Mega Mover Empire

6. Run

7. Better than life

8. Jesus culture alive

9. North point worship-Every beat

10. Death was arrested

11. North point worship-Love come down

12. Forgiven by Crowder Wallace

13. Casting crowns-The power of the cross

CHRIS TOMLIN

1. Nonstop gospel music by Chris Tomlin

2. Passion-White flag

3. Top 30 worship songs of Chris Tomlin

NIGERIAN AND WEST AFRICA

1. Excess love by Mercy Kinwo

2. I know who I am by Sinach

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1. ANDROID APPS DOWNLOAD

2. WINDOWS SOFTWARE DOWNLOADS

3. MEGA MOVER EMPIRE ON YOUTUBE

4. UGANDA GOSPEL MUSIC

Godfrey Kateregga as the author and administrator of this page, is a Ugandan youth male Graduate from Mbarara University of Science and Technology, Faculty of Medicine, Western Uganda. He is a medical scientist with over half a decade in instructing medical students and, interested in sharing medical information and medical informatics plus ICT, widely experienced in training Adults with special needs.

Friday, June 10, 2022

RENAL FAILURE

INTRODUCTION: Renal failure results when the kidneys are unable to remove metabolic waste and perform their regulatory functions. Acute renal failure (ARF) is a rapid loss of renal function due to damage to the kidneys. Three major categories of ARF are prerenal (hypoperfusion, as from volume depletion disorders, extreme vasodilation, or impaired cardiac performance); intrarenal (parenchymal damage to the glomeruli or kidney tubules, as from burns, crush injuries, infections, transfusion reaction, or nephrotoxicity, which may lead to acute tubular necrosis [ATN]); and postrenal (urinary tract obstruction, as from calculi, tumor, strictures, prostatic hyperplasia, or blood clots).

CLINICAL STAGES: Initiation period: initial insult and oliguria. Oliguric period (urine volume less than 400 mL/day): Uremic symptoms first appear and hyperkalemia may develop.

Diuresis period: gradual increase in urine output signaling beginning of glomerular filtration’s recovery. Laboratory values stabilize and start to decrease.

Recovery period: improving renal function (may take 3 to 12 months).

CLINICAL MANIFESTATIONS: Critical illness and lethargy with persistent nausea, vomiting, and diarrhea. Skin and mucous membranes are dry. Central nervous system manifestations: drowsiness, headache, muscle twitching, seizures. Urine output scanty to normal; urine may be bloody with low specific gravity. Steady rise in blood urea nitrogen (BUN) may occur depending on degree of catabolism; serum creatinine values increase with disease progression. Hyperkalemia may lead to dysrhythmias and cardiac arrest. Progressive acidosis, increase in serum phosphate concentrations, and low serum calcium levels may be noted. Anemia from blood loss due to uremic GI lesions, reduced red blood cell life-span, and reduced erythropoietin production.

ASSESSMENT AND DIAGNOSTIC METHODS: Urine output measurements. Renal ultrasonography, CT and magnetic resonance imaging (MRI) scans. BUN, creatinine, electrolyte analyses.

MEDICAL MANAGEMENT: Treatment objectives are to restore normal chemical balance and prevent complications until renal tissues are repaired and renal function is restored. Possible causes of damage are identified and treated. Fluid balance is managed on the basis of daily weight, serial measurements of central venous pressure, serum and urine concentrations, fluid losses, blood pressure, and clinical status. Fluid excesses are treated with mannitol, furosemide, or ethacrynic acid to initiate diuresis and prevent or minimize subsequent renal failure. Blood flow is restored to the kidneys with the use of intravenous (IV) fluids, albumin, or blood product transfusions. Dialysis (hemodialysis, hemofiltration, or peritoneal dialysis) is started to prevent complications, including hyperkalemia, metabolic acidosis, pericarditis, and pulmonary edema. Cation-exchange resins (orally or by retention enema). IV dextrose 50%, insulin, and calcium replacement for the patient who is hemodynamically unstable (low blood pressure, changes in mental status, dysrhythmia). Shock and infection are treated if present. Arterial blood gases are monitored when severe acidosis is present. Sodium bicarbonate to elevate plasma pH. If respiratory problems develop, ventilatory measures are started. Phosphate-binding agents to control elevated serum phosphate concentrations. Replacement of dietary proteins is individualized to provide the maximum benefit and minimize uremic symptoms. Caloric requirements are met with high-carbohydrate feedings; parenteral nutrition (PN). Foods and fluids containing potassium and phosphorus are restricted. Blood chemistries are evaluated to determine amount of sodium, potassium, and water replacement during oliguric phase. After the diuretic phase, high-protein, high-calorie diet is given with gradual resumption of activities.

