ORGANS OF THE IMMUNE SYSTEM

INTRODUCTION: Several tissues and organs play roles in host defenses and are functionally classified as the immune system. In the human body, the primary immune parts are the lymphoid organs; the thymus and the bone marrow. All cells of the immune system are originally derived from bone marrow and that cellular lineage is known as the Pluripotent stem cells.

IMMUNE CELLS FROM THE BONE MALLOW: Pluripotent stem cells differentiate into lymphocyte, granulocyte, monocyte, erythrocyte, and megakaryocyte populations. Deficiency or dysfunction of the pluripotent stem cell or the various cell lines developing from it can result in immune deficiency disorders of varying expression and severity.

THYMUS GLAND AND IT’S ROLE IN IMMUNITY: The thymus, derived from the third and fourth embryonic pharyngeal pouches, functions to produce T lymphocytes and is the site of initial T lymphocyte differentiation. Developing T cells in the thymic cortex are first positively selected for their ability to recognize self-peptides which are, major histocompatibility complex (MHC). In subsequent negative selection, T cells that avidly recognize self-peptides are destroyed, thus removing deleterious self-reactive clones. The thymus also regulates immune function by secreting multiple bioactive substances that promote T-lymphocyte differentiation and are essential for T-lymphocyte–mediated immunity.

OTHER LYMPHOID ORGANS IN THE HUMAN BODY: In mammals, the lymph nodes, spleen, and gut-associated lymphoid tissue are secondary lymphoid organs connected by blood and lymphatic vessels. Lymph nodes are strategically dispersed throughout the vasculature and are the principal organs of the immune system that deliver and localize antigen, promoting adaptive immunity through cell–cell interaction and lymphocyte activation.

LYMPH NODE AND THEIR ROLE IN IMMUNITY: Lymph nodes have a framework of reticular cells and fibers that are arranged into a cortex and medulla. B lymphocytes, the precursors of antibody-producing cells, or plasma cells, are found in the cortex, as well as in the medulla. T lymphocytes are found chiefly in the medullary and paracortical areas of the lymph node.

THE SPLEEN AND IT’S ROLE IN IMMUNITY: The spleen filters and processes antigens from the blood and is functionally and structurally divided into B-lymphocyte and T-lymphocyte areas, similar to those of the lymph nodes. The spleen also removes damaged blood cells and immune complexes, including antibody-coated microbes. Loss of the spleen, through traumatic causes or therapeutic splenectomy, increases host susceptibility to encapsulated bacteria, which are normally cleared through opsonization and phagocytosis in splenic tissue.

THE GASTROINTESTINAL TRACT AND IT’S ROLE IN IMMUNITY: Gut-associated lymphoid tissue, adjacent to the mucosal epithelium, includes the tonsils, the Peyer patches of the small intestine, and the appendix, all of which facilitate immune responses to the multitude of ingested antigens and commensal microbes. Like the lymph nodes and spleen, these tissues exhibit separation into B-lymphocyte–dependent and T-lymphocyte–dependent areas. Mucosal immune responses tend to generate antigen-specific IgA, and, with some orally administered antigens, T-cell anergy or tolerance may occur rather than immune stimulation. Increasingly, the commensal microbiome of the gastrointestinal tract has been recognized to shape both local and systemic innate and adaptive immune responses, influencing both health and disease for example the case of allergy or autoimmunity.

RELATED;

1. LINEAGES OF STEM CELLS FROM THE BORN MARROW

2. THE MAJOR HISTOCOMPATIBILITY COMPLEX

3. ADAPTIVE IMMUNITY

4. IMMUNOGLOBULINS

5. ALLERGY

6. AUTOIMMUNITY

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INSULIN AS A CHEMICAL OF LIFE

 

Introduction: Insulin increases the transport of glucose from the blood into cells by increasing the permeability of cell membranes to glucose. It should be noted however that the Brain, liver, and kidney cells, are not dependent on insulin for glucose intake.

Role of glucose in cells: Once inside cells, glucose is used in cell respiration to produce energy in form of ATP. The liver and skeletal muscles also change glucose to glycogen, a process biochemically known as glycogenesis, which means glycogen production and the implication is that glucose can be stored for later use.

Other roles of insulin other than glucose metabolism: Insulin is also important in the metabolism of other food types; it enables cells to take in fatty acids and amino acids to use in the synthesis of lipids and proteins and in this case not energy production. Without insulin, blood levels of lipids tend to rise and cells accumulate excess fatty acids. With respect to blood glucose, insulin decreases its level by promoting the use of glucose for energy production.

Secretion of Insulin and consequences of it’s deficiency: Insulin is a vital hormone that we cannot survive for very long without. A deficiency of insulin or in its functioning is called diabetes mellitus. Secretion of insulin is stimulated by hyperglycemia which is a condition of high blood glucose level. This state occurs after eating, especially of meals high in carbohydrates. As glucose is absorbed from the small intestine into the blood, insulin is secreted to enable cells to use the glucose for immediate energy. At the same time, any excess glucose will be stored in the liver and muscles as glycogen.

RELATED;

1.  Glucagon

2.  The endocrine pancreas

3.  Diabetes mellitus

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BREAST CANCER

INTRODUCTION: Cancer of the breast is a pathologic entity that starts with a genetic alteration in a single cell and may take several years to become palpable. The most common histologic type of breast cancer is infiltrating ductal carcinoma, whereby tumors arise from the duct system and invade the surrounding tissues. These tumors arise from the lobular epithelium and typically occur as an area of ill-defined thickening in the breast. Infiltrating ductal and lobular carcinomas usually spread to bone, lung, liver, adrenals, pleura, skin, or brain.

