OVULATION AND THE MENSTRUAL CYCLE

INTRODUCTION: The menstrual cycle includes the activity of the hormones of the ovaries and anterior pituitary gland and the resultant changes in the ovaries that we sometimes call, the ovarian cycle. This then is preceded by changes in the uterus which we sometimes call the uterine cycle.

HORMONES INVOLVED IN THE PROCESS: Follicle Stimulating (FSH) and Luteinizing Hormone (LH) from the anterior pituitary gland, estrogen from the ovarian follicle, and progesterone from the corpus luteum are the four hormones involved. It is the fluctuation and production of these hormones that influence the ovulation cycle and and then menstruations.

THE CYCLE: A cycle may be described in terms of three phases: menstrual phase, follicular phase, and luteal phase.

1. Menstrual phase: The loss of the functional layer of the endometrium is called menstruation or the menses. Although this is actually the end of a menstrual cycle, the onset of menstruation is easily pinpointed and is, therefore, a useful starting point. Menstruation may last 2 to 8 days, with an average of 3 to 6 days. At this time, secretion of FSH is increasing, and several ovarian follicles begin to develop.

2. Follicular phase: FSH stimulates growth of ovarian follicles and secretion of estrogen by the follicle cells. The secretion of LH is also increasing, but more slowly. FSH and estrogen promote the growth and maturation of the ovum, and estrogen stimulates the growth of blood vessels in the endometrium to regenerate the functional layer. This phase ends with ovulation, when a sharp increase in LH causes rupture of a mature ovarian follicle.

3. Luteal phase: Under the influence of LH, the ruptured follicle becomes the corpus luteum and begins to secrete progesterone as well as estrogen. Progesterone stimulates further growth of blood vessels in the functional layer of the endometrium and promotes the storage of nutrients such as glycogen. As progesterone secretion increases, LH secretion decreases, and if the ovum is not fertilized, the secretion of progesterone also begins to decrease. Without progesterone, the endometrium cannot be maintained and begins to slough off in menstruation. FSH secretion begins to increase (as estrogen and progesterone decrease), and the cycle begins again.

OCCURANCE OF CYCLES: Women may have cycles of anywhere from 23 to 35 days, the normal range. Women who engage in strenuous exercise over prolonged periods of time may experience amenorrhea, that is, cessation of menses. This seems to be related to reduction of body fat. Apparently the reproductive cycle ceases if a woman does not have sufficient reserves of energy for herself and a developing fetus. The exact mechanism by which this happens is not completely understood at present. Amenorrhea may also accompany states of physical or emotional stress, anorexia nervosa, or various endocrine disorders.

RELATED;

1.  INFERTILITY

2.  DYSMENORRHEA

3.  PELVIC INFLAMMATORY DISEASE

4.  ENDOMETRIOSIS

REFERENCES

THE APGAR SCORING SYSTEM

 

SIGN	0	1	2
Color	Blue or pale	Acrocynotic	Complex pink
Heart rate	Absent	Less than 100 bpm	More than 100 bpm
Reflex activity response to stimulation	No response	Grimace	Cry or active withdrawal
Muscle tone	Limp	Some flexion	Active motion
Respirations	Absent	Weak cry; hypoventilatio	Good, crying

INTRODUCTION: The Apgar scoring system is commonly used as an objective means to assess the newborn’s condition. In this system, five signs are given scores of 0, 1, or 2, for a total of up to 10. Scores are assigned at 1 minute and 5 minutes, and at every 5 minutes until 20 minutes thereafter if the 5-minute Apgar score is less than 7. Although these continued assessments are not part of the original Apgar scoring system, many clinicians find them to be of value in evaluating how an infant is responding to resuscitation.

SIGNIFICANCE OF THE APGAR SCORE: In the term and late-preterm infant, a 5-minute Apgar score of 7 to 10 is reassuring; a 5-minute score of 4 to 6 is considered indicative of a mildly to moderately depressed infant; and a 5-minute score of less than 4 is suggestive of a severely depressed infant. It should be noted however that, the Apgar score should not be used to define birth asphyxia, because it is not designed to do so and, it does not provide such information.

