ASCORBIC ACID (VITAMIN C)

  

INTRODUCTION:  Vitamin C is a water soluble vitamin which is easily destroyed by heat, alkali and storage. In the process of cooking, 70% of vitamin C is lost. It is a reducing agent and it’s strong reducing property depends on the double-bonded (enediol) carbons.

METABOLISM OF ASCORBIC ACID: Ascorbic acid is readily absorbed from gastrointestinal tract. The vitamin is excreted in urine. Since vitamin C is a strong reducing agent, the Benedict's test will be positive in the urine sample after the vitamin administration.

Oxidation of ascorbic acid yields dehydro ascorbic acid, which is oxidized further to oxalic acid. Ascorbic acid is partly excreted unchanged and partly as oxalic acid. Most of the oxalates in urine are derived from ascorbic acid, and the rest from glycine metabolism. The ascorbic acid level varies between 0.7 to 1.2 mg/100 ml of plasma and 25 mg/100 cc of WBC. A low level in blood is noted in women taking contraceptive pills and also in chronic alcoholics.

BIOCHEMICAL FUNCTIONS OF VITAMIN C

1)  Reversible oxidation-reduction:  It can change between ascorbic acid and dehydroascorbic acid.

2)  Hydroxylation of proline and lysine: Ascorbic acid is necessary for the post-translational hydroxylation of proline and lysine residues. Hydroxyproline and hydroxylysine are essential for the formation of cross links in the collagen, which gives the tensile strength to the fibres. This process is absolutely necessary for the normal production of supporting tissues such as osteoid, collagen and intercellular cement substance of capillaries.

3)  Tryptophan metabolism:  Ascorbic acid is necessary for the hydroxylation of tryptophan to 5-hydroxy tryptophan. This is required for the formation of serotonin.

4.  Tyrosine metabolism:  Vitamin C helps in the oxidation of parahydroxy phenyl pyruvate to homogentisic acid.

5.  Iron metabolism:  Ascorbic acid enhances the iron absorption from the intestine.

6.  Hemoglobin metabolism:  It is useful for re-conversion of met-hemoglobin to hemoglobin.

7.  Folic acid metabolism:  Ascorbic acid is helping the enzyme folate reductase to reduce folic acid to tetrahydrofolic acid. Thus it helps in the maturation of RBC.

8.  Steroid synthesis:  Large quantities of vitamin C are present in adrenal cortex. The ascorbic acid is depleted by ACTH stimulation. So the vitamin has some role in adrenal steroidogenesis. Vitamin C helps in the synthesis of bile acids from cholesterol. The initial 7-alphahydroxylase step is stimulated by the vitamin.

9.  Phagocytosis: Ascorbic acid stimulates phagocytic action of leukocytes and helps in the formation of antibodies.

10.  Anti-oxidant property: As an anti-oxidant, it may prevent cancer formation. Aniline dyes are known to induce bladder cancer in factory workers. Daily intake of vitamin C reduces this risk for cancer.

11.  Cataract:  Vitamin C is concentrated in the lens of eye. Regular intake of ascorbic acid reduces the risk of cataract formation. Deficiency Manifestations of Vitamin C results in scurvy and Infantile scurvy (Barlow's disease).

RELATED;

1.  Vitamin A

2.  Magnesium

3.  Calcium and the human body

4.  Biomolecules of life

REFERENCES

CONSTIPATION

 

INTRODUCTION:  Constipation refers to an abnormal infrequency or irregularity of defecation, abnormal hardening of stools that makes their passage difficult and sometimes painful, decrease in stool volume, or prolonged retention of stool in the rectum. 

CAUSES OF CONSTIPATION:  It can be caused by certain medications; rectal or anal disorders; obstruction; metabolic, neurologic, and neuromuscular conditions; endocrine disorders; lead poisoning; connective tissue disorders; and a variety of disease conditions. 

Other causes may include weakness, immobility, debility, fatigue, and inability to increase intra-abdominal pressure to pass stools. Constipation develops when people do not take the time or ignore the urge to defecate or as the result of dietary habits such as, low consumption of fiber and inadequate fluid intake, lack of regular exercise, and a stress-filled life. 

CLINICAL MANIFESTATIONS:  Fewer than three bowel movements per week, abdominal distention, and pain and pressure.  Decreased appetite, headache, fatigue, indigestion, sensation of incomplete emptying.  Straining at stool; elimination of small volume of hard, dry stool.  Complications such as hypertension, hemorrhoids and fissures, fecal impaction, and megacolon.

ASSESSMENT AND DIAGNOSTIC METHODS:  Diagnosis is based on history, physical examination, possibly a barium enema or sigmoidoscopy, stool for occult blood, anorectal manometry (pressure studies), defecography, and colonic transit studies. Newer tests such as pelvic floor MRI may identify occult pelvic floor defects. 

