TEN RULES OF BEING FREE FROM STRESS:
THE WORLD IS CHANGING NOWADAYS ESPECIALLY WHEN IT COMES TO EDUCATION. DURING THIS PERIOD AND POST COVID 19 PANDEMIC, A MODERN MEDICAL SCHOLAR WILL NEED TO BE UPDATED WITH THE LATEST ICT SKILLS TO MEET THE CHALLENGES OF THE PAST. THIS SITE WAS CREATED AT THE BEGINNING OF COVID 19 LOCKDOWN WITH THE AIM TO PROVIDE MEDICAL STUDENTS WITH SELF STUDY NOTES IN MEDICINE, PHARMACOLOGY, RESEARCH METHODS, MICROBIOLOGY, PATHOPHYSIOLOGY AND BIOCHEMISTRY.
Friday, July 14, 2023
TEN RULES OF BEING FREE FROM STRESS AT THE WORKPLACE
Wednesday, June 21, 2023
INFLAMMATORY CONDITIONS AND THE HUMAN BODY
OBJECTIVES: By the end of the discussion, the reader/medical student will be able to;
Saturday, June 03, 2023
PATHOPHYSIOLOGY OF DIABETES MELLITUS
OBJECTIVES OF THE DISCUSSION: By the end of this discussion, the learner/Medical student/reader will be able to;
METABOLISM OF GLUCOSE: Glucose also commonly known as blood sugar, is a monomer of polysaccharides, many disaccharides and oligosaccharides, and is a constituent of many carbohydrate food stuffs. When taken in the body especially in form of food, carbohydrates yield this precious source of fuel in the body as part of digestion in the gastrointestinal tract. Digestion of carbohydrates
DEVELPMENT OF DIABETES MELLITUS: Development of diabetes follows the body's inability to absorb glucose from the blood circulation either as a result of insufficient production of insulin from the pancreas, cellular resistance to circulating insulin or both and therefore increasing load of glucose in circulation.
TYPES OF DIABETS: Now that we have seen the issue is insulin and glucose, there are two aspects; The insulin produced in the pancreas is not enough or it is not produced at all, and this will be termed Diabetes mellitus type 1 or Insulin dependent diabetes mellitus.
The other aspect will be, the pancreas is normal and producing enough insulin but the body cells are not sensitive to the produced insulin and therefore the produced insulin noes not work despite it's presence. This is termed Diabetes mellitus type 2 or Non Insulin dependent diabetes mellitus.
SUMMERY: That describes the out goings of glucose metabolism, insulin production, and development of diabetes. To read about the detailed description for the types of diabetes, possible causes of pancreatic failure and management of diabetes click here.
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6. MEDICAL MANAGEMENT OF DIABETES MELLITUS
7. PANCREATITIS
Wednesday, May 24, 2023
PATHOPHYSIOLOGY OF PEPTIC ULCER DISEASE
OBJECTIVES OF THE DISCUSSION: By the end of the discussion, the reader/medical student will be able to;
2) Hypersecretion of gastric juice in the stomach which may lead to autodigestion of the protein portions of the stomach walls.
3. Use of aggressive factors including but not limited to alcohol, smoking or use of Nicotine and tar.
The pathophysiology of peptic ulcer disease is erosion of the mucus layer protecting the stomach from corrosive Hydrochloric acid co-produced with pepsin, and subsequent autodigestion of stomach walls leading to inflammation, followed by wounds and if not treated in time, perforation. If you would like to read more about peptic ulcers management and treatment options, follow the links in the related section below.
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2. Nicotine
Sunday, May 07, 2023
DISSEMINATED INTRAVASCULAR COAGULATION (DIC)
INTRODUCTION: Disseminated intravascular coagulation (DIC) is a potentially life-threatening sign and not a disease itself, of a serious underlying disease mechanism. In this condition there is a problem that predominates and over activate the immune system which in turn over responds.
TRIGGERS OF DIC: Disseminated Intravascular Coagulation may be triggered by sepsis, trauma, cancer, shock, abruptio placentae, toxins, or allergic reactions. The severity of DIC is variable, but it is potentially life threatening.
PATHOPHYSIOLOGY OF DIC: In DIC, the normal hemostatic mechanisms are altered so that tiny clots form within the microcirculation of the body. These clots consume platelets and clotting factors, eventually causing coagulation to fail and bleeding to result. This bleeding disorder is characterized by low platelet and fibrinogen levels; prolonged prothrombin time (PT), partial thromboplastin time (PTT), and thrombin time; and elevated fibrin degradation products (D-dimers).
CLINICAL MANIFESTATIONS: Clinical manifestations of DIC are primarily reflected in compromised organ function or failure, clot formation followed by ischemia to all or part of the organ and or, less often, bleeding.
1. Patient may bleed from mucous membranes, venipuncture sites, and gastrointestinal and urinary tracts.
2. Bleeding can range from minimal occult internal bleeding to profuse hemorrhage from all orifices.
3. Patients typically develop multiple organ dysfunction syndrome (MODS), and they may exhibit renal failure as well as pulmonary and multifocal central nervous system infarctions as a result of microthromboses, macrothromboses, or hemorrhages.
4. Initially, the only manifestation is a progressive decrease in the platelet count; then, progressively, the patient exhibits signs and symptoms of thrombosis in the organs involved.
ASSESSMENT AND DIAGNOSTIC FINDINGS: Clinically, the diagnosis of DIC is often established by a drop in platelet count, an increase in PT and activated partial thromboplastin time (aPTT), an elevation in fibrin degradation products, and measurement of one or more clotting factors and inhibitors.
MEDICAL MANAGEMENT: The most important management issue is treating the underlying cause of DIC. A second goal is to correct the secondary effects of tissue ischemia by improving oxygenation, replacing fluids, correcting electrolyte imbalances, and administering vasopressor medications. If serious hemorrhage occurs, the depleted coagulation factors and platelets may be replaced. A heparin infusion, which is a controversial management method, may be used to interrupt the thrombosis process. Other therapies include recombinant activated protein C and AT infusions.
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1. BLOOD CLOTTING AND IT'S PREVENTION
4. BLOOD PLASMA
Saturday, April 22, 2023
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.
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3. OVULATION AND THE MENSTRAUL CYCLE
4. OXYTOCIN
Friday, April 14, 2023
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