LUNG CANCER

 

INTRODUCTION: Lung cancers arise from a single transformed epithelial cell in the tracheobronchial airways. A carcinogen such as; cigarette smoke, radon gas and other occupational and environmental agents, damages the cell, causing abnormal growth and development into a malignant tumor. Most lung cancers are classified into one of two major categories: small cell lung cancer which contribute 15% to 20% of tumors, and non–small cell lung cancer that contribute approximately 80% of tumors. Most small cell cancers arise in the major bronchi and spread by infiltration along the bronchial wall.

RISK FACTORS OF LUNG CANCER: Risk factors include tobacco smoke and especially second-hand also known as passive smoke, environmental and occupational exposures, gender, genetics, and dietary deficits. Other factors that have been associated with lung cancer include genetic predisposition and underlying respiratory diseases, such as chronic obstructive pulmonary disease (COPD) and tuberculosis (TB).

CLINICAL MANIFESTATIONS: Lung cancer often develops insidiously and is asymptomatic until late in its course. Signs and symptoms depend on location, tumor size, degree of obstruction, and existence of metastases to regional or distant sites.

1.  Most common symptom is cough or change in a chronic cough.

2.  Dyspnea may occur early in the disease.

3.  Hemoptysis or blood-tinged sputum may be expectorated.

4.  Chest pain or shoulder pain may indicate chest wall or pleural involvement. Pain is a late symptom and may be related to bone metastasis.

5.  Recurring fever may be an early symptom.

Chest pain, tightness, hoarseness, dysphagia, head and neck edema, and symptoms of pleural or pericardial infusion exist if the tumor spreads to adjacent structures and lymph nodes.  Common sites of metastases are lymph nodes, bone, brain, contralateral lung, adrenal glands, and liver.  Weakness, anorexia, and weight loss may appear.

ASSESSMENT AND DIAGNOSTIC METHODS: Chest x-ray, CT scans, bone scans, abdominal scans, PET scans, liver ultrasound, and MRI.  Sputum examinations, fiberoptic bronchoscopy, transthoracic fine-needle aspiration, endoscopy with esophageal ultrasound, mediastinoscopy or mediastinotomy, and biopsy.  Pulmonary function tests, ABG analysis scans, and exercise testing.  Staging of the tumor refers to the size of the tumor, its location, whether lymph nodes are involved, and whether the cancer has spread.

MEDICAL MANAGEMENT: The objective of management is to provide a cure if possible. Treatment depends on cell type, stage of the disease, and physiologic status. Treatment may involve surgery, radiation therapy, or chemotherapy—or a combination of these.

RELATED;

1.  THE ORIGIN OF CANCER

2.  GASEOUS EXCHANGE

3.  ACIDITY AND ALKALINITY OF BODY SYSTEMS

REFERENCES

BREAST EXAMINATION

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

1.  List the importance of conducting breast examination

2.  Describe the normal findings that follows breast examination

3.  Explain the possible abnormal finding that can follow breast examination

INTRODUCTION: The breast examination by a physician remains the best means of early detection of breast cancer when combined with appropriately scheduled mammography. The results of the breast examination may be expressed by description or diagram, or both, usually with reference to the quadrants and tail region of the breast or by allusion to the breast as a clock face with the nipple at the center.

INSPECTION OF THE BREASTS: The breasts are first examined by inspection, with the patient’s arms at her sides, and then with her hands pressed against her hips, and/or with her arms raised over her head. If the patient’s breasts are especially large and pendulous, she may be asked to lean forward so that the breasts hang free of the chest, facilitating inspection.

FINDINGS: Tumors often distort the relations of these tissues, causing disruption of the shape, contour, and symmetry of the breast or position of the nipple. Some asymmetry of the breasts is common, but marked differences or recent changes deserve further evaluation.

1. Discolorations or ulcerations of the skin of the breast, areola, or nipple, or edema of the lymphatics that causes a leathery puckered appearance of the skin are abnormal.

2. A clear or milky breast discharge is usually bilateral and associated with stimulation or elevated prolactin levels also medically termed galactorrhea.

3. Bloody discharge from the breast is abnormal and usually unilateral; it usually does not represent carcinoma, but rather inflammation of a breast structure with intraductal papilloma is often found. Evaluation is necessary to exclude malignancy.