MEDICAL MANAGEMENT:  Treatment should target the underlying cause of constipation and aim to prevent recurrence, including education, bowel habit training, increased fiber and fluid intake, and judicious use of laxatives. Discontinue laxative abuse; increase fluid intake; include fiber in diet; try biofeedback, exercise routine to strengthen abdominal muscles.  If laxative is necessary, use bulk-forming agents, saline and osmotic agents, lubricants, stimulants, or fecal softeners.  Specific medication therapy to increase intrinsic motor function such as cholinergics, cholinesterase inhibitors, or prokinetic agents.

RELATED;

1.  ULCERATIVE COLITIS  

2.  DIARRHEA

3.  MEDICAL CONDITIONS

REFERENCES

CORTICOSTEROIDS (GLUCOCORTICOIDS)

 

OBJECTIVES OF THE DISCUSSION:  By the end of this discussion the learner/medical student will be able to;

1.  Describe the role of corticosteroids in management of pain

2.  Explain the effect of corticosteroids on the human body

3.  List the possible side and adverse effect encountered with use of corticosteroids

INTRODUCTION:  Corticosteroids have numerous therapeutic applications. One of their most useful properties is the ability to suppress severe inflammation. Because of potentially serious adverse effects, however, systemic corticosteroids are reserved for the short-term treatment of severe disease. Corticosteroids are often referred to as glucocorticoids.

TREATING ACUTE OR SEVERE INFLAMMATION WITH CORTICOSTEROIDS:  Corticosteroids are natural hormones released by the adrenal cortex that have powerful effects on nearly every cell in the body. When corticosteroids are used as drugs to treat inflammatory disorders, the doses are many times higher than the amount naturally present in the blood. The uses of corticosteroids include the treatment of neoplasia, asthma, arthritis, and corticosteroid deficiency.  Asthma 

PHARMACODYNAMICS:  Like the NSAIDs, corticosteroids inhibit the biosynthesis of prostaglandins. Corticosteroids, however, affect inflammation by multiple mechanisms. They have the ability to suppress histamine release and can inhibit certain functions of phagocytes and lymphocytes. These multiple actions markedly reduce inflammation, making corticosteroids the most effective medications available for the treatment of severe inflammatory disorders.  Inflammation 

ADVERSE EFFECTS:  When given by the oral or parenteral routes, corticosteroids have a number of serious adverse effects that limit their therapeutic utility. These include suppression of the normal functions of the adrenal gland a condition known as adrenal insufficiency, hyperglycemia, mood changes, cataracts, peptic ulcers, electrolyte imbalances, and osteoporosis.  Peptic ulcers

Because of their effectiveness at reducing the signs and symptoms of inflammation, corticosteroids can mask infections that may be present in a patient. This combination of masking signs of active infection and suppressing the immune response creates a potential for infections to grow rapidly and remain undetected. In that regard therefore, active infection is usually a contraindication for corticosteroids therapy. 

Because the appearance of these adverse effects is a function of the dose and duration of therapy, treatment is often limited to the short-term control of acute disease. When longer therapy is indicated, doses are kept as low as possible and alternate-day therapy is sometimes implemented; the medication is taken every other day to encourage the patient’s adrenal glands to function on the days when no drug is given.

RELATED;

1.  OPIOID ANALGESICS

2.  OPIOID ANALGESICS

3.  MORPHINE

4.  INFLAMMATORY CONDITIONS OF THE HUMAN BODY

REFERENCES

HEPATITIS DISEASE

 

HEPATITIS A: Hepatitis A is caused by an RNA virus of the genus Enterovirus. This form of hepatitis is transmitted primarily through the fecal–oral route, by the ingestion of food or liquids infected by the virus. The virus is found in the stool of infected patients before the onset of symptoms and during the first few days of illness. The incubation period is estimated to be 2 to 6 weeks, with a mean of approximately 4 weeks. The course of illness may last 4 to 8 weeks. The virus is present only briefly in the serum; by the time jaundice appears, the patient is likely to be noninfectious. A person who is immune to hepatitis A may contract other forms of hepatitis. Recovery from hepatitis A is usual; it rarely progresses to acute liver necrosis and fulminant hepatitis. No carrier state exists, and no chronic hepatitis is associated with hepatitis A.

CLINICAL MANIFESTATIONS: Many patients are anicteric (without jaundice) and symptomless. When symptoms appear, they are of a mild, flulike, upper respiratory infection, with low-grade fever. Anorexia is an early symptom and is often severe. Later, jaundice and dark urine may be apparent. Indigestion is present in varying degrees. Liver and spleen are often moderately enlarged for a few days after onset. Patient may have an aversion to cigarette smoke and strong odors; symptoms tend to clear when jaundice reaches its peak. Symptoms may be mild in children; in adults, they may be more severe, and the course of the disease prolonged.

