CERVICAL CANCER

INTRODUCTION: Cancer of the cervix is predominantly squamous cell cancer and also includes adenocarcinomas. It is less common than it once was because of early detection by the Pap test, but it remains the third most common reproductive cancer in women.

RISK FACTORS: Risk factors vary from multiple sex partners to smoking to chronic cervical infection all of which predispose one to exposure to human papillomavirus [HPV].

CLINICAL MANIFESTATIONS: Cervical cancer is most often asymptomatic. When discharge, irregular bleeding, or pain or bleeding after sexual intercourse occurs, the disease may be advanced. Vaginal discharge gradually increases in amount, becomes watery, and finally is dark and foul smelling because of necrosis and infection of the tumor. Bleeding occurs at irregular intervals between periods or after menopause, may be slight, and is usually noted after mild trauma. As disease continues, bleeding may persist and increase. Leg pain, dysuria, rectal bleeding, and edema of the extremities signal advanced disease.

Nerve involvement, producing excruciating pain in the back and legs, occurs as cancer advances and tissues outside the cervix are invaded, including the fundus and lymph glands anterior to the sacrum. Extreme emaciation and anemia, often with fever due to secondary infection and abscesses in the ulcerating mass, and fistula formation may occur in the final stage.

ASSESSMENT AND DIAGNOSTIC FINDINGS: Pap smear and biopsy results show severe dysplasia, highgrade epithelial lesion, or carcinoma in situ. Other tests may include x-rays, laboratory tests, special examinations (eg, punch biopsy and colposcopy), dilation and curettage (D & C), CT scan, MRI, IV urography, cystography, PET, and barium x-ray studies.

MEDICAL MANAGEMENT: Disease may be staged (usually TNM system) to estimate the extent of the disease so that treatment can be planned more specifically and prognosis. Conservative treatments include monitoring, cryotherapy (freezing with nitrous oxide), laser therapy, loop electrosurgical excision procedure (LEEP), or conization (removing a cone-shaped portion of cervix). Simple hysterectomy if preinvasive cervical cancer (carcinoma in situ) occurs when a woman has completed childbearing. Radical trachelectomy is an alternative to hysterectomy. For invasive cancer, surgery, radiation (external beam or brachytherapy), platinum-based agents, or a combination of these approaches may be used.

RELATED;

1.  THE ORIGIN OF CANCER

2.  PATHOPHYSIOLOGY OF CANCER

3.  PATHOLOGY

4.  BIOCHEMISTRY

REFERENCES

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

IMPETIGO

 

INTRODUCTION:  Impetigo is a superficial infection of the skin caused by staphylococci, streptococci, or multiple bacteria. Exposed areas of the body, face, hands, neck, and extremities are most frequently involved. Impetigo is contagious and may spread to other parts of the skin or to other members of the family who touch the patient or who use towels or combs that are soiled with the exudate of the lesion. Impetigo is seen in people of all ages. It is particularly common among children living in poor hygienic conditions. Chronic health problems, poor hygiene, and malnutrition may predispose adults to impetigo.

CLINICAL MANIFESTATIONS: Lesions begin as small, red macules that become discrete, thin-walled vesicles that rupture and become covered with a honey-yellow crust. These crusts, when removed, reveal smooth, red, moist surfaces on which new crusts develop. If the scalp is involved, the hair is matted, distinguishing the condition from ringworm.  Bullous impetigo, a deep-seated infection of the skin caused by Staphylococcus aureus, is characterized by the formation of bullae from original vesicles. The bullae rupture, leaving a raw, red area.

MEDICAL MANAGEMENT:  Pharmacologic Therapy: Systemic antibiotic therapy is the usual treatment for impetigo. It reduces contagious spread, treats deep infection, and prevents acute glomerulonephritis (kidney infection). Agents for nonbullous impetigo: benzathine penicillin, oral penicillin, or erythromycin. Topical antibacterial therapy is the usual treatment for disease that is limited to a small area. The topical preparation is applied to lesions several times daily for 1 week. Lesions are soaked or washed with soap solution to remove central site of bacterial growth and to give the topical antibiotic an opportunity to reach the infected site.