4. Pus usually indicates infection, although an underlying tumor may be encountered.

PALPATION OF THE BREASTS: Palpation follows inspection, first with the patient’s arms at her sides and then with the arms raised over her head. This part of the examination is usually done with the patient in the supine position. The patient may also be seated, with her arm resting on the examiner’s shoulder or over her head, for examination of the most lateral aspects of the axilla. Palpation should be done with slow, careful maneuvers, using the flat part of the fingers rather than the tips. The fingers are moved up and down in a wavelike motion, moving the tissues under them back and forth, so that any breast masses that are present can be more easily felt.

FINDINGS: If masses are found, their size, shape, consistency, and mobility as well as their position should be determined. Women with large breasts may have a firm ridge of tissue located transversely along the lower edge of the breast. This is the inframammary ridge and is a normal finding. The examination is concluded with gentle pressure inward and then upward at the sides of the areola to express fluid. If fluid is noted on inspection or is expressed, it should be sent for culture and sensitivity investigations.

RELATED;

1.  PELVIC INFLAMMATORY DISEASE

2.  OXYTOCIN

3.  OVULATION AND MENSTRUAL CYCLE

REFERENCES

PREMATURE RAPTURE OF MEMBRANES

INTRODUCTION: Rapture of membranes is associated with loss from the uterus of amniotic fluids. Amniotic fluid is normally produced continuously and, after approximately 16 weeks of gestation, is predominantly dependent on fetal urine production. However, passage of fluid across the fetal membranes, skin, and umbilical cord; fetal saliva production; and fetal pulmonary effluent also contribute.

IMPORTANCE OF AMNIOTIC FLUIDS: Amniotic fluid protects the fetus against infection, fetal trauma by acting as a shock absorber, and umbilical cord compression. It also allows for fetal movement and fetal breathing, which, in turn, permits fetal skeletal, chest, and lung development. Decreased or absent amniotic fluid can lead to compression of the umbilical cord and decreased placental blood flow. Disruption of the fetal membranes is associated with loss of the protective effects and developmental roles of amniotic fluid.

PREMATURE RAPTURE OF MEMBRANES: Premature rupture of membranes (PROM) is the rupture of the chorioamniotic membrane before the onset of labor. PROM is associated with about 8% of term pregnancies, which is about 37 weeks or more of gestational age, and is generally followed by the onset of labor. Preterm PROM (PPROM), defined as PROM that occurs before 37 weeks of gestation, is a leading cause of neonatal morbidity and mortality and is associated with approximately 30% of preterm deliveries.

CONSEQUENCES THAT FOLLOW PROM: PROM leading to preterm delivery is associated with neonatal complications of prematurity such as respiratory distress syndrome, intraventricular hemorrhage, neonatal infection, necrotizing enterocolitis, neurologic and neuromuscular dysfunction, and sepsis.

The most significant maternal risk of term PROM is intrauterine infection, a risk that increases with the duration of membrane rupture. The presence of lower genital tract infections with Neisseria gonorrhoeae and group B streptococcus (GBS), as well as bacterial vaginosis (BV) increases the risk of intrauterine infection associated with PROM.

Other complications include prolapsed umbilical cord and abruptio placentae. Consequences of PPROM depend on the gestational age at the time of occurrence. Rupture of the membranes before viability occurs in less than 1% of pregnancies. The probability of neonatal death and morbidity associated with PROM decreases with longer latency and advancing gestational age.

CAUSES OF PROM: The cause of PROM is not clearly understood. Sexually transmitted infections (STIs) and other lower genital tract conditions, such as BV, may play a role, insofar as women with these infections are at higher risk for PROM than those without STI or BV. However, intact fetal membranes and normal amniotic fluid do not fully protect the fetus from infection, because it appears that subclinical intra-amniotic infection may contribute to PROM. Metabolites produced by bacteria and inflammatory mediators may either weaken the fetal membranes or initiate uterine contractions by stimulating prostaglandin synthesis.