ASSESSMENT AND DIAGNOSTIC METHODS: Stool analysis for hepatitis A antigen. Serum hepatitis A virus antibodies; immunoglobulin.

PREVENTION: Scrupulous hand washing, safe water supply, proper control of sewage disposal. Hepatitis vaccine. Administration of immune globulin, if not previously vaccinated, to prevent hepatitis A if given within 2 weeks of exposure. Immune globulin is recommended for household members and for those who are in sexual contact with people with hepatitis A. Preexposure prophylaxis is recommended for those traveling to developing countries or settings with poor or uncertain sanitation conditions who do not have sufficient time to acquire protection by administration of hepatitis A vaccine.

MANAGEMENT: Bed rest during the acute stage; encourage a nutritious diet. Give small, frequent feedings supplemented by IV glucose if necessary during period of anorexia. Promote gradual but progressive ambulation to hasten recovery. Patient is usually managed at home unless symptoms are severe. Assist patient and family to cope with the temporary disability and fatigue that are common problems in hepatitis. Teach patient and family the indications to seek additional health care if the symptoms persist or worsen. Instruct patient and family regarding diet, rest, follow-up blood work, avoidance of alcohol, and sanitation and hygiene measures (hand washing) to prevent spread of disease to other family members.

RELATED;

1. IMMUNISATION

2. IMMUNOGLOBULINS

3.  VIROLOGY

REFERENCES

CATEGORIES OF DRUGS IN RELATION TO PREGNANCY

 

INTRODUCTION:  Drug use during pregnancy is one of the most important threats to worry about in order to ensure the safety of the mother and the baby.  In the first place although the mother may have less or no effect, our fear rotates around the growing fetus that may take in the drug via the placenta and develop fetal malformations.

1.  RISK CATEGORY A

INTERPRETATION: Adequate, well-controlled studies in pregnant women have not shown an increased risk of fetal abnormalities to the fetus in any trimester of pregnancy.

EXAMPLE OF DRUGS: Prenatal multivitamins, insulin, thyroxine, folic acid.

2.  RISK CATEGORY B

INTERPRETATION: Animal studies have revealed no evidence of harm to the fetus; however, there are no adequate and well-controlled studies in pregnant women.

OR

Animal studies have shown an adverse effect, but adequate and well-controlled studies in pregnant women have failed to demonstrate risk to the fetus in any trimester.

EXAMPLE OF DRUGS: Penicillins, cephalosporins, azithromycin, acetaminophen, ibuprofen in the first and second trimesters.

3.  RISK CATEGORY C

INTERPRETATION: Animal studies have shown an adverse effect and there are no adequate and well controlled studies in pregnant women.

OR

No animal studies have been conducted and there are no adequate and well controlled studies in pregnant women.

EXAMPLE OF DRUGS: Most prescription medicines; antimicrobials such as clarithromycin, fluoroquinolones, and Bactrim; selective serotonin reuptake inhibitors (SSRIs); corticosteroids; and most antihypertensives.

4.  RISK CATEGORY D

INTERPRETATION: Adequate well-controlled or observational studies in pregnant women have demonstrated a risk to the fetus. However, the benefits of therapy may outweigh the potential risk. For example, the drug may be acceptable if needed in a life-threatening situation or serious disease for which safer drugs cannot be used or are ineffective.

EXAMPLE OF DRUGS: Alcohol, ACE inhibitors, angiotensin receptor blockers (ARBs) in the second and third trimesters, gentamicin, carbamazepine, cyclophosphamide, lithium carbonate, methimazole, mitomycin, nicotine, nonsteroidal antiinflammatory drugs (NSAIDs) in the third trimester, phenytoin, propylthiouracil, streptomycin, tetracyclines, valproic acid.

5.  RISK CATEGORY X

INTERPRETATION: Adequate well-controlled or observational studies in animals or pregnant women have demonstrated positive evidence of fetal abnormalities or risks. The use of the product is contraindicated in women who are or may become pregnant. There is no indication for use in pregnancy.

EXAMPLE OF DRUGS: Clomiphene, fluorouracil, isotretinoin, leuprolide, menotropins, methotrexate, misoprostol, nafarelin, oral contraceptives, raloxifene, ribavirin, statins, temazepam, testosterone and thalidomide, and warfarin.