RELATED;

1.  STREPTOCOCCUS

2.  STAPHYLOCOCCUS

3.  SEBORRHEIC DERMATITIS

REFERENCES

CANDIDIASIS

INTRODUCTION:  This is a fungal infection that is common especially in immunocompromised patients.  Usually fungi microbes are not a big burden in immunocompetent individuals and if the do infect an individual, in most cases they will be asymptomatic.  The commonest of these fungal species is Candida albicans.  Other important species include; Candida tropicalis, C. pseudotropicalis, C. brumptii, C. parapsilosis, C. guilliermondii, C. krusei.  

MORPHOLOGY AND REPRODUCTION:  The thallus of Candida consists of yeast cells and pseudohyphae. They reproduce by budding, ferment a number of sugars and assimilate nitrogen.  Microscopic examination of pathological material shows round or oval yeast cells in the process of budding and often exhibiting pseudohyphae.

PATHOGENESIS:  Under normal conditions this fungus is not pathogenic. Many factors predispose to pathogenic effect and these include the following;

1.  Impaired immune defences,

2. Pregnancy

3. Spontaneous hormonal

4. Menopause changes

5. Premature birth

6. Use of Corticosteroids

7. Immunosuppression

8. Long-term antibiotic therapy

9. Oral contraceptives

10. Diabetes mellitus

11. Pre-existing lesions of skin

CLINICAL FEATURES:  A variety of infections are caused by Candida species though it is an opportunistic fungus.  In addition to general predisposing factors, following local conditions also predispose to this infection: Chemical, mechanical or biological irritants, Reduced salivation, Digestive disorders, Remnants of milk left fermenting in the mouth of infants.

LABORATORY DIAGNOSIS:  Collection of Infected Material Skin or nail scrapings, mucous patches from the mouth, vagina or anus, sputum, blood, CSF or faeces may be collected for diagnosis in the laboratory. The material should be collected in sterile containers or as smears on slides.

TREATMENT:  Predisposing factors should be eliminated. The affected area should be kept dry.  Topical application of nystatin and systemic treatment with Amphotericin B, oral ketoconazole and fluconazole is effective.

 

RELATED;

1.  INTRODUCTION TO FUNGI

2.  AMPHOTERICIN B

3.  OPPORTUNISTIC MYCOSES

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

EDEMA

 

Objectives of the discussion:  By the end of this discussion, the learner/medical student will be able to;

1.  Explain the cause of the swelling of the different human body parts

2.  Describe the difference between systemic and localised edema

Introduction: Edema is an abnormal increase in the amount of tissue fluid, which may be localized or systemic. Sometimes edema is inapparent, and sometimes it is apparent as swelling. 

Localized edema follows injury and inflammation of a body part.  I have discussed a lot about inflammation and the drugs used to treat it.  You can read more about inflammation from the link in the related below.

Pathophysiology of edema: Spraining an ankle, for example, damages tissues that then release histamine. Histamine increases the permeability of capillaries, and more tissue fluid is formed. As tissue fluid accumulates, the ankle may become swollen.

Systemic edema:  Systemic edema is the result of an imbalance between the movement of water out of and into capillaries, that is, between filtration and osmosis. Excessive filtration will occur when capillary pressure rises. This may be caused by venous obstruction due to blood clots or by congestive heart failure.  Edema of this type is often apparent in the lower extremities. Systemic bacterial infections may increase capillary permeability, and loss of plasma to tissue spaces is one aspect of septicemia. In this situation, however, the edema is of secondary importance to the hypotension, which may be life-threatening. 

Insufficient osmosis, the return of tissue fluid into capillaries, is a consequence of a decrease in plasma proteins, especially albumin. This may occur in severe liver diseases such as cirrhosis, kidney disease involving loss of protein in urine, malnutrition, or severe burn injuries.  Because edema is a symptom rather than a disease, treatment is aimed at correcting the specific cause. If that is not possible, the volume of tissue fluid may be diminished by a low-salt diet and the use of diuretics

RELATED;

1. THE INFLAMMATORY PROCESS

2. BIOCHEMISTRY OF HISTAMINE

3. CONGESTIVE HEART FAILURE

4.  MEDICAL CONDITIONS

REFERENCES

THROMBOCYTOPENIA

 

INTRODUCTION: Thrombocytopenia which is a condition of low platelet count, is the most common cause of abnormal bleeding.