RELATED;

1.  NORMAL LABOR AND VAGINAL DELIVERY

2.  SEXUALLY TRANSMITTED DISEASES

3.  FETAL CIRCULATION

4.  ANATOMY AND PHYSIOLOGY

REFERENCES

DYSMENORRHEA

INTRODUCTION: Dysmenorrhea is defined as painful menstruation. This is often sufficiently severe that it prevents a woman from performing normal activities. It may also be accompanied by other symptoms, including diarrhea, nausea, vomiting, headache, and dizziness. Dysmenorrhea may be because of a clinically identifiable cause and in that case we call it secondary dysmenorrhea, or by an excess of prostaglandins, leading to painful uterine muscle activity in which case we call it primary dysmenorrhea.

THE CASCADE OF DYSMENORRHEA: Primary and secondary dysmenorrhea are a source of recurrent disability for a significant number of women in their early reproductive years. It is uncommon for primary dysmenorrhea to occur during the first three to six menstrual cycles, when regular ovulation is not yet well established. The incidence of primary dysmenorrhea is greatest in women in their late teens to early twenties and it tends to declines with age. On the other hand, secondary dysmenorrhea becomes more common as a woman ages, because it accompanies the rising prevalence of causal factors. Childbearing does not affect the occurrence of either primary or secondary dysmenorrhea.

ETIOLOGY AND PATHOPHYSIOLOGY

Primary Dysmenorrhea: Primary dysmenorrhea is caused by excess prostaglandin F2α (PGF2α) produced in the endometrium. Prostaglandin production in the endometrium normally increases under the influence of progesterone, reaching a peak at, or soon after, the start of menstruation. With the onset of menstruation, formed prostaglandins are released from the shedding endometrium. In addition to the increase in prostaglandins from endometrial shedding, necrosis of endometrial cells provides increased substrate arachidonic acid from cell walls for prostaglandin synthesis.

Prostaglandins are potent smooth muscle stimulants that cause intense uterine contractions, resulting in intrauterine pressures to increase. PGF2α also causes contractions in smooth muscle elsewhere in the body, resulting in nausea, vomiting, and diarrhea. Besides PGF2α, prostaglandin E2 (PGE2) is also produced in the uterus. PGE2, a potent vasodilator and inhibitor of platelet aggregation, has been implicated as a cause of primary menorrhagia.

Secondary Dysmenorrhea: Secondary dysmenorrhea is caused by structural abnormalities or disease processes that occur outside the uterus, within the uterine wall, or within the uterine cavity. Common causes of secondary dysmenorrhea include endometriosis described as; the presence of endometrial glands and stroma outside of the uterus, adenomyosis also described as; the presence of ectopic endometrial tissue within the myometrium, adhesions, pelvic inflammatory disease (PID), and leiomyomata (uterine fibroids).

DIAGNOSIS: Patients with primary dysmenorrhea present with recurrent, month-aftermonth, spasmodic lower abdominal pain that occurs on the first 1 to 3 days of menstruation. Dyspareunia is generally not found in patients with primary dysmenorrhea and, if present, should suggest a secondary cause. Symptoms In patients with primary dysmenorrhea, the pain is often diffusely located in the lower abdomen and suprapubic area, with radiation around or through to the back. The pain is described as “coming and going,” or similar to labor. This pain is frequently accompanied by moderate-to-severe nausea, vomiting, and diarrhea. Fatigue, low backache, and headache are also common.

In patients with secondary dysmenorrhea, the pain often lasts longer than the menstrual period. It may start before menstrual bleeding begins, become worse during menstruation, then persist after menstruation ends. Secondary dysmenorrhea often starts later in life than primary dysmenorrhea.

THERAPY: Patients with primary dysmenorrhea generally experience exceptional pain relief through the use of nonsteroidal anti-inflammatory drugs (NSAIDs), which are prostaglandin synthetase inhibitors. Other useful components of therapy for primary dysmenorrhea include the application of heat; exercise; psychotherapy and reassurance; and, on occasion, endocrine therapy; that is to say, oral contraceptives to induce anovulation and pain relief.

Combined Oral Contraceptives: Combined oral contraceptives can be useful in patients who do not desire childbearing and who do not have contraindications to their use. They work by suppressing ovulation and stabilizing estrogen and progesterone levels, with a resultant decrease in endometrial prostaglandins and spontaneous uterine activity. Oral contraceptives may be taken in the traditional 28-day cycle, or in an extended fashion that increases the interval between menses. The continuous use of oral contraceptives to eliminate menses can often eliminate dysmenorrhea altogether.