RELATED;

1.  HEMORRHAGIC DISEASE OF THE NEW BORN  

2.  ENDOMETRIOSIS

3.  OBSTETRICS AND GYNECOLOGY

REFERENCES

INTESTINAL OBSTRUCTION

 

INTRODUCTION: Intestinal obstruction occurs when blockage prevents the flow of contents through the intestinal tract. Large bowel obstruction results in an accumulation of intestinal contents, fluid, and gas proximal to the obstruction. Obstruction in the colon can lead to severe distention and perforation unless gas and fluid can flow back through the ileal valve. Dehydration occurs more slowly than in small bowel obstruction. If the blood supply is cut off, intestinal strangulation and necrosis occur; this condition is life threatening. Necrosis

CLINICAL MANIFESTATIONS: Symptoms develop and progress relatively slowly. Constipation may be the only symptom for months for obstruction in sigmoid colon or rectum.  Blood loss in the stool, which may result in iron-deficiency anemia. The patient may experience weakness, weight loss, and anorexia. Abdomen eventually becomes markedly distended, loops of large bowel become visibly outlined through the abdominal wall, and patient has crampy lower abdominal pain. Fecal vomiting develops; symptoms of shock may occur. Shock

ASSESSMENT AND DIAGNOSTIC METHODS: Symptoms plus imaging studies including; abdominal x-ray and abdominal CT scan or MRI; barium studies are contraindicated in this case.

MEDICAL MANAGEMENT: Restoration of intravascular volume, correction of electrolyte abnormalities, and nasogastric aspiration and decompression are instituted immediately. Colonoscopy to untwist and decompress the bowel, if obstruction is high in the colon. Cecostomy may be performed for patients who are poor surgical risks and urgently need relief from the obstruction. Rectal tube to decompress an area that is lower in the bowel. Usual treatment is surgical resection to remove the obstructing lesion; a temporary or permanent colostomy may necessary; an ileoanal anastomosis may be performed if entire large bowel must be removed.

RELATED;

1.  ULCERATIVE COLITIS  

2.  CONSTIPATION

REFERENCES

SEPSIS & SEPTIC SHOCK

 

Clinical Presentation: Sepsis is a clinical syndrome characterized by a dysregulated inflammatory response to infection. Rates of sepsis continue to rise secondary to medical advances such as the widespread use of indwelling intravascular catheters, increased implantation of prosthetic material such as, cardiac valves and artificial joints, and administration of immunosuppressive drugs and chemotherapeutic agents. These interventions serve to increase the risk of infection and subsequent sepsis. Sepsis is a continuum of conditions, from infection and bacteremia to sepsis and septic shock.  Shock

The septic condition:  Patients with early sepsis have infection and bacteremia and are at risk for progressing to sepsis and septic shock. Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated immune response to infection.  We have previously discussed the body's response to incoming infectious agents under specific immunity, which you can read about in the link below. 

Specific immunity

Etiology: Although evidence of infection is a diagnostic criterion for sepsis, only 28% of patients with sepsis have bacteremia, and slightly more than 10% will have primary bacteremia, defined as positive blood cultures without an obvious source of bacterial seeding. Common sites of infection among patients with sepsis syndrome include the respiratory tract, the genitourinary tract, abdominal sources such as, gall bladder, colon, and wound or soft tissue infections.  Respiratory tract infections

Bacteremia and sepsis:  Gram-negative bacteria including but not limited to; Enterobacteriaceae and Pseudomonas, previously the most common cause of sepsis, have been supplanted by gram-positive organisms, which now cause more than 50% of cases. Staphylococci are the most common bacteria cultured from the bloodstream, presumably because of an increase in the prevalence of chronic indwelling venous access devices and implanted prosthetic material. 

The incidence of fungal sepsis has risen dramatically owing to an increase in immunosuppressed and neutropenic patients.  Sepsis associated with P. aeruginosa, Candida, or mixed (polymicrobial) organisms is an independent predictor of mortality.

Pathogenesis. The normal host response to infection is recognition via pathogen recognition receptors and immune cell migration, primarily by neutrophils, to the site of infection, where they release inflammatory mediators. The process is highly regulated, with anti-inflammatory cytokines such as IL-10 suppressing release of inflammatory cytokines (eg, TNF-α). 

Pathophysiology:  Sepsis occurs when the inflammatory response overwhelms the local environment and becomes systemic. The cause of the systemic reaction is likely multifactorial and may include the effect of the microorganism, the release of large quantities of proinflammatory mediators, and even the genetic susceptibility of the individual. The different stages of sepsis (early sepsis to septic shock) represent a continuum, with patients often progressing from one stage to the next within days or even hours after admission.

Sepsis generally starts with a localized infection. Bacteria may then invade the bloodstream directly or may proliferate locally and release toxins into the bloodstream. These toxins can arise from a structural component of the bacteria such as endotoxin or may be exotoxins, which are proteins synthesized and released by the bacteria. 

