar puncture.  Key diagnostic tests: bacterial culture and Gram staining of CSF and blood.

PREVENTION:  The Advisory Committee on Immunization Practices of the Centers for Disease Control and Prevention (CDC) (2008) recommends that the meningococcal conjugated vaccine be given to adolescents entering high school and to college freshmen living in dormitories.  Vaccination should also be considered as an adjunct to antibiotic chemoprophylaxis for anyone living with a person who develops meningococcal infection. Vaccination against H. influenzae and S. pneumoniae should be encouraged for children and at-risk adults. People in close contact with patients with meningococcal meningitis should be treated with antimicrobial chemoprophylaxis using rifampin, ciprofloxacin hydrochloride (Cipro), or ceftriaxone sodium (Rocephin). Therapy should be started within 24 hours after exposure because a delay in the initiation of therapy limits the effectiveness of the prophylaxis.

MEDICAL MANAGEMENT:  Vancomycin hydrochloride in combination with one of the cephalosporins (eg, ceftriaxone sodium, cefotaxime sodium) is administered by intravenous (IV) injection. Dexamethasone has been shown to be beneficial as adjunct therapy in the treatment of acute bacterial meningitis and in pneumococcal meningitis. Dehydration and shock are treated with fluid volume expanders. Seizures, which may occur early in the course of the disease, are controlled with phenytoin. Increased ICP is treated as necessary.

 

RELATED;

1.  CEREBRAL VASCULAR ACCIDENT

2.  THE BLOOD BRAIN BARRIER

3.  MEDICAL CONDITIONS 

REFERENCES

EPISTAXIS

 

INTRODUCTION:  Epistaxis is a hemorrhage from the nose caused by the rupture of tiny, distended vessels in the mucous membrane of any area of the nasal passage. The anterior septum is the most common site.

RISK FACTORS OF NOSEBLEEDS:  Risk factors include infections, low humidity, nasal inhalation of illicit drugs, trauma (including vigorous nose blowing and nose picking), arteriosclerosis, hypertension, nasal tumors, thrombocytopenia, aspirin use, liver disease, and hemorrhagic syndromes.

MEDICAL MANAGEMENT:  A nasal speculum, penlight, or headlight may be used to identify the site of bleeding in the nasal cavity. The patient sits upright with the head tilted forward to prevent swallowing and aspiration of blood and is directed to pinch the soft outer portion of the nose against the midline septum for 5 or 10 minutes continuously. Alternatively, a cotton tampon may be used to try to stop the bleeding. Suction may be used to remove excess blood and clots from the field of inspection. Application of anesthetics and nasal decongestants (phenylephrine, one or two sprays) to act as vasoconstrictors may be necessary. 

Visible bleeding sites may be cauterized with silver nitrate or electrocautery (high-frequency electrical current). If the origin of the bleeding cannot be identified, the nose may be packed with gauze impregnated with petrolatum jelly or antibiotic ointment. The packing may remain in place for 48 hours or up to 5 or 6 days if necessary to control bleeding. Antibiotics may be prescribed to prevent and manage infection.

 

RELATED;

1.  Anemia

2.  Thrombocytopenia

3.  Medical conditions

REFERENCES

ENDOMETRIOSIS

 

INTRODUCTION:  Endometriosis is a benign lesion with cells similar to those lining the uterus, growing aberrantly in the pelvic cavity outside the uterus. During menstruation, this ectopic tissue bleeds, mostly into areas having no outlet, which causes pain and adhesions. Endometrial tissue can also be spread by lymphatic or venous channels. There is a high incidence among patients who bear children later and have fewer children. It is usually found in nulliparous women between 25 and 35 years of age and in adolescents, particularly those with dysmenorrhea that does not respond to nonsteroidal anti-inflammatory drugs (NSAIDs) or oral contraceptives. There appears to be a familial predisposition to endometriosis. It is a major cause of chronic pelvic pain and infertility.

CLINICAL MANIFESTATIONS:  Symptoms vary but include dysmenorrhea, dyspareunia, and pelvic discomfort or pain (some patients have no pain).  Dyschezia (pain with bowel movements) and radiation of pain to the back or leg may occur.  Depression, inability to work due to pain, and difficulties in personal relationship may result.  Infertility may occur.

ASSESSMENT AND DIAGNOSTIC METHODS:  A health history, including an account of the menstrual pattern, is necessary to elicit specific symptoms. On pelvic examination, fixed tender nodules are sometimes palpated, and uterine mobility may be limited, indicating adhesions. Laparoscopic examination confirms the diagnosis and enables clinicians to determine the disease’s stage.