Although a low 1-minute Apgar score identifies the newborn that requires particular attention, it does not predict any individual infant’s outcome. The 5-minute Apgar score can be used to evaluate the effectiveness of any resuscitative efforts that have been undertaken or to identify an infant who needs continuing evaluation and management. It too should not be used to predict neurologic outcome in term infants.

RELATED;

1.  PREGNANCY AND CHILD BIRTH

2.  RHESUS DISEASE OF THE NEWBORN

3.  DRUG USE IN RELATION TO PREGNANCY

REFERENCES

CONTRACEPTION

INTRODUCTION: On average, more than 50% of all pregnancies in many communities are unplanned. Despite the fact that every year new contraceptive options are introduced with various improvements, there are still many myths and misconceptions when it comes to child spacing. Although no family planning method is effective if it is not used correctly, many methods are very reliable. In our discussion here, we will take a look at the various contraceptive options from the most reliable to the least and compare their risks, benefits, and reliability.

DYNAMICS OF FAMILY PLANNING: Although there are many kinds of contraceptives, all work either by inhibiting the development or release of ova or blocking the meeting of ova and sperm. This goal is accomplished by two general mechanisms, each with many variations:

(1) Inhibiting the development and release of the egg, a basis for oral contraceptive pills [OCPs], long-acting progesterone injection such as Sayana press and depo provera, or contraceptive patch and ring.

(2) Imposing a mechanical, chemical, or temporal barrier between the sperm and egg, which is the basis for the condom, diaphragm, spermicide, intrauterine contraception, and fertility awareness.

FAMILY PLANNING USING INTRAUTERINE DEVICES (IUD): As a secondary mechanism, intrauterine devices (IUDs) placed as emergency contraception (EC) alter the ability of the fertilized egg to implant and grow. It is important to understand that the mechanism of action of the IUD not placed for EC is via changes in the amount and viscosity of cervical mucus, endometrial suppression, inhibition of sperm migration and viability, changes in transport speed of the ovum, and damage to or destruction of the ovum.

MAKING A CHOICE FOR FAMILY PLANNING: Before helping any woman or couple choose among the many contraceptive options, the physician must consider two things. First, the physician must understand and be able to explain, in language the woman and partner can understand, the physiologic or pharmacologic mechanism of action of all of the available contraceptive methods, along with their effectiveness rates, indications, contraindications, complications, advantages, and disadvantages.

Second, the physician must know the woman and her partner well enough to recognize personal, physical, religious, or cultural values affecting the use of each contraceptive method under consideration and be able to help them deal with those issues using empathic evidence-based discussions, regardless of any personal bias. When done correctly, these discussions allow the couple to understand the contraceptive options and the physician to freely provide evidence-based recommendations.  In this manner, an appropriate individualized contraceptive method can be chosen whose correct, regular use is highly likely.

RELATED;

1.  ECTOPIC PREGNANCY

2.  DRUG USE IN RELATION TO PREGNANCY

3.  PRETERM LABOR AND CHILD BIRTH

4.  OVULATION AND THE MENSTRUAL CYCLE

REFERENCES

ECTOPIC PREGNANCY

INTRODUCTION: An ectopic or extrauterine pregnancy is one in which the blastocyst implants anywhere other than the endometrial lining of the uterine cavity. Ectopic pregnancies account for less than 5% on average. In most cases, 98% of ectopic pregnancies implant in the fallopian tube, with 80% occurring in the ampullary segment. Other locations include, but are not limited to, the ovary, cervix, and abdomen.

TUBAL ECTOPIC PREGNANCY: Without intervention, the natural course of a tubal pregnancy will result in any of three outcomes: tubal abortion, tubal rupture, or spontaneous resolution. Tubal abortion is the expulsion of the pregnancy through the fimbriated end. This tissue can then either regress or reimplant in the abdominal cavity. Tubal rupture is associated with significant intraabdominal hemorrhage, often necessitating surgical intervention.

PATHOPHYSIOLOGY AND RISK FACTORS: Inflammation resulting in tubal damage can disrupt the normal migration of a fertilized ovum through the tube, thereby predisposing to an ectopic pregnancy. Specific examples of an inflammatory process include salpingitis.  An acute chlamydial infection causes intraluminal inflammation and subsequent fibrin deposition with tubal scarring. Whereas endotoxin-producing Neisseria gonorrhoeae causes virulent pelvic inflammation with a rapid clinical onset, chlamydial inflammatory response has a bit slow onset and peaks at 7 to 14 days.