RELATED;

1.  HAEMATOLOGICAL CONDITIONS

2.  STROKE

3.  ALTERED LEVEL OF CONSCIOUSNESS

4.  THE INTRAVENOUS DRUG ADMINISTRATION

5.  ENTEROBACTERIACEAE

6.  PSEUDOMONAS

7.  STAPHYLOCOCCUS

HEART FAILURE

INTRODUCTION: Heart failure (HF), sometimes referred to as congestive HF, is the inability of the heart to pump sufficient blood to meet the needs of the tissues for oxygen and nutrients. HF is a clinical syndrome characterized by signs and symptoms of fluid overload or inadequate tissue perfusion. The underlying mechanism of HF involves impaired contractile properties of the heart (systolic dysfunction) or filling of the heart (diastolic) that leads to a lower-than-normal cardiac output. The low cardiac output can lead to compensatory mechanisms that cause increased workload on the heart and eventual resistance to filling of the heart. HF is a progressive, life-long condition that is managed with lifestyle changes and medications to prevent episodes of acute decompensated HF, which are characterized by an increase in symptoms, decreased CO, and low perfusion.

RISK FACTORS: HF results from a variety of cardiovascular conditions, including chronic hypertension, coronary artery disease, and valvular disease. These conditions can result in systolic failure, diastolic failure, or both. Several systemic conditions (eg, progressive renal failure and uncontrolled hypertension) can contribute to the development and severity of cardiac failure. 

CLINICAL MANIFESTATIONS: The signs and symptoms of HF can be related to which ventricle is affected. Left-sided HF (left ventricular failure) causes different manifestations than right-sided HF (right ventricular failure). In chronic HF, patients may have signs and symptoms of both left and right ventricular failure.

Left-Sided HF:  Most often precedes right-sided cardiac failure; Pulmonary congestion: dyspnea, cough, pulmonary crackles, and low oxygen saturation levels; an extra heart sound, the S3, or “ventricular gallop,” may be detected on auscultation. Dyspnea on exertion (DOE), orthopnea, paroxysmal nocturnal dyspnea (PND). Cough initially dry and nonproductive; may become moist over time. Large quantities of frothy sputum, which is sometimes pink (blood-tinged). Bibasilar crackles advancing to crackles in all lung fields. Inadequate tissue perfusion. Oliguria and nocturia. With progression of HF: altered digestion; dizziness, lightheadedness, confusion, restlessness, and anxiety; pale or ashen and cool and clammy skin. Tachycardia, weak, thready pulse; fatigue.

Right-Sided HF: Congestion of the viscera and peripheral tissues. Edema of the lower extremities (dependent edema), hepatomegaly (enlargement of the liver), ascites (accumulation of fluid in the peritoneal cavity), anorexia and nausea, and weakness and weight gain due to retention of fluid.

ASSESSMENT AND DIAGNOSTIC METHODS: Assessment of ventricular function. Echocardiogram, chest x-ray, electrocardiogram (ECG). Laboratory studies: serum electrolytes, blood urea nitrogen (BUN), creatinine, thyroid-stimulating hormone (TSH), CBC count, brain natriuretic peptide (BNP), and routine urinalysis. Cardiac stress testing, cardiac catheterization.

MEDICAL MANAGEMENT: The overall goals of management of HF are to relieve patient symptoms, to improve functional status and quality of life, and to extend survival. Treatment options vary according to the severity of the patient’s condition and may include oral and IV medications, major lifestyle changes, supplemental oxygen, implantation of assistive devices, and surgical approaches, including cardiac transplantation. Lifestyle recommendations include restriction of dietary sodium; avoidance of excessive fluid intake, alcohol, and smoking; weight reduction when indicated; and regular exercise.

Pharmacologic Therapy: Alone or in combination: vasodilator therapy (angiotensinconverting enzyme [ACE] inhibitors), angiotensin II receptor blockers (ARBs), selective beta-blockers, calcium channel blockers, diuretic therapy, cardiac glycosides (digitalis), and others. IV infusions: nesiritide, milrinzne, dobutamine. Medications for diastolic dysfunction. Possibly anticoagulants, medications that manage hyperlipidemia (statins). 

SURGICAL MANAGEMENT: Coronary bypass surgery, percutaneous transluminal coronary angioplasty (PTCA), other innovative therapies as indicated (eg, mechanical assist devices, transplantation).

RELATED;

1.  CORONARY ARTERY DISEASE

2.  ARTERIOSCLEROSIS

3.  HYPERTENSION

REFERENCES  

PELVIC INFLAMMATORY DISEASE

 

INTRODUCTION: Pelvic inflammatory disease (PID) is an inflammatory condition of the pelvic cavity that may begin with cervicitis and may involve the uterus (endometritis), fallopian tubes (salpingitis), ovaries (oophoritis), pelvic peritoneum, or pelvic system. Infection, which may be acute, subacute, recurrent, or chronic and localized or widespread, is usually caused by bacteria but may be attributed to a virus, fungus, or parasite. 

PATHOPHYSIOLOGY: Pathogenic organisms usually enter the body through the vagina, pass through the cervical canal into the uterus, and may proceed to one or both fallopian tubes and ovaries, and into the pelvis. Infection most commonly occurs through sexual transmission but also may be caused by invasive procedures such as endometrial biopsy, surgical abortion, hysteroscopy, or insertion of an intrauterine device (IUD). The most common organisms involved are gonorrhea and chlamydia. The infection is usually bilateral.

