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

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

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

FETAL CIRCULATION

 

INTRODUCTION: The fetus depends upon the mother for oxygen and nutrients and for the removal of carbon dioxide an other waste products. The site of exchange between fetus and mother is the placenta, which contains fetal and maternal blood vessels that are very close to one another.

THE FETAL-MATERNAL BLOOD: The blood of the fetus does not mix with the blood of the mother; substances are exchanged by diffusion and active transport mechanisms. The fetus is connected to the placenta by the umbilical cord, which contains two umbilical arteries and one umbilical vein.

THE UMBILICAL CODE: The umbilical arteries are branches of the fetal internal iliac arteries; they carry blood from the fetus to the placenta. In the placenta, carbon dioxide and waste products in the fetal blood enter maternal circulation, and oxygen and nutrients from the mother’s blood enter fetal circulation. The umbilical vein carries this oxygenated blood from the placenta to the fetus. Within the body of the fetus, the umbilical vein branches: One branch takes some blood to the fetal liver, but most of the blood passes through the ductus venosus to the inferior vena cava, to the right atrium.

NEONATAL CIRCULATION: After birth, when the umbilical cord is cut, the remnants of these fetal vessels constrict and become nonfunctional. The other modifications of fetal circulation concern the fetal heart and. Because the fetal lungs are deflated and do not provide for gas exchange, blood is shunted away from the lungs and to the body. The foramen ovale is an opening in the interatrial septum that permits some blood to flow from the right atrium to the left atrium, not, as usual, to the right ventricle. The blood that does enter the right ventricle is pumped into the pulmonary artery. The ductus arteriosus is a short vessel that diverts most of the blood in the pulmonary artery to the aorta, to the body. Both the foramen ovale and the ductus arteriosus permit blood to bypass the fetal lungs. Just after birth, the baby breathes and expands its lungs, which pulls more blood into the pulmonary circulation. More blood then returns to the left atrium, and a flap on the left side of the foramen ovale is closed. The ductus arteriosus constricts, probably in response to the higher oxygen content of the blood, and pulmonary circulation becomes fully functional within a few days.

RELATED;

1.  FETAL DIAGNOSIS

2.  HEMORRHAGIC DISEASE OF THE NEW BORN

3.  ANATOMY AND PHYSIOLOGY

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

MEASLES

 

INTRODUCTION: Measles is a highly contagious, acute, febrile illness. In the developing countries it has the highest morbidity and mortality among all vaccine preventable illnesses. Measles is one of the most ubiquitous and persistent of human viruses. Its distribution is worldwide and it causes disease in any climate and under any conditions, provided enough susceptible human beings are brought together to enable it to spread.

CLINICAL FEATURES: Measles is one of the most important childhood infections. After an incubation period of 10-12 days, the disease manifests with prodromal symptoms of fever and upper respiratory tract infection marked with coryza, cough and conjunctivitis. Early diagnosis can be made by detecting Koplik’s spots, which are red macules or ulcers with a bluish white centre, seen on the mucous membrane of the inside of cheek. Rashes appear on different parts of the body starting from head followed by chest, trunk and then limbs. After a few days they start fading and then recovery is rapid and complete. Measles can cause severe and multiple complications in a large number of patients (10-20%). Encephalomyelitis has an incidence of less than one out of 1000, but carries a mortality of 15%. It also has sequelae of epilepsy and personality changes.

PATHOGENESIS: Measles, like mumps, is a typical systemic viral infection. Virus gains entry through respiratory tract, multiplies in the epithelial lining and then spreads to lymph nodes where another phase of replication occurs. Further spread to organs takes place and skin, brain and lungs get involved. Lesions produced are characterised by the presence of multinucleated giant cells with well defined intranuclear and intracytoplasmic inclusions. It is now well established that the maculopapular rash of measles is mediated by immunopathological mechanism. Such rashes do not appear in immunologically compromised patients who develop pneumonia and in case of adults, the disease proves fatal.

IMMUNE RESPONSE: High titres of IgG, IgM as well as secretory IgA are seen after primary infection with measles virus. IgM and IgA disappear after sometime but IgG persist lifelong making the individual immune to reinfection. Though a strong immune response is mounted by the body on getting infected with measles virus, the disease has got an immunosuppressive action.

LABORATORY DIAGNOSIS: Clinical Samples: Diagnosis of a typical case of measles can be made based upon clinical symptoms. However, demonstration of the virus or seroconversion against the virus is necessary to confirm the diagnosis. Best results for isolation of virus are obtained when specimens are taken during the first few days of illness.

RELATED;

1.  MUMPS

2.  HEPATITIS

3.  MEDICAL CONDITIONS

REFERENCES

SALMONELLA (GASTROENTERITIS, TYPHOID FEVER, PARATYPHOID FEVER)

 

INTRODUCTION: All salmonellae are classified in the species Salmonella enterica with seven subspecies. Nearly all human pathogen salmonellae are grouped under S. enterica, subsp. enterica. Salmonellae are further subclassified in over 2000 serovars based on their O and H antigens, which used to be designated as species. Typhoid salmonelloses are caused by the serovars typhi and paratyphi A, B, and C.

MODES OF TRANSMISSION: The salmonellae are taken up orally and the invasion pathway is through the intestinal tract, from where they enter lymphatic tissue, first spreading lymphogenously, then hematogenously. A generalized septic clinical picture results. Human carriers are the only source of infection. Transmission is either direct by smear infection or indirect via food and drinking water.  Anti-infective agents are required for therapy including but not limited to; ampicillin, cotrimoxazole, 4-quinolones). An active vaccine is available to protect against typhoid fever. Enteric salmonelloses develop when pathogens are taken up with food. The primary infection source is usually livestock. These relatively frequent infections remain restricted to the gastrointestinal tract. Treatment with antiinfective agents is necessary in exceptional cases only.  It is not known why typhoid salmonellae only cause systemic disease in humans, whereas enteric salmonella infections occur in animals as well and are usually restricted to the intestinal tract.

DIAGNOSIS: The method of choice is detection of the pathogens in cultures. Selective indicator mediums are used to isolate salmonellae in stool. Identification is done using metabolic patterns. Serovar classification is determined with specific antisera in the slide agglutination test. Culturing requires at least two days. Typhoid salmonelloses can be diagnosed indirectly by measuring the titer of agglutinating antibodies to O and H antigens (according to Gruber-Widal). To provide conclusive proof the titer must rise by at least fourfold from blood sampled at disease onset to a sample taken at least one week later.

THERAPY: Typhoid salmonelloses must be treated with anti-infective agents, whereas symptomatic treatment will suffice for enteric infections. Symptomatic treatment encompasses slowing down intestinal activity (e.g., with loperamide) and replacing fluid and electrolyte losses orally as required. Eliminating the infection in chronic stool carriers of typhoid salmonellae, 2–5% of cases, presents a problem. Chronic carriers are defined as convalescents who are still eliminating pathogens three months after the end of the manifest illness. The organisms usually persist in the scarified wall of the gallbladder. Success is sometimes achieved with high-dose administration of anti-infective agents, e.g., 4-quinolones or aminopenicillins.

PREVENTION: The main method of effective prevention is to avoid exposure: this means clean drinking water, prevention of food contamination, avoidance of uncooked foods in countries where salmonellae occur frequently, disinfection of excreta containing salmonellae or from chronic carriers, etc. It is also important to report all cases to health authorities so that appropriate measures can be taken.

RELATED;

1.  BRUCELLA  

2.  GRAM NEGATIVE ENTERIC BACTERIA

3.  BACTERIOLOGY

4. MEDICAL MICROBIOLOGY

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