2. EXCRETION OF DRUGS

Saturday, January 09, 2021

DISORDERS OF THE INTESTINES

DUODENAL ULCERS: These are erosions of the duodenal wall caused by the gastric juice that enters from the stomach. The most serious consequences are bleeding and perforation.

PARALYTIC ILEUS: This is the cessation of contraction of the smooth muscle layer of the intestine. This is a possible complication of abdominal surgery, but it may also be the result of peritonitis or inflammation elsewhere in the abdominal cavity. In the absence of peristalsis, intestinal obstruction may occur. Bowel movements cease, and vomiting occurs to relieve the pressure within the alimentary tube. Treatment involves suctioning the intestinal contents to eliminate any obstruction and to allow the intestine to regain its normal motility.

LACTOSE INTOLERANCE: This is the inability to digest lactose because of deficiency of the enzyme lactase. Lactase deficiency may be congenital, a consequence of prematurity, or acquired later in life. The delayed form is quite common among people of African or Asian ancestry, and in part is genetic. When lactose, or milk sugar, is not digested, it undergoes fermentation in the intestine. Symptoms include diarrhea, abdominal pain, bloating, and flatulence (gas formation).

SALMONELLA FOOD POISONING: This is caused by bacteria in the genus Salmonella. These are part of the intestinal flora of animals, and animal foods such as meat and eggs may be sources of infection. These bacteria are not normal for people, and they cause the intestines to secrete large amounts of fluid. Symptoms include diarrhea, abdominal cramps, and vomiting and usually last only a few days. For elderly or debilitated people, however, salmonella food poisoning may be very serious or even fatal.

DIVERTICULA: These are small outpouchings through weakened areas of the intestinal wall. They are more likely to occur in the colon than in the small intestine and may exist for years without causing any symptoms. The presence of diverticula is called diverticulosis. Inflammation of diverticula is called diverticulitis, which is usually the result of entrapment of feces and bacteria. Symptoms include abdominal pain and tenderness and fever. If uncomplicated, diverticulitis may be treated with antibiotics and modifications in diet. The most serious complication is perforation of diverticula, allowing fecal material into the abdominal cavity, causing peritonitis. A diet high in fiber is believed to be an important aspect of prevention, to provide bulk in the colon and prevent weakening of its wall.

RELATED;

1. PEPTIC ULCER DISEASE

2. FOOD POISONING

3. LACTOSE INTOLERANCE

Friday, July 17, 2020

GASTROESOPHAGEAL REFLUX DISEASE

GASTROESOPHAGEAL REFLUX DISEASE

Friday, June 26, 2020

LUGANDA CHURCH MUSIC

UGANDAN CHURCH MUSIC

1. Mukulike nnyo mwasoba

COLLAGEN

Introduction: Collagen is the most abundant protein in mammals, occupying up to a third of the total mass. There are at least 16 types of collagen. Its fibers are a major component of tendons and they are also found abundantly in skin. Collagen is also prominent in cornea, cartilage, bone, blood vessels and the gut.

Structure of Collagen: Collagen’s structure is an example of a helix of helices, being composed of three left handed helical chains that each are coiled together in a right-handed fashion to make the collagen fiber. Each helix is stretched out more than an α-helix, giving it an extended appearance. On the inside of the triple helical structure, only residues of glycine are found, since the side chains of other amino acids are too bulky. Collagen chains have the repeating structure glycinem-n where m is often proline and n is often hydroxyproline. Collagen is synthesized in a pre-procollagen form. Processing of the pre-procollagen in the endoplasmic reticulum results in glycosylation, removal of the ‘pr sequence, and hydroxylation of lysine and proline residues. The hydroxides can form covalent cross-links with each other, strengthening the collagen fibers. As pro-collagen is exported out of the cell, proteases trim it, resulting in a final form of collagen called tropocollagen.