MEDICAL MANAGEMENT:  Treatment depends on symptoms, desire for pregnancy, and extent of the disease. In asymptomatic cases, routine examination may be all that is required. Other therapy for varying degrees of symptoms may be NSAIDs, oral contraceptives, gonadotropin-releasing hormone (GnRH) agonists, or surgery. Pregnancy often alleviates symptoms because neither ovulation nor menstruation occurs.

Pharmacologic Therapy:  Palliative measures (eg, use of medications, such as analgesic agents and prostaglandin inhibitors) for pain.  Oral contraceptives.  Synthetic androgen, causes atrophy of the endometrium and subsequent amenorrhea.  GnRH agonists decrease estrogen production and cause subsequent amenorrhea. Side effects are related to low estrogen levels (eg, hot flashes and vaginal dryness).

Surgical Management:  Laparoscopy to fulgurate endometrial implants and to release adhesions.  Laser surgery to vaporize or coagulate endometrial implants, thereby destroying the tissue.

RELATED;

1.  PELVIC INFLAMMATORY DISEASE

2.  OVULATION AND THE MENSTRUAL CYCLE

REFERENCES

RENAL FAILURE

 

INTRODUCTION:  Renal failure results when the kidneys are unable to remove metabolic waste and perform their regulatory functions. Acute renal failure (ARF) is a rapid loss of renal function due to damage to the kidneys. Three major categories of ARF are prerenal (hypoperfusion, as from volume depletion disorders, extreme vasodilation, or impaired cardiac performance); intrarenal (parenchymal damage to the glomeruli or kidney tubules, as from burns, crush injuries, infections, transfusion reaction, or nephrotoxicity, which may lead to acute tubular necrosis [ATN]); and postrenal (urinary tract obstruction, as from calculi, tumor, strictures, prostatic hyperplasia, or blood clots).

CLINICAL STAGES:  Initiation period: initial insult and oliguria.  Oliguric period (urine volume less than 400 mL/day): Uremic symptoms first appear and hyperkalemia may develop.  

Diuresis period: gradual increase in urine output signaling beginning of glomerular filtration’s recovery. Laboratory values stabilize and start to decrease.

Recovery period: improving renal function (may take 3 to 12 months).

CLINICAL MANIFESTATIONS:  Critical illness and lethargy with persistent nausea, vomiting, and diarrhea.  Skin and mucous membranes are dry.  Central nervous system manifestations: drowsiness, headache, muscle twitching, seizures.  Urine output scanty to normal; urine may be bloody with low specific gravity.  Steady rise in blood urea nitrogen (BUN) may occur depending on degree of catabolism; serum creatinine values increase with disease progression.  Hyperkalemia may lead to dysrhythmias and cardiac arrest.  Progressive acidosis, increase in serum phosphate concentrations, and low serum calcium levels may be noted.  Anemia from blood loss due to uremic GI lesions, reduced red blood cell life-span, and reduced erythropoietin production.

ASSESSMENT AND DIAGNOSTIC METHODS: Urine output measurements.  Renal ultrasonography, CT and magnetic resonance imaging (MRI) scans.  BUN, creatinine, electrolyte analyses.

MEDICAL MANAGEMENT:  Treatment objectives are to restore normal chemical balance and prevent complications until renal tissues are repaired and renal function is restored. Possible causes of damage are identified and treated.  Fluid balance is managed on the basis of daily weight, serial measurements of central venous pressure, serum and urine concentrations, fluid losses, blood pressure, and clinical status. Fluid excesses are treated with mannitol, furosemide, or ethacrynic acid to initiate diuresis and prevent or minimize subsequent renal failure.  Blood flow is restored to the kidneys with the use of intravenous (IV) fluids, albumin, or blood product transfusions.  Dialysis (hemodialysis, hemofiltration, or peritoneal dialysis) is started to prevent complications, including hyperkalemia, metabolic acidosis, pericarditis, and pulmonary edema.  Cation-exchange resins (orally or by retention enema).  IV dextrose 50%, insulin, and calcium replacement for the patient who is hemodynamically unstable (low blood pressure, changes in mental status, dysrhythmia).  Shock and infection are treated if present.  Arterial blood gases are monitored when severe acidosis is present.  Sodium bicarbonate to elevate plasma pH.  If respiratory problems develop, ventilatory measures are started.  Phosphate-binding agents to control elevated serum phosphate concentrations.  Replacement of dietary proteins is individualized to provide the maximum benefit and minimize uremic symptoms.  Caloric requirements are met with high-carbohydrate feedings; parenteral nutrition (PN).  Foods and fluids containing potassium and phosphorus are restricted.  Blood chemistries are evaluated to determine amount of sodium, potassium, and water replacement during oliguric phase.  After the diuretic phase, high-protein, high-calorie diet is given with gradual resumption of activities.

 

RELATED;

1.  GENITAL URINARY TRACT CONDITIONS AND INFECTIONS

2.  EXCRETION OF DRUGS

REFERENCES