Therapy for Secondary Dysmenorrhea: For secondary dysmenorrhea, when a specific diagnosis is possible, therapy directed at the underlying condition is most likely to succeed.

RELATED;

1.  Endometriosis

2.  Pelvic inflammatory disease

3.  Infertility

4.  Ectopic pregnacy

REFERENCES

PRETERM LABOR AND BIRTH

INTRODUCTION: Preterm labor is defined as the presence of regular uterine contractions that occur before 37 completed weeks of gestation and are associated with cervical changes. It is often difficult to diagnose preterm labor because of the absence of definitive measurements. Preterm birth is delivery that occurs prior to the completion of 37 completed weeks or an equivalent of 259 days of gestation. Because it is the most common cause of perinatal morbidity and mortality in many countries, prevention and treatment of preterm birth is one of the major focus of obstetric care.

COMPLICATIONS OF PRETERM BIRTH: In addition to perinatal death in the very young fetus, common complications of preterm birth include respiratory distress syndrome, intraventricular hemorrhage, necrotizing enterocolitis, sepsis, neurologic impairment, and seizures. Long-term morbidity associated with preterm delivery includes bronchopulmonary dysplasia and developmental abnormalities, including cerebral palsy.

CLASSIFICATION: Preterm births may be classified into two general presentations: Spontaneous and indicated. Approximately 50% of preterm births result from spontaneous preterm labor with intact membranes; around 40% result from preterm premature rupture of membranes. The remaining more than 10% occur following deliberate intervention for a variety of maternal or obstetric complications such as, eclampsia.

CAUSE OF PRETERM LABOR: Preterm labor may represent a final common pathway for a number of pathogenic processes. The four main processes include;

(1) activation of the maternal or fetal hypothalamic–pituitary–adrenal axis due to maternal or fetal stress,

(2) decidual–chorioamniotic or systemic inflammation caused by infection,

(3) decidual hemorrhage, and

(4) pathologic uterine distention.

FACTORS ASSOCIATED WITH PRETERM LABOR

1. Prior history of preterm birth

2. Preterm uterine contractions

3. Premature rupture of membranes

4. Behavorial risk factors: Low maternal pregnancy, weight, Smoking, Substance abuse, Short interpregnancy interval

5. Current pregnancy factors: Short cervical length, Multifetal gestation, Vaginal bleeding, Urinary tract infections, Genital tract infection and Periodontal disease

RELATED;

1.  PREGNANCY AND CHILDBIRTH

2.  PARTURITION AND LABOR

3.  DRUGS USED IN LABOR

REFERENCES

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

INFERTILITY

 

Definition: Infertility is defined as the absence of conception after at least 1 year of regular sexual intercourse.

Causes: Males are found to be solely responsible for 20-30% of infertility cases and these are related to issues such as, inadequate sperm count which contribute to 50% of cases.  For female infertility, about 40% of cases are due to ovulatory failure, about 40% are due to endometrial or tubal disease, about 10% are due to rarer causes such as, thyroid disease or hyperprolactinemia, and about 10% remain unexplained after full workup.

Pathophysiology of female infertility

Ovulatory Causes:  Infertility due to ovarian dysfunction can result from disorders of the hypothalamus or pituitary, resulting in inadequate gonadotropic stimulation of the ovary.  This can bring problems ranging from ovarian disorders, resulting either in inadequate secretory products or failure to ovulate; and occasionally from both types of disorder occurring at the same time. Correction of the underlying cause will often restore fertility. In many cases, the administration of exogenous gonadotropins will stimulate the ovaries to produce follicular growth. The oocytes can then be released in vivo and fertilized by intercourse or by artificial insemination.

Tubal and Pelvic Causes:  With normal follicles and reproductive neuroendocrine axis function, the major cause of infertility is an abnormality in the endometrium or fallopian tubes. Prior or ongoing pelvic infections, with adhesions or inflammation, can result in a failure of sperm or egg transport, a failure of implantation, or implantation in an inappropriate location (ectopic pregnancy).