PATHOPHYSIOLOGY: Thrombocytopenia can result from decreased production of platelets within the bone marrow or from increased destruction or consumption of platelets.

CAUSES: Causes include failure of production as a result of hematologic malignancies, myelodysplastic syndromes, metastatic involvement of bone marrow from solid tumors, certain anemias, toxins, medications, infections, alcohol, and chemotherapy; increased destruction as a result of idiopathic thrombocytopenia purpura, lupus erythematosus, malignant lymphoma, chronic lymphocytic leukemia, medications, infections, and sequestration; and increased utilization, such as results from disseminated intravascular coagulopathy (DIC).

CLINICAL MANIFESTATIONS: With platelet count below 50,000/mm³ : bleeding and petechiae. With platelet count below 20,000/mm³ : petechiae, along with nasal and gingival bleeding, excessive menstrual bleeding, and excessive bleeding after surgery or dental extractions. With platelet count below 5,000/mm³: spontaneous, potentially fatal central nervous system hemorrhage or gastrointestinal hemorrhage.

ASSESSMENT AND DIAGNOSTIC FINDINGS: Bone marrow aspiration and biopsy, if platelet deficiency is secondary to decreased production. Increased megakaryocytes (the cells from which platelets originate) and normal or even increased platelet production in bone marrow, when platelet destruction is the cause.

MEDICAL MANAGEMENT: The management of secondary thrombocytopenia is usually treatment of the underlying disease. Platelet transfusions are used to raise platelet count and stop bleeding or prevent spontaneous hemorrhage if platelet production is impaired; if excessive platelet destruction is the cause, the patient is treated as indicated for idiopathic thrombocytopenia purpura.

For some patients a splenectomy can be therapeutic, although it may not be an option for other patients for example, patients in whom the enlarged spleen is due to portal hypertension related to cirrhosis.

RELATED;

1. BLOOD PLATELETS

2. THE COAGULATION CASCADE

3. BLEEDING DISORDERS

4.  MEDICAL CONDITIONS

REFERENCES

ALLERGY

 

INTRODUCTION: An allergy is a hypersensitivity to a particular foreign antigen, called an allergen. Allergens include plant pollens, foods, chemicals in cosmetics, antibiotics such as penicillin, dust, and mold spores. Such allergens are not themselves harmful. Most people, for example, can inhale pollen, eat peanuts, or take penicillin with no ill effects.

HYPERSENSITIVITY: Hypersensitivity means that the immune system overresponds to the allergen, and produces tissue damage by doing so. Allergic responses are characterized by the production of IgE antibodies, which bond to mast cells. Mast cells are specialized connective tissue cells and are numerous in the connective tissue of the skin and mucous membranes.

INFLAMMATORY MEDIATORS: Chemicals in mast cells include histamine and leukotrienes, which are released by the bonding of IgE antibodies or when tissue damage occurs. These chemicals contribute to the process of inflammation by increasing the permeability of capillaries and venules. Tissue fluid collects and more WBCs are brought to the damaged area. In an allergic reaction, the effects of inflammatory chemicals create symptoms such as watery eyes and runny nose (hay fever) or the more serious wheezing and difficult breathing that characterize asthma. Several medications are available to counteract these effects.

ANAPHYLACTIC SHOCK: Anaphylactic shock is an extreme allergic response that may be elicited by exposure to penicillin or insect venoms. On the first exposure, the person becomes highly sensitized to the foreign antigen. On the second exposure, histamine is released from mast cells throughout the body and causes a drastic decrease in blood volume. The resulting drop in blood pressure may be fatal in only a few minutes. People who know they are allergic to bee stings, for example, may obtain a self-contained syringe of epinephrine to carry with them. Epinephrine can delay the progression of anaphylactic shock long enough for the person to seek medical attention.