RISK FACTORS: Risk factors include early age at first intercourse, multiple sexual partners, frequent intercourse, intercourse without condoms, sex with a partner with a sexually transmitted disease (STD), and a history of STDs or previous pelvic infection.

CLINICAL MANIFESTATIONS: Symptoms may be acute and severe or low-grade and subtle. Vaginal discharge, dyspareunia, lower abdominal pelvic pain, and tenderness that occurs after menses; pain increases during voiding or defecating. Systemic symptoms include fever, general malaise, anorexia, nausea, headache, and possibly vomiting. Intense tenderness is noted on palpation of the uterus or movement of cervix (cervical motion tenderness) during pelvic examination.

COMPLICATIONS: Pelvic or generalized peritonitis, abscesses, strictures, and fallopian tube obstruction. Adhesions that eventually may require removal of the uterus, tubes, and ovaries. Bacteremia with septic shock and thrombophlebitis with possible embolization.

MEDICAL MANAGEMENT: Broad-spectrum antibiotic therapy is instituted, with mild to moderate infections being treated on an outpatient basis. If the patient is acutely ill, hospitalization may be required. Once hospitalized, the patient is placed on a regimen of bed rest, IV fluids, and IV antibiotic therapy. Nasogastric intubation and suction are used if ileus is present; vital signs are monitored. Treatment of sexual partners is necessary to prevent reinfection.

RELATED;

1. BACTERIOLOGY  

2. ANTIBIOTICS  

3.  MEDICINE AND SURGERY

4.  OBSTETRICS AND GYNECOLOGY

REFERENCES

ROLES OF A RESEARCH SUPERVISOR

ROLES OF A RESEARCH SUPERVISOR:  A research supervisor is on of the most important aspects of a research project.  With the help of a supervisor, the research student is guided step by step from the formulation and approval of a research topic, to the final sign up leading to submission of the research report.  This is of course a long process and that alone clarifies the significance of such a post.  In the this article, we are going to look at the most important roles of a research supervisor, the qualities of a good supervisor and the most common mistakes made by research supervisors.

1.  Roles and crucial steps accomplished by a research supervisor

A student must be assigned a research supervisor before even a research topic is approved and one of the most immediate responsibilities of a supervisor is to make sure that the student choose among the specialties of the discipline he/she is mostly interested in.  For a student conducting the research project from the field they are most interested in, will enjoy the process to maximum and help them add on their theory and practicum.  If you would like to know more about choosing research topics click here.

2.  Qualities of a good supervisor:  A good supervisor will have to bear these qualities to do their job very well.

1.  Use moral judgement to predetermine the student's readiness to conduct the research study.

3.  The most common mistakes made by research supervisors.

One of the most common mistakes made by research supervisors is thinking that the student is at the same level of understanding as they do.

SEBORRHEIC DERMATITIS

 

INTRODUCTION: Seborrhea is an excessive production of sebum (secretion of sebaceous glands). Seborrheic dermatitis is a chronic inflammatory disease of the skin with a predilection for areas that are well supplied with sebaceous glands or that lie between folds of the skin, where the bacterial count is high. Seborrheic dermatitis has a genetic predisposition; hormones, nutritional status, infection, and emotional stress influence its course. There are remissions and exacerbations of this condition. 

AREAS MOST AFFECTED: Areas most often affected are the face, scalp, cheeks, ears, axillae, and various skin folds.

CLINICAL MANIFESTATIONS: Two forms can occur: an oily form and a dry form. Either form may start in childhood with fine scaling of the scalp or other areas.  Oily Form: Moist or greasy patches of sallow, greasy-appearing skin, with or without scaling, and slight erythema (redness); small pustules or papulopustules on trunk resembling acne.  Dry Form: Flaky desquamation of the scalp (dandruff); asymptomatic mild forms or scaling often accompanied by pruritus, leading to scratching and secondary infections and excoriation. 

MEDICAL MANAGEMENT: Because there is no known cure for seborrhea, the objectives of therapy are to control the disorder and allow the skin to repair itself. Treatment measures include the following: Administering topical corticosteroid cream to body and face. These should however be used with caution near eyes. Aerating skin and careful cleansing of creases or folds to prevent candidal yeast infection (evaluate patients with persistent candidiasis for diabetes). Shampooing hair daily or at least three times weekly with medicated shampoos. Two or three different types of shampoos are used in rotation to prevent the seborrhea from becoming resistant to a particular shampoo.

RELATED.