CAUSES OF BREAST CANCER: There is no one specific cause of breast cancer; rather, a combination of genetic, hormonal, and possibly environmental events may contribute to its development. If lymph nodes are unaffected, the prognosis is better. The key to improved cure rates is early diagnosis, before metastasis.

RISK FACTORS:

1. Gender and in specific female, and increasing age.

2. Previous breast cancer: The risk of developing cancer in the same or opposite breast is significantly increased.

3. Family history: Having first-degree relative with breast cancer (mother, sister, daughter) increases the risk twofold; having two first-degree relatives increases the risk fivefold.

4. Genetic mutations account for majority of inherited breast cancers.

5. Hormonal factors: early menarche for example before 12 years of age, nulliparity, first birth after 30 years of age, late menopause that is to say; after 55 years of age, and hormone therapy also formerly referred to as hormone replacement therapy.

6. Other factors may include exposure to ionizing radiation during adolescence and early adulthood obesity, alcohol intake.

PROTECTIVE FACTORS: Protective factors may include regular vigorous exercise, pregnancy before age 30 years, and breastfeeding.

PREVENTION STRATEGIES: Patients at high risk for breast cancer may consult with specialists regarding possible or appropriate prevention strategies such as the following:

1. Long-term surveillance consisting of twice-yearly clinical breast examinations starting at age 25 years, yearly mammography, and possibly MRI

2. Chemoprevention to prevent disease before it starts, using tamoxifen and possibly raloxifene

CLINICAL MANIFESTATIONS: Generally, lesions are nontender, fixed, and hard with irregular borders; most occur in the upper outer quadrant. Some women have no symptoms and no palpable lump but have an abnormal mammogram. Advanced signs may include skin dimpling, nipple retraction, or skin ulceration.

ASSESSMENT AND DIAGNOSTICS: Biopsy for example percutaneous or surgical, and histologic examination of cancer cells. Tumor staging and analysis of additional prognostic factors are used to determine the prognosis and optimal treatment regimen. Chest x-rays, CT, MRI, PET scan, bone scans, and blood work, that is, complete blood cell count, comprehensive metabolic panel, tumor markers.

Medical Management: Various management options are available. The patient and physician may decide on surgery, radiation therapy, chemotherapy, or hormonal therapy or a combination of therapies. Modified radical mastectomy involves removal of the entire breast tissue, including the nipple–areola complex and a portion of the axillary lymph nodes. Total mastectomy involves removal of the breast and nipple–areola complex but does not include axillary lymph node dissection.

Chemotherapy to eradicate micrometastatic spread of the disease: cyclophosphamide, methotrexate, fluorouracil, anthracycline-based regimens (eg, doxorubicin, taxanes (paclitaxel, docetaxel).

Hormonal therapy based on the index of estrogen and progesterone receptors: Tamoxifen is the primary hormonal agent used to suppress hormonal-dependent tumors; others are inhibitors anastrazole.

RELATED;

1.  BREAST EXAMINATION

2.  THE ORIGIN OF CANCER

3.  OVULATION AND THE MENSTRAUL CYCLE

4.  OXYTOCIN

REFERENCES

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

HUMAN PAPILLOMAVIRUSES

 

INTRODUCTION: Papillomaviruses cannot be grown in cultures and existence of a large number of distinct human papillomaviruses became evident only after the development recombinant DNA technology. Different types of human papillomaviruses (HPV) are associated with lesions of specific morphology and at specific anatomic sites some of which include the cervix.

MORPHOLOGY: The virion is non-enveloped and has a diameter of 55 nm, icosahedral symmetry and 72 capsomers. The viral genome is a double stranded, circular DNA molecule with molecular weight of 5.2 million daltons. The viral capsid proteins consist of a major polypeptide and a number of minor polypeptides. Purified virion contains four histones of host origin.

PATHOGENESIS: Human papillomaviruses infect only epithelium of skin and mucous membranes. The virus probably infects cells of the lower layers of the epithelium which undergo proliferation and form the warts. Histologically, a wart is localised epithelial hyperplasia with a defined boundary and an intact basement membrane. Clinically warts can be of various types.

DIAGNOSIS: It is essentially clinical. History can confirm the diagnosis of warts but it does not indicate the type of HPV responsible. No serological tests are available for virus identification. Human papillomaviruses cannot be grown in culture. A broadly cross-reactive genus-specific antiserum is available, which is capable of recognising capsid antigen of all human and animal papillomaviruses by immunoperoxidase or immunofluorescent tests. Identification of viral genotype is possible by DNA hybridisation methods.

TREATMENT: Most skin and genital warts regress spontaneously. The patient seeks treatment for cosmetic reasons, pain, discomfort, and disability depending on the location and size of warts. The treatment includes application of caustic agents such as podophyllin and salicylic acid, cryotherapy, surgical removal, and antimetabolites such as 5-fluorouracil.

RELATED;

1.  HUMAN IMMUNE VIRUS

2.  INFECTION BY THE MUMPS VIRUS

3.  VIRAL HEPATITIS

4.  RETROVIRUSES

REFERENCES

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1.  CASTING CROWNS MUSIC

2.  UGANDAN GOSPEL MUSIC

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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