RELATED;

1. Proteins

2. Diversity of biomolecules

3. Amino acids

4. TRADITIONAL AND COMPLIMENTARY MEDICATIONS

VALERIAN FOR ANXIETY AND INSOMNIA

Valerian (Valeriana officinalis) is a perennial plant grown in Europe, Asia, and North America. Valerian has several substances in its roots that affect the CNS; its effects appear to be due to a mixture of various chemicals within the herb. Valerian has been used to treat nervousness, anxiety, and insomnia for thousands of years and is one of the most widely used herbal CNS depressants. The drug likely acts by a mechanism similar to the benzodiazepines: increasing the amount of GABA at synapses in the CNS. The herb is considered to be safe, when used at recommended doses for 4-to 6-week periods. At higher doses, the major side effects of valerian are drowsiness and decreased alertness, especially the morning after taking the herb. Valerian should not be combined with alcohol or other drugs that cause sedation or drowsiness.

RELATED;

1. BARBITURATES

2. BENZODIAZEPINES

3. SEDATIVE-HYPNOTICS

3. PHARMACOLOGY AND THERAPEUTICS

Wednesday, June 24, 2020

CEPHALOSPORINS & CEPHAMYCINS

INTRODUCTION: Cephalosporins are similar to penicillins, but more stable to many bacterial β-lactamases and therefore have a broader spectrum of activity. However, there are some strains of E. coli and Klebsiella expressing extended-spectrum β-lactamases and they can hydrolyze most cephalosporins, sparking the burden of antibiotic resistance. Cephalosporins are not active against enterococci and L. monocytogenes. Antimicrobialdrug resistance: Beta-lactamase inhibitors: Penicillins

MOLECULAR CHARACTERISTICS: The nucleus of the cephalosporins, 7-aminocephalosporanic acid, bears a close resemblance to 6-aminopenicillanic acid. The intrinsic antimicrobial activity of natural cephalosporins is low, but the attachment of various functional groups has yielded hundreds of potent compounds of low toxicity. Cephalosporins can be classified into four major groups or generations, depending mainly on the spectrum of antimicrobial activity.

FIRST-GENERATION CEPHALOSPORINS: First-generation cephalosporins include; cefazolin, cefadroxil, cephalexin, cephalothin, cephapirin, and cephradine. These drugs are very active against gram-positive cocci, such as pneumococci, streptococci, and staphylococci. Traditional cephalosporins are not active against methicillin-resistant strains of staphylococci; however, new compounds have been developed that have activity against methicillin-resistant strains.

CLINICAL USES: Oral drugs may be used for the treatment of urinary tract infections and staphylococcal or streptococcal infections, including cellulitis or soft tissue abscess. However, oral cephalosporins should not be relied on in serious systemic infections. Cefazolin penetrates well into most tissues. It is therefore a drug of choice for surgical prophylaxis. Cefazolin may also be a choice in infections for which it is the least toxic drug such as in penicillinase producing E. coli or K. pneumonia, and in individuals with staphylococcal or streptococcal infections who have a history of penicillin allergy other than immediate hypersensitivity.

SECOND-GENERATION CEPHALOSPORINS: Members of the second-generation cephalosporins include cefaclor, cefamandole, cefonicid, cefuroxime, cefprozil, loracarbef, and ceforanide. They are structurally related cephamycins including; cefoxitin, cefmetazole , and cefotetan , which have activity against anaerobes. This is a heterogeneous group with marked individual differences in activity, pharmacokinetics, and toxicity.

In general, they are active against organisms inhibited by first-generation drugs, but in addition they have extended gram-negative coverage. Klebsiella sp including those resistant to cephalothin are usually sensitive. Cefamandole, cefuroxime, cefonicid, ceforanide, and cefaclor are active against H. influenzae but not against serratia or B. fragilis.