The incidence of ectopic pregnancy has increased consistently with the rise in chlamydial infections. Pregnancy after tubal sterilization is rare, but, when it does occur, there is a substantial risk that the pregnancy will be ectopic due to the distorted tubal anatomy created by the tubal ligation.  Additional risk factors include prior ectopic pregnancy, smoking, prior tubal surgery, and advanced age.

SYMPTOMS: The classic symptoms associated with ectopic pregnancy are amenorrhea followed by vaginal bleeding and abdominal pain on the affected side; however, there is no constellation of symptoms that are diagnostic. Normal pregnancy symptoms, such as breast tenderness, nausea, and urinary frequency, may accompany more ominous findings. These include shoulder pain worsened by inspiration. As long as placental hormones are produced, there is usually no vaginal bleeding. Irregular vaginal bleeding results from the sloughing of the decidua from the endometrial lining.

Vaginal bleeding in patients with an ectopic gestation may range from little or none to heavy, menstrual-like flow. In some patients, the entire “decidual cast” is passed intact, simulating a spontaneous abortion.  In any pregnant patient with no histopathologic confirmation of chorionic villi within the uterus, an ectopic implantation should be assumed to be present until proven otherwise.

RELATED;

1.  PRETERM LABOR AND BIRTH

2.  PARTURITION AND LABOR

3.  RHESUS DISEASE OF THE NEWBORN

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

CALCIUM AND THE HUMAN BODY

ROLE OF CALCIUM AND VITAMIN D IN BONE HOMEOSTASIS: Calcium is the primary mineral responsible for bone formation and for maintaining bone health throughout the life span. This major mineral constitutes about 2% of our body weight and is also critical to proper functioning of the nervous, muscular, and cardiovascular systems. To maintain homeostasis, calcium balance in the body is regulated by parathyroid hormone (PTH), calcitonin, and vitamin. Acting together, these three substances regulate the rate of absorption of calcium from the gastrointestinal (GI) tract, the excretion of calcium from the kidney, and the movement of calcium into and out of bone.

BONE RESORPTION AND DEPOSITION: Secreted by the parathyroid glands, PTH stimulates bone cells called osteoclasts. These cells accelerate the process of bone resorption, demineralization that breaks down bone into its mineral components. Once bone is broken down (resorbed), calcium becomes available for transport to areas in the body where it is needed. The opposite of this process is bone deposition, or bone building, accomplished by cells called osteoblasts. This process, which removes calcium from the blood to be placed in bone, is stimulated by the hormone calcitonin. When serum calcium levels become elevated, calcitonin is released by the thyroid gland.

ROLE OF VITAMIN D IN CALCIUM METABOLISM: Vitamin D and calcium metabolism are intimately related: Absorption of calcium is increased in the presence of vitamin D, and inhibited by vitamin D deficiency. Thus, calcium disorders are often associated with vitamin D disorders. Vitamin D is unique among vitamins because the body is able to synthesize it from precursor molecules. Several steps, however, are required before vitamin D can act on target tissues. The inactive form of vitamin D, cholecalciferol, is synthesized in the skin from cholesterol. Exposure of the skin to sunlight or ultraviolet light increases the level of cholecalciferol in the blood. Cholecalciferol can also be obtained from dietary products such as milk or other foods fortified with vitamin D. Enzymes in the kidneys metabolize calcifediol to calcitriol, the active form of vitamin D. Parathyroid hormone stimulates the formation of calcitriol at the level of the kidneys. Patients with extensive kidney disease are unable to adequately synthesize calcitriol and thus frequently experience calcium and vitamin D abnormalities. The primary function of calcitriol is to increase calcium absorption from the GI tract. Dietary calcium is absorbed more efficiently in the presence of active vitamin D and parathyroid hormone, resulting in higher serum levels of calcium, which is then transported to bone, muscle, and other tissues.

ROLES OF CALCIUM IN THE BODY: The importance of proper calcium balance in the body cannot be overstated. Calcium ion influences the excitability of all neurons. When calcium concentrations are too high (hypercalcemia), sodium permeability decreases across cell membranes. This is a dangerous state, because nerve conduction depends on the proper influx of sodium into cells. When calcium levels in the bloodstream are too low (hypocalcemia), cell membranes become hyperexcitable. If this situation becomes severe, convulsions or muscle spasms may result. Calcium is also important for the normal functioning of other body processes such as blood coagulation and muscle contraction.