 

RELATED;

1.  PELVIC INFLAMMATORY DISEASE

2.  OBSTETRICS AND GYNECOLOGY

3.  CONTRACEPTION

4.  MEDICAL CONDITIONS

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

CANCER

 

INTRODUCTION: Cancer is a disease process that begins when an abnormal cell is transformed by the genetic mutation of the cellular DNA. The abnormal cell forms a clone and begins to proliferate abnormally, ignoring growth-regulating signals in the environment surrounding the cell. The cells acquire invasive characteristics, and changes occur in surrounding tissues. The cells infiltrate these tissues and gain access to lymph and blood vessels, which carry the cells to other areas of the body. This phenomenon is called metastasis. In otherwards the cancer spread to other parts of the body.

DESCRIPTION OF CANCER: Cancerous cells are described as malignant neoplasms and are classified and named by tissue of origin. The failure of the immune system to promptly destroy abnormal cells permits these cells to grow too large to be managed by normal immune mechanisms. Certain categories of agents or factors implicated in carcinogenesis include viruses and bacteria, physical agents, chemical agents, genetic or familial factors, dietary factors, and hormonal agents.

CLINICAL MANIFESTATIONS: Cancerous cells spread from one organ or body part to another by invasion and metastasis; therefore, manifestations are related to the system affected and degree of disruption. Generally, cancer causes anemia, weakness, weight loss, and pain which is often in late stages. Symptoms are from tissue destruction and replacement with nonfunctional cancer tissue or overproductive cancer tissue such as, bone marrow disruption and anemia or excess adrenal steroid production; pressure on surrounding structures; increased metabolic demands; and disruption of production of blood cells.

ASSESSMENT AND DIAGNOSTIC METHODS: Screening to detect early cancer usually focuses on cancers with the highest incidence or those that have improved survival rates if diagnosed early. Examples of these cancers include breast, colorectal, cervical, endometrial, testicular, skin, and oropharyngeal cancers. Patients with suspected cancer undergo extensive testing to;

1) Determine the presence and extent of tumor.

2) Identify possible spread (metastasis) of disease or invasion of other body tissues.

3) Evaluate the function of involved and uninvolved body systems and organs.

4) Obtain tissue and cells for analysis, including evaluation of tumor stage and grade.

Diagnostic tests may include tumor marker identification, genetic profiling, imaging studies (mammography, magnetic resonance imaging [MRI], computed tomography [CT], fluoroscopy, ultrasonography, endoscopy, nuclear medicine imaging, positron emission tomography [PET], PET fusion, radioimmunoconjugates), and biopsy.

RELATED;

1.  THE ORIGIN OF CANCER

2.  PATHOLOGY

REFERENCES

INTRAVENOUS INFUSION OF FLUIDS

 

INTRODUCTION: When fluid output exceeds fluid intake, volume deficits may result. Shock, dehydration, or electrolyte loss may occur; large deficits are fatal, unless treated. The following are some common reasons for fluid depletion: 

1) Loss of gastrointestinal (GI) fluids due to vomiting, diarrhea, chronic laxative use, or GI suctioning. 

2) Excessive sweating during hot weather, athletic activity, or prolonged fever. 

3) Severe burns. 

4) Hemorrhage. 

5) Excessive diuresis due to diuretic therapy or uncontrolled diabetic ketoacidosis.

PURPOSE OF ADMINISTERING IV FLUIDS: The immediate goal in treating a volume deficit disorder is to replace the depleted fluid. In non-acute circumstances, this may be achieved by drinking more liquids or by administering fluids via a feeding tube. In acute situations, IV fluid therapy is indicated. Regardless of the route, careful attention must be paid to restoring normal levels of blood elements and electrolytes as well as fluid volume. IV replacement fluids are of two basic types namely; crystalloids and colloids.

CRYSTALLOIDS: Crystalloids are IV solutions that contain electrolytes and other substances that closely mimic the body’s ECF. They are used to replace depleted fluids and to promote urine output. Crystalloid solutions are capable of quickly diffusing across membranes, leaving the plasma and entering the interstitial fluid and ICF. It is estimated that two thirds of infused crystalloids will distribute in the interstitial space.

COMPONENTS OF IV FLUIDS: Isotonic, hypotonic, and hypertonic solutions are available for that purpose. Sodium is the most common crystalloid added to solutions. Some crystalloids contain dextrose, a form of glucose, commonly in concentrations of 2.5%, 5%, or 10%. Dextrose is added to provide nutritional value: 1 L of 5% dextrose supplies 170 calories. In addition, water is formed during the metabolism of dextrose, enhancing the rehydration of the patient. When dextrose is infused, it is metabolized, and the solution becomes hypotonic.