1.  PRURITUS

2.  MEDICAL CONDITIONS

3.  THE INTEGUMENTARY SYSTEM

REFERENCES

MEDICAL ERRORS AND MISDIAGNOSIS

MEDICAL ERRORS AND MISDIAGNOSIS:  the medical field is one of the most sensitive fields that require extreme carefulness in everything done.  This is because it deals with the human life and any error, can lead to automatic termination of the life of either the health work and or the patient.  The errors that are more likely to happen in the medical field are usually counteracted by making thorough and frequent checkups by more than one medical personnel to make sure that in case a mistake is done by one individual, it can be corrected by the other before it reaches the target patient.  However, since the human brain is not an automatic machine, several aspects of errors tend to arise especially in resource limited setting as we are going to look at them one by one, and the way they are watched over the time not to happen frequently or again.

Cont...................

ASTHMA

 

INTRODUCTION: Asthma is a chronic inflammatory disease of the airways characterized by hyper-responsiveness, mucosal edema, and mucus production. This inflammation ultimately leads to recurrent episodes of asthma symptoms: cough, chest tightness, wheezing, and dyspnea. Patients with asthma may experience symptom-free periods alternating with acute exacerbations that last from minutes to hours or days. Asthma, the most common chronic disease of childhood, can begin at any age.

RISK FACTORS: Risk factors for asthma include family history, allergy (strongest factor), and chronic exposure to airway irritants or allergens such as, grass, weed pollens, mold, dust, or animals. Common triggers for asthma symptoms and exacerbations include airway irritants such as, pollutants, cold, heat, strong odors, smoke, perfumes. Others include; exercise, stress or emotional upset, rhinosinusitis with postnasal drip, medications, viral respiratory tract infections, and gastroesophageal reflux.

CLINICAL MANIFESTATIONS: Most common symptoms of asthma are cough (with or without mucus production), dyspnea, and wheezing (first on expiration, then possibly during inspiration as well). Asthma attacks frequently occur at night or in the early morning. An asthma exacerbation is frequently preceded by increasing symptoms over days, but it may begin abruptly. Chest tightness and dyspnea occur. Expiration requires effort and becomes prolonged. As exacerbation progresses, central cyanosis secondary to severe hypoxia may occur. Additional symptoms, such as diaphoresis, tachycardia, and a widened pulse pressure, may occur.

ASSESSMENT AND DIAGNOSTIC METHODS: Family, environment, and occupational history is essential. During acute episodes, sputum and blood test, pulse oximetry, ABGs, hypocapnia and respiratory alkalosis, and pulmonary function (forced expiratory volume [FEV] and forced vital capacity [FVC] decreased) tests are performed.

MEDICAL MANAGEMENT: Pharmacologic Therapy: There are two classes of medications; long-acting control and quick-relief medications, as well as combination products. Short-acting include; beta2-adrenergic agonists, Anticholinergics. Corticosteroids: metered-dose inhaler (MDI). Leukotriene modifiers inhibitors/antileukotrienes. Methylxanthines. The immediate medical care of patients with asthma depends on the severity of symptoms. The patient and family are often frightened and anxious because of the patient’s dyspnea. Therefore, a calm approach is an important aspect of care. Assess the patient’s respiratory status by monitoring the severity of symptoms, breath sounds, peak flow, pulse oximetry, and vital signs. Obtain a history of allergic reactions to medications before administering medications. Identify medications the patient is currently taking. Administer medications as prescribed and monitor the patient’s responses to those medications; medications may include an antibiotic if the patient has an underlying respiratory infection. Administer fluids if the patient is dehydrated. Assist with intubation procedure, if required.  Teach patient and family about asthma (chronic inflammatory), purpose and action of medications, triggers to avoid and how to do so, and proper inhalation technique.

RELATED;

1.  ACUTE RESPIRATORY DISTRESS SYNDROME  

2.  TUBERCULOSIS

3.  ALLERGY

4.  MEDICAL CONDITIONS

REFERENCES

BENIGN PROSTATIC HYPERPLASIA (BPH)

 

INTRODUCTION: This is enlargement, or hypertrophy, of the prostate gland. The prostate gland enlarges, extending upward into the bladder and obstructing the outflow of urine. Incomplete emptying of the bladder and urinary retention leading to urinary stasis may result in hydronephrosis, hydroureter, and urinary tract infections (UTIs). The cause is not well understood, but evidence suggests hormonal involvement. BPH is common in men older than 40 years.

CLINICAL MANIFESTATIONS: The prostate is large, rubbery, and nontender. Prostatism (obstructive and irritative symptom complex) is noted. Hesitancy in starting urination, increased frequency of urination, nocturia, urgency, abdominal straining. Decrease in volume and force of urinary stream, interruption of urinary stream, dribbling. Sensation of incomplete emptying of the bladder, acute urinary retention (more than 60 mL), and recurrent UTIs. Fatigue, anorexia, nausea and vomiting, and pelvic discomfort are also reported, and ultimately azotemia and renal failure result with chronic urinary retention and large residual volumes.