RELATED;

1.  IMMUNOGLOBULINS  

2.  IMMUNISATION

3.  MEDICAL CONDITIONS

REFERENCES

FETAL DIAGNOSIS

INTRODUCTION: Several procedures are currently available to determine certain kinds of abnormalities in a fetus or to monitor development.  We should once again remember that the human gestation age goes 40 weeks from the days of the last normal menstruations period.  And although for some people this period may be less or slightly more, the fetus is always monitored with non invasive procedures to make sure that it's life is not in danger and any concerns diagnosed are addressed right away.

ULTRASOUND (OR FETAL ULTRASONOGRAPHY): This is a non-invasive procedure; high-frequency sound waves are transmitted through the abdominal wall into the uterus. The reflected sound waves are converted into an image called a sonogram. This method is used to confirm multiple pregnancies, fetal age or position, or to detect fetal abnormalities such as heart defects or malformations of other organs. Ultrasound may also be used to determine the thickness of the fetal neck, which is an indicator of Down syndrome.

AMNIOCENTESIS: This procedure is usually performed at 16 to 18 weeks of gestation. A hypodermic needle is inserted through the wall of the abdomen into the amniotic sac, and about 10 to 20 mL of amniotic fluid is removed. Within this fluid are fetal cells, which can be cultured so that their chromosomes may be examined. Through such examination and biochemical tests, a number of genetic diseases or chromosome abnormalities may be detected. Because women over the age of 35 years are believed to have a greater chance of having a child with Down syndrome, amniocentesis is often recommended for this age group. A family history of certain genetic diseases is another reason a pregnant woman may wish to have this procedure.

CHORIONIC VILLUS SAMPLING (CVS): In this procedure, a biopsy catheter is inserted through the vagina and cervix to collect a small portion of the chorionic villi. These cells are derived from the fetus but are not part of the fetus itself. The information obtained is the same as that for amniocentesis, but CVS may be performed earlier in pregnancy, at about 8 weeks. Although there is a risk that the procedure may cause a miscarriage, CVS is considered comparable in safety to amniocentesis. It is important to remember that no invasive procedure is without risks.

MATERNAL BLOOD TESTS: Alpha-fetoprotein (AFP) is produced by the fetus and is found in maternal circulation. The level reaches a peak between 12 and 15 weeks of gestation, and should then decrease. If AFP is still high after 16 to 18 weeks, there is a 95% chance that the fetus has spina bifida or anencephaly, malformations of the central nervous system. Maternal blood levels of pregnancy-associated plasma protein A (PAPP-A) and beta hCG can be measured during the first trimester. These tests, in conjunction with ultrasound, can reliably detect Down syndrome.

RELATED;

1. DRUG USE AND PREGNANCY  

2. HEMMOLYTIC DISEASE OF THE NEW BORN

3.  NORMAL LABOR AND VARGINAL DELIVERY

REFERENCES

DEPRESSION

 

INTRODUCTION:  Depression is a disorder characterized by a sad or despondent mood. Many symptoms are associated with depression, including lack of energy, sleep disturbances, abnormal eating patterns, and feelings of despair, guilt, or hopelessness. Depression is the most common mental health disorder of elderly adults, encompassing a variety of physical, emotional, cognitive, and social considerations.

CRITERIA FOR DIAGNOSIS OF DEPRESSION:  The American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV), describes the following criteria for diagnosis of a major depressive disorder:

A depressed affect plus at least five of the following symptoms lasting for a minimum of 2 weeks: 

1)  Difficulty sleeping or sleeping too much.  

2)  Extremely tired; without energy.

3)  Abnormal eating patterns (eating too much or not enough).

4)  Vague physical symptoms (gastrointestinal [GI] pain, joint/muscle pain, or headaches).

5)  Inability to concentrate or make decisions.

6)  Feelings of despair, guilt, and misery; lack of self-worth.

7)  Obsessed with death (expressing a wish to die or to commit suicide).