EFFECTS OF IV FLUIDS: Infusion of crystalloids will increase total fluid volume in the body, but the compartment that is most expanded depends on the solute in this case, sodium, concentration of the fluid administered. Isotonic crystalloids can expand the circulating intravascular (plasma) fluid volume without causing major fluid shifts between compartments. Isotonic crystalloids such as normal saline are often used to treat fluid loss due to vomiting, diarrhea, or surgical procedures, especially when the blood pressure is low.

Because isotonic crystalloids can rapidly expand circulating blood volume, care must be taken not to cause fluid overload in the patient. Infusion of hypertonic crystalloids expands plasma volume by drawing water away from the cells and tissues.

RELATED;

1.  PLASMA VOLUME EXPANDERS

2.  BODY FLUIDS

3.  ANATOMY AND PHYSIOLOGY

REFERENCES

INFECTIVE ENDOCARDITIS

 

INTRODUCTION: Infective endocarditis is a microbial infection of the endothelial surface of the heart. A deformity or injury of the endocardium leads to accumulation on the endocardium of fibrin and platelets involving clot formation. Infectious organisms, usually staphylococci, streptococci, enterococci, pneumococci, or chlamydia invade the clot and endocardial lesion. Other causative microorganisms include fungi such as, Candida, Aspergillus and rickettsiae

RISK FACTORS: Prosthetic heart valves or structural cardiac defects such as, valve disorders, hypertrophic cardiomyopathy

Age: More common in older people, who are more likely to have degenerative or calcific valve lesions, reduced immunologic response to infection, and the metabolic alterations associated with aging.

Intravenous (IV) drug use: There is a high incidence of staphylococcal endocarditis among IV drug users.

Hospitalization: Hospital-acquired endocarditis occurs most often in patients with debilitating disease or indwelling catheters and in those receiving hemodialysis or prolonged IV fluid or antibiotic therapy.

Immunosuppression: Patients taking immunosuppressive medications or corticosteroids are more susceptible to fungal endocarditis.

CLINICAL MANIFESTATIONS: Primary presenting symptoms are fever and a heart murmur: Fever may be intermittent or absent, especially in elderly patients, patients receiving antibiotics or corticosteroids, or those who have heart failure or renal failure. Vague complaints of malaise, anorexia, weight loss, cough, and back and joint pain.

A heart murmur may be absent initially but develops in almost all patients. Small, painful nodules (Osler nodes) may be present in the pads of fingers or toes. Irregular, red or purple, painless, flat macules may be present on the palms, fingers, hands, soles, and toes. Hemorrhages with pale centers (Roth spots) caused by emboli may be observed in the fundi of the eyes. Splinter hemorrhages (ie, reddish brown lines and streaks) may be seen under the fingernails and toenails. Petechiae may appear in the conjunctiva and mucous membranes. Cardiomegaly, heart failure, tachycardia, or splenomegaly may occur.

ASSESSMENT AND DIAGNOSTIC METHODS: A diagnosis of acute infective endocarditis is made when the onset of infection and resulting valvular destruction are rapid, occurring within days to weeks. Blood cultures Doppler or transesophageal echocardiography.

COMPLICATIONS: Complications include heart failure, cerebral vascular complications, valve stenosis or regurgitation, myocardial damage, and mycotic aneurysms.

MEDICAL MANAGEMENT: Objectives of treatment are to eradicate the invading organism through adequate doses of an appropriate antimicrobial agent (continuous IV infusion for 2 to 6 weeks at home). Treatment measures include the following:

1) Isolating causative organism through serial blood cultures. Blood cultures are taken to monitor the course of therapy.

2) Monitoring patient’s temperature for effectiveness of the treatment. After recovery from the infectious process, seriously damaged valves may require debridement or replacement. For example, surgical valve replacement is required if heart failure develops, if patient has more than one serious systemic embolic episode, if infection cannot be controlled or is recurrent, or if infection is caused by a fungus.

REFERENCES;

1. HEART MURMURS

2. HEART FAILURE

3.  ANGINA PECTORIS

REFERENCES