ASSESSMENT AND DIAGNOSTIC METHODS: Physical examination, including digital rectal examination (DRE), and health history. Urinalysis to screen for hematuria and UTI. Urodynamic studies, urethrocystoscopy, and ultrasound may be performed. Complete blood studies, including clotting studies.

Medical Management: The treatment plan depends on the cause, severity of obstruction, and condition of the patient. Treatment measures include the following: Immediate catheterization if patient cannot void (an urologist may be consulted if an ordinary catheter cannot be inserted). A suprapubic cystostomy is sometimes necessary. Watchful waiting, to monitor disease progression.

PHARMACOLOGIC MANAGEMENT: Alpha-adrenergic blockers (fpr example, alfuzosin, terazosin), which relax the smooth muscle of the bladder neck and prostate, and 5-alpha-reductase inhibitors. Hormonal manipulation with antiandrogen agents (finasteride [Proscar]) decreases the size of the prostate and prevents the conversion of testosterone to dihydrotestosterone (DHT).

SURGICAL MANAGEMENT: Minimally invasive therapy: transurethral microwave heat treatment (TUMT; application of heat to prostatic tissue); transurethral needle ablation (TUNA; via thin needles placed in prostate gland); prostatic stents (but only for patients with urinary retention and in patients who are poor surgical risks). Surgical resection: transurethral resection of the prostate (TURP; benchmark for surgical treatment); transurethral incision of the prostate (TUIP).

RELATED;

1.  PELVIC INFLAMMATORY DISEASE

2.  MEDICINE AND SURGERY TOPICS

REFERENCES

ULCERATIVE COLITIS

 

INTRODUCTION: Ulcerative colitis is a recurrent ulcerative and inflammatory disease of the mucosal and submucosal layers of the colon and rectum. It is a serious disease, accompanied by systemic complications and a high mortality rate; approximately 5% of patients with ulcerative colitis develop colon cancer. It is characterized by multiple ulcerations, diffuse inflammations, and desquamation or shedding of the colonic epithelium, with alternating periods of exacerbation and remission. Bleeding occurs from the ulceration and the mucosa becomes edematous and inflamed, with continuous lesions and abscesses.

INDIVIDUALS MOST AFFECTED: Ulcerative colitis most commonly affects people of Caucasian and Jewish heritage.

CLINICAL MANIFESTATIONS: Predominant symptoms: diarrhea, passage of mucus and pus, left lower quadrant abdominal pain, intermittent tenesmus, and rectal bleeding. Bleeding may be mild or severe; pallor, anemia, and fatigue result. Anorexia, weight loss, fever, vomiting, dehydration, cramping, and feeling an urgent need to defecate. Hypocalcemia may occur. Rebound tenderness in right lower quadrant. Skin lesions, eye lesions (uveitis), joint abnormalities, and liver disease.

ASSESSMENT AND DIAGNOSTIC METHODS: Assess for tachypnea, tachycardia, hypotension, fever, and pallor. Abdomen is examined for bowel sounds, distention, and tenderness. Stool examination to rule out dysentery, occult blood test. Abdominal x-rays, computed tomography (CT), magnetic resonance imaging (MRI). Sigmoidoscopy or colonoscopy and barium enema. Blood studies (low hematocrit and hemoglobin, high white blood cell count, decreased albumin level, electrolyte imbalance).

MEDICAL MANAGEMENT: Medical treatment for both Crohn’s disease and ulcerative colitis is aimed at reducing inflammation, suppressing inappropriate immune responses, providing rest for a diseased bowel so that healing may take place, improving quality of life, and preventing or minimizing complications.

NUTRITIONAL THERAPY: Initial therapy consists of diet and fluid management with oral fluids; low-residue, high-protein, high-calorie diets; supplemental vitamin therapy; and iron replacement. Fluid and electrolyte balance may be corrected by intravenous (IV) therapy. Additional treatment measures include smoking cessation and avoiding foods that exacerbate symptoms, such as milk and cold foods.

PHARMACOLOGIC THERAPY: Sedative, antidiarrheal, and antiperistaltic medications. Aminosalicylates: sulfasalazine; effective for mild or moderate inflammation. Corticosteroids such as, oral: prednisone; parenteral: hydrocortisone; topical: budesonide. Immunomodulator agents such as, azathioprine. Biologic agents such as, infliximab.

SURGICAL MANAGEMENT: When nonsurgical measures fail to relieve the severe symptoms of inflammatory bowel disease, surgery may be recommended. A common procedure performed for strictures of the small intestines is laparoscope-guided strictureplasty. In some cases, a small bowel resection is performed. In cases of severe Crohn’s disease of the colon, a total colectomy and ileostomy may be the procedure of choice.

RELATED;

1.  ANTIEMETIC AGENTS    

2. CONSTIPATION    

3. DIARRHEA

4.  INFLAMMATORY BOWEL DISEASE

REFERENCES