RELATED;

1.  Magnesium

2.  Vitamin D

3.  Osteoporosis 

REFERENCES

INFLUENZA

INTRODUCTION: Influenza is an acute viral disease that causes worldwide epidemics every 2 to 3 years with a highly variable degree of severity. The virus is easily spread from host to host through droplet exposure. Previous infection with influenza does not guarantee protection from future exposure. Mortality is probably attributable to accompanying pneumonia which maybe viral or superimposed bacterial pneumonia, and other chronic cardiopulmonary condition.

MANAGEMENT: Goals of medical and nursing management include relieving symptoms, treating complications, and preventing transmission.

PREVENTION: Annual influenza vaccinations are recommended for those at high risk for complications of influenza. These include people older than 50 years, children 6 to 59 months of age, pregnant women, residents of extended care facilities, and those with chronic medical diseases or disabilities. In addition, health care providers and household members of those in high-risk groups should receive the vaccine to reduce the risk of transmission to people vulnerable to influenza sequelae.

RELATED;

1. SYMPTOMATIC MANAGEMENT OF PATIENTS

2.  EBOLA VIRUS DISEASE

3.  IMMUNISATION

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

THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS)

 

INTRODUCTION: The renin–angiotensin–aldosterone system (RAAS) is one of the primary homeostatic mechanisms controlling blood pressure and fluid balance in the body. Drugs that affect the RAAS decrease blood pressure and increase urine volume. They are widely used in the pharmacotherapy of Hypertension, heart failure, and myocardial infarction (MI).

PHYSIOLOGY OF RAAS: Renin is an enzyme secreted by specialized cells in the kidney when blood pressure falls, or when there is a decrease in sodium ion (Na+) flowing through the kidney tubules. Once in the blood, renin converts the inactive liver protein angiotensinogen to angiotensin I. When it passes through the lungs, angiotensin I is converted to angiotensin II, one of the most potent natural vasoconstrictors known. The enzyme responsible for the final step in this system is angiotensin-converting enzyme (ACE). The intense vasoconstriction of arterioles caused by angiotensin II raises blood pressure by increasing peripheral resistance. Angiotensin II also stimulates the secretion of aldosterone, a hormone from the adrenal cortex. The primary action of aldosterone is to increase Na+ reabsorption in the kidney. The enhanced Na+ reabsorption causes the body to retain water, increasing blood volume and raising blood pressure.

CONCLUSION: Thus, angiotensin II increases blood pressure through two distinct mechanisms: direct vasoconstriction and increased water retention.

RELATED;

1.  FUNCTION OF THE LIVER

2.  ENZYMES

3.  BLOOD PRESSURE AND HYPERTENSION

4.  HEART FAILURE

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

THE FORCES THAT INTERACT WITH BIOLOGICAL MOLECULES

 

COVALENT BONDS:  Molecules are formed by sharing of electrons between atoms and for covalent bonding, basically the atoms will be of the same type for example, the oxygen molecule O2, nitrogen molecule N2 are diatomic molecules made up of two atoms each.

IONIC BONDS OR ELECTROSTATIC BONDS: Ionic bonds result from the electrostatic attraction between two ionized groups of opposite charges. They are formed by transfer of one or more electrons from the outermost orbit of an electropositive atom to the outermost orbit of an electronegative atom. This transfer results in the formation of a cation and an anion, which get consequently bound by an ionic bond.  Common examples of such compounds include NaCl, KBr and NaF.

HYDROGEN BONDS:  These are formed by sharing of a hydrogen between two electron donors. Hydrogen bonds result from electrostatic attraction between an electro-negative atom and a hydrogen atom that is bonded covalently to a second electronegative atom. Normally, a hydrogen atom forms a covalent bond with only one other atom. However, a hydrogen atom covalently bonded to a donor atom, may form an additional weak association, the hydrogen bond with an acceptor atom.