CLINICAL USES: The oral second-generation cephalosporins are active against β-lactamase-producing H influenzae or Moraxella catarrhalis and have been primarily used to treat sinusitis, otitis, and lower respiratory tract infections, in which these organisms have an important role. Because of their activity against anaerobes (including many B. fragilis strains) , cefoxitin, cefotetan, or cefmetazole can be used to treat mixed anaerobic infections such as peritonitis, diverticulitis, and pelvic inflammatory disease. Cefuroxime is used to treat community-acquired pneumonia because it is active against β-lactamase-producing H. influenzae or K. pneumoniae and some penicillin-non-susceptible pneumococci. Although cefuroxime crosses the blood-brain barrier, it is less effective in treatment of meningitis than ceftriaxone or cefotaxime and should not be used.

THIRD-GENERATION CEPHALOSPORINS: Third-generation agents include cefoperazone, cefotaxime, ceftazidime, ceftizoxime, ceftriaxone, cefixime, cefpodoxime proxetil, cefdinir, cefditoren pivoxil, ceftibuten, and moxalactam .

ANTIMICROBIAL ACTIVITY: Compared with second-generation agents, these drugs have expanded gram-negative coverage, and some are able to cross the blood-brain barrier. Third-generation drugs are active against Citrobacter, S. marcescens, and Providencia (although resistance can emerge during treatment of infections caused by these species due to selection of mutants that constitutively produce cephalosporinase). They are also effective against β-lactamase-producing strains of haemophilus and neisseria. Ceftazidime and cefoperazone are the only two drugs with useful activity against P. aeruginosa. Like the second-generation drugs, third-generation cephalosporins are hydrolyzed by constitutively produced AmpC β lactamase, and they are not reliably active against Enterobacter species. Serratia, Providencia, and Citrobacter also produce a chromosomally encoded cephalosporinase that, when constitutively expressed, can confer resistance to third-generation cephalosporins.

RELATED;

1. PENICILLINS

2. SULFONAMIDES

2. Antimicrobial resistance to Quinine

MEBENDAZOLE

INTRODUCTION: Mebendazole is a synthetic benzimidazole that has a wide spectrum of antihelminthic activity and a low incidence of adverse effects.

PHARMACOTHERAPEUTICS: Less than 10% of orally administered mebendazole is absorbed. In fact to be precise, only if you take it with a heavy fatty meal, the bioavailability will exceed 3%. The absorbed drug is protein-bound (> 90%), is rapidly converted to inactive metabolites, primarily during its first pass in the liver, and has a half-life of 2–6 hours. It is excreted mostly in the urine, principally as decarboxylated derivatives. In addition, a portion of absorbed drug and its derivatives are excreted in the bile. Absorption is increased if the drug is ingested with a fatty meal.

PHARMACODYNAMICS: Mebendazole probably acts by inhibiting microtubule synthesis; the parent drug appears to be the active form. Efficacy of the drug varies with gastrointestinal transit time, with intensity of infection, and perhaps with the strain of parasite. The drug kills hookworm, ascaris, and trichuris eggs.

CLINICAL USES: Mebendazole is indicated for use in ascariasis, trichuriasis, hookworm and pinworm infections, and certain other helminthic infections. It can be taken before or after meals; the tablets should be chewed before swallowing.

For pinworm infection, the dose is 100 mg once, repeated at 2 weeks.

For ascariasis, trichuriasis, hookworm, and trichostrongylus infections, a dosage of 100 mg twice daily for 3 days is used for adults and for children older than 2 years of age. Cure rates are good for pinworm infections and ascariasis, but have been disappointing in recent studies of trichuriasis. For intestinal capillariasis, mebendazole is used at a dosage of 200 mg twice daily for 21 or more days.

ADVERSE REACTIONS, CONTRAINDICATIONS, AND CAUTIONS: Short-term mebendazole therapy for intestinal nematodes is nearly free of adverse effects. Mild nausea, vomiting, diarrhea, and abdominal pain have been reported infrequently. Rare side effects, usually with high-dose therapy, are hypersensitivity reactions which includes rash and urticaria, agranulocytosis, alopecia, and elevation of liver enzymes.