8)  Avoiding psychosocial and interpersonal interactions.

9)  Lack of interest in personal appearance or sex.

10)  Delusions or hallucinations. 

AGGREVIATING FACTORS TO DEPRESSION:  The majority of depressed patients are not found in psychiatric hospitals but in mainstream society. For proper diagnosis and treatment to occur, recognition of depression is often a collaborative effort among health care providers.  For example, it might be the pharmacist who recognizes that a customer is depressed when the customer buys natural or over-the-counter (OTC) remedies to control anxiety symptoms or to induce sleep.

Situational depression occurs when the depression is the result of a circumstance in a person’s life, for example, loss of a job or unfavorable event at home such as death, children leaving home, or divorce.  Dysthymic disorder is characterized by less severe depressive symptoms that may prevent a person from feeling well or functioning normally. Because depressed patients may be found in multiple settings, health workers should be proficient in the assessment of patients afflicted with these conditions. Some women experience intense mood shifts associated with hormonal changes during the menstrual cycle, pregnancy, childbirth, and menopause. 

WOMEN AND DEVELOPMENT DEPRESSIVE DISORDER:  Up to 80% of women who give birth experience postpartum depression during the first several weeks after birth of their baby. About 10% of new mothers experience a major depressive episode within 6 months related to the dramatic hormonal shifts that occur during postdelivery. Along with the hormonal changes, additional situational stresses, such as responsibilities at home or work, single parenthood, and caring for children or for aging parents, may contribute to the onset of symptoms. If mood is severely depressed and persists long enough, many women will likely benefit from medical treatment, including women with premenstrual dysphoric disorder, depression during pregnancy, postpartum mood disorders, or menopausal distress. Because of the possible consequences of perinatal mood disorders, some state agencies mandate that all new  mothers receive information about mood shifts prior to their discharge after giving birth.  Health care providers in obstetrician’s offices, pediatric outpatient settings, and family medicine centers are encouraged to conduct routine screening for symptoms of perinatal mood disorders.

RELATED;

1.  SEDATIVE-HYPNOTICS  

2.  ZOLPIDEM

3.  PHARMACOLOGY AND THERAPEUTICS

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

JAUNDICE

 

Objectives this article:  By the end of this article, the learner will be able to; 

1.  understand the cause of the yellow color that appear in mucous membranes.

2.  Explain the role of the liver in elimination of bilirubin

INTRODUCTION: Jaundice is not a disease, but rather a sign caused by excessive accumulation of bilirubin in the blood. Because one of the liver’s many functions is the excretion of bilirubin, jaundice may be a sign of liver disease such as hepatitis or cirrhosis. Hepatitis

This may be called hepatic jaundice, because the problem is with the liver. Other types of jaundice are prehepatic jaundice and posthepatic jaundice: The name of each tells us where the problem is. Recall that bilirubin is the waste product formed from the heme portion of the hemoglobin of old RBCs. Hemoglobin: The human red blood cells

PATHOPHYSIOLOGY: Prehepatic jaundice means that the problem is “before” the liver; that is, hemolysis of RBCs is taking place at a more rapid rate. Rapid hemolysis is characteristic of sickle cell anemia, malaria, and Rh disease of the newborn; these are hemolytic anemias. Sickle cell anaemia: Rh disease of the newborn

As excessive numbers of RBCs are destroyed, bilirubin is formed at a faster rate than the liver can excrete it. The bilirubin that the liver cannot excrete remains in the blood and causes jaundice. Another name for this type is hemolytic jaundice.

Posthepatic jaundice means that the problem is “after” the liver. The liver excretes bilirubin into bile, which is stored in the gallbladder and then moved to the small intestine. If the bile ducts are obstructed, perhaps by gallstones or inflammation of the gallbladder, bile cannot pass to the small intestine and backs up in the liver. Bilirubin may then be reabsorbed back into the blood and cause jaundice. Another name for this type is obstructive jaundice.

RELATED;

1.  THE CYTOCHROME P450 ENZYME SYSTEM  

2.  CATALASE

3.  FUNCTIONS OF THE LIVER

4.  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