In biological systems, both donors and acceptors are usually nitrogen or oxygen atoms, especially those atoms in amino (NH2) and hydroxyl (OH) groups. With regard to protein chemistry, hydrogen releasing groups are -NH (imidazole, indole,peptide); -OH (serine, threonine) and -NH2 (arginine lysine). Hydrogen accepting groups are COO–, (aspartic, glutamic) C=O (peptide); and S–S (disulphide).  The DNA structure for example is maintained by hydrogen bonding between the purine and pyrimidine residues.

HYDROPHOBIC INTERACTIONS:  Non-polar groups have a tendency to associate with each other in an aqueous environment; this is referred to as hydrophobic interaction. These are formed by interactions between nonpolar hydrophobic side chains by eliminating water molecules. The force that causes hydrophobic molecules or nonpolar portions of molecules to aggregate together rather than to dissolve in water is called the ‘hydrophobic bond’.  This serves to hold lipophilic side chains of amino acids together. Thus, nonpolar molecules will have minimum exposure to water molecules.  To understand more clearly, look at the structure of a cell membrane listed below.

 

RELATED;

1.  THE GLYCOSIDIC BOND

2. DNA THE GENETIC MATERIAL

3. NUCLEOTIDES

4. STRUCTURE AND PHYSIOLOGY OF A CELL MEMBRANE

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

TERTIARY STRUCTURE OF PROTEINS

INTRODUCTION:  Secondary structure denotes the configurational relationship between residues which are about 3-4 amino acids apart; or secondary level defines the organization at immediate vicinity of amino acids. The tertiary structure denotes three dimensional structure of the whole protein. The tertiary structure defines the steric relationship of amino acids which are far apart from each other in the linear sequence, but are close in the three-dimensional aspect.

STABILITY OF THE TERTIARY STRUCTURE: The tertiary structure is maintained by non-covalent interactions such as hydrophobic bonds, electrostatic bonds and van der Waals forces. The tertiary structure acquired by native protein is always thermodynamically most stable.

DOMAIN:  This is the term used to denote a compact globular functional unit of a protein. A domain is a relatively independent region of the protein, and may represent a functional unit. The domains are usually connected with relatively flexible areas of protein. To give an example, Phenyl alanine hydroxylase enzyme contains 3 domains, one regulatory, one catalytic and one protein-protein interaction domains.

 

RELATED;

1.  BIOCHEMISTRY OF PROTEINS

2. BIOCHEMISTRY OF BONDS

3. IMMUNOGLOBULINES

4. ENZYMES

REFERENCES

MAGNESIUM (Mg++)

INTRODUCTION:  Magnesium is the fourth most abundant cation in the body and second most prevalent intracellular cation. Magnesium is mainly seen in intracellular fluid. Total body magnesium is about 25 g, 60% of which is complexed with calcium in bone.  One-third of skeletal magnesium is exchangeable with serum.  Magnesium orally produces diarrhea; but intravenously it produces CNS depression.

REQUIREMENT:  The requirement is about 400 mg/day for men and 300 mg/day for women. Doses above 600 mg may cause diarrhea. More is required during lactation. Major sources are cereals, beans, leafy vegetables and fish.

NORMAL SERUM LEVEL OF MAGNESIUM: Normal serum level Mg++ is 1.8-2.2 mg/dl. Inside the RBC, the magnesium content is 5 mEq/L. In muscle tissue Mg++ is 20 mEq/L. About 70% of magnesium exists in free state and remaining 30% is protein-bound (25% to albumin and 5% to globulin).  Homeostasis is maintained by intestinal absorption as well as by excretion by kidney.  Magnesium is reabsorbed from loop of Henle and not from proximal tubules.

FUNCTIONS OF MAGNESIUM:  1.  Mg++ is the activator of many enzymes requiring ATP. Alkaline phosphatase, hexokinase, fructokinase, phosphofructokinase, adenyl cyclase, cAMP dependent kinases among others. need magnesium.

2. Neuromuscular irritability is lowered by magnesium.

3. Insulin-dependent uptake of glucose is reduced in magnesium deficiency. Magnesium supplementation improves glucose tolerance.

 

RELATED;

1.  PLASMA PROTEINS

2. ENZYMES

3. VITAMIN C

4.  VITAMIN A

5.  VITAMINS AND MINERALS

6.  BIOCHEMISTRY

REFERENCES