Mebendazole is teratogenic in animals and therefore contraindicated in pregnancy. It should be used with caution in children younger than 2 years of age because of limited experience and rare reports of convulsions in this age group. Plasma levels may be decreased by concomitant use of carbamazepine or phenytoin and increased by cimetidine.

Mebendazole should be used with caution in patients with cirrhosis.

RELATED;

1. Metronidazole

2. Water, the universal solvent

Monday, June 08, 2020

WATER INTAKE AND OUTPUT

INTRODUCTION: Most of the water the body requires comes from the ingestion of liquids, and this amount averages 1600 ml per day. The food we eat also contains water. Even foods we think of as somewhat dry, such as bread, contain significant amounts of water. The daily water total from food averages 700 ml. The last source of water, about 200 ml per day, is the metabolic water that is a product of cell respiration. The total intake of water per day, therefore, is about 2500 ml, or 2.5 liters.

DAILY WATER OUTPUT: Most of the water lost from the body is in the form of urine produced by the kidneys; this averages 1500 ml per day. About 500 ml per day is lost in the form of sweat, another 300 ml per day is in the form of water vapor in exhaled air, and another 200 ml per day is lost in feces. The total output of water is thus about 2500 ml per day. Naturally, any increase in water output must be compensated for by an increase in intake. Someone who exercises strenuously, for example, may lose 1 to 2 liters of water in sweat and must replace that water by drinking more fluids. In a healthy individual, water intake equals water output, even though the amounts of each may vary greatly from the averages just mentioned.

REGULATION OF WATER INTAKE AND OUTPUT: The hypothalamus in the brain contains osmoreceptors that detect changes in the osmolarity of body fluids. Osmolarity is the concentration of dissolved materials present in a fluid. Dehydration raises the osmolarity of the blood; that is, there is less water in proportion to the amount of dissolved materials. Another way to express this is to simply say that the blood is now a more concentrated solution. When dehydrated, we feel the sensation of thirst, characterized by dryness of the mouth and throat, as less saliva is produced. Thirst is an uncomfortable sensation, and we drink fluids to relieve it. The water we drink is readily absorbed by the mucosa of the stomach and small intestine and has the effect of decreasing the osmolarity of the blood. In other words, we can say that the water we just drank is causing the blood to become a more dilute solution, and, as the serum osmolarity returns to normal, the sensation of thirst diminishes.

WATER BALANCE AND THE ROLE OF ANTIDIURETIC HORMONE: As you may recall, the hypothalamus is also involved in water balance because of its production of antidiuretic hormone (ADH), which is stored in the posterior pituitary gland. In a state of dehydration, the hypothalamus stimulates the release of ADH from the posterior pituitary. Antidiuretic hormone then increases the reabsorption of water by the kidney tubules. Water is returned to the blood to preserve blood volume, and urinary output decreases.

WATER BALANCE AND THE ROLE OF ALDOSTERONE: The hormone aldosterone, from the adrenal cortex, also helps regulate water output. Aldosterone increases the reabsorption of Na ions by the kidney tubules, and water from the renal filtrate follows the Na ions back to the blood. Aldosterone is secreted when the Na ion concentration of the blood decreases or whenever there is a significant decrease in blood pressure (the renin-angiotensin mechanism). Several other factors may also contribute to water loss. These include excessive sweating, hemorrhage, diarrhea or vomiting, severe burns, and fever. In these circumstances, the kidneys will conserve water, but water must also be replaced by increased consumption. Following hemorrhage or during certain disease states, fluids may also be replaced by intravenous administration. A less common occurrence is that of too much water in the body. This may happen following overconsumption of fluids. The osmolarity of the blood decreases, and there is too much water in proportion to electrolytes (or, the blood is too dilute). This condition may become symptomatic, and is called water intoxication. Symptoms are dizziness, abdominal cramps, nausea, and lethargy. Convulsions are possible in severe cases, and fluids must be restricted until the kidneys can excrete the excess water. A hormone that will contribute to that is atrial natriuretic peptide (ANP), which is secreted by the atria when blood volume or blood pressure increases. ANP then decreases the reabsorption of Na ions by the kidneys, which increases urinary output of sodium and water. Also, secretion of ADH will diminish, which will contribute to a greater urinary output that will return the blood osmolarity to normal.

RELATED;

1. Body fluids

1. ACUTE RESPIRATORY DISTRESS SYNDROME

PULMONARY EMBOLISM

INTRODUCTION: PE refers to the obstruction of the pulmonary artery or one of its branches by a thrombus (or thrombi) that originates somewhere in the venous system or in the right side of the heart. Gas exchange is impaired in the lung mass supplied by the obstructed vessel. Massive PE is a life-threatening emergency; death commonly occurs within 1 hour after the onset of symptoms.

RISK FACTORS: It is a common disorder associated with trauma, surgical operation including but not limited to; orthopedic, major abdominal, pelvic, and gynecologic surgeries. Among other factors we have pregnancy, Heart Failure, age more than 50 years, hypercoagulable states, and prolonged immobility. It also may occur in apparently healthy people where most thrombi originate in the deep veins of the legs.

CLINICAL MANIFESTATIONS: Symptoms depend on the size of the thrombus and the area of the pulmonary artery occlusion. Dyspnea is the most common symptom. Tachypnea is the most frequent sign. Chest pain is common, usually sudden in onset and pleuritic in nature; it can be substernal and may mimic angina pectoris or a myocardial infarction. Anxiety, fever, tachycardia, apprehension, cough, diaphoresis, hemoptysis, syncope, shock, and sudden death may occur. Clinical picture may mimic that of bronchopneumonia or HF. In atypical instances, PE causes few signs and symptoms, whereas in other instances it mimics various other cardiopulmonary disorders.

ASSESSMENT AND DIAGNOSTIC METHODS: Because the symptoms of PE can vary from few to severe, a diagnostic workup is performed to rule out other diseases. The initial diagnostic workup may include chest x-ray, ECG, ABG analysis, and ventilation-perfusion scan. Pulmonary angiography is considered the best method to diagnose PE; however, it may not be feasible, cost-effective, or easily performed, especially with critically ill patients. Spiral CT scan of the lung, D-dimer assay (blood test for evidence of blood clots), and pulmonary arteriogram may be warranted.

PREVENTION: Ambulation or leg exercises in patients on bed rest. Application of sequential compression devices. Anticoagulant therapy for patients whose hemostasis is adequate and who are undergoing major elective abdominal or thoracic surgery.

MEDICAL MANAGEMENT: Immediate objective is to stabilize the cardiopulmonary system. Nasal oxygen is administered immediately to relieve hypoxemia, respiratory distress, and central cyanosis. IV infusion lines are inserted to establish routes for medications or fluids that will be needed. A perfusion scan, hemodynamic measurements, and ABG determinations are performed. Spiral (helical) CT or pulmonary angiography may be performed. Hypotension is treated by a slow infusion of dobutamine, which has a dilating effect on the pulmonary vessels and bronchi, or dopamine. The ECG is monitored continuously for dysrhythmias and right ventricular failure, which may occur suddenly. Digitalis glycosides, IV diuretics, and antiarrhythmic agents are administered when appropriate. Blood is drawn for serum electrolytes, complete blood cell count, and hematocrit. If clinical assessment and ABG analysis indicate the need, the patient is intubated and placed on a mechanical ventilator. If the patient has suffered massive embolism and is hypotensive, an indwelling urinary catheter is inserted to monitor urinary output. Small doses of IV morphine or sedatives are administered to relieve patient anxiety, to alleviate chest discomfort, to improve tolerance of the endotracheal tube, and to ease adaptation to the mechanical ventilator.

Anticoagulation Therapy: Anticoagulant therapy (heparin, warfarin sodium [Coumadin]) has traditionally been the primary method for managing acute DVT and PE. Patients must continue to take some form of anticoagulation for at least 3 to 6 months after the embolic event. Major side effects are bleeding anywhere in the body and anaphylactic reaction resulting in shock or death. Other side effects include fever, abnormal liver function, and allergic skin reaction.

Thrombolytic Therapy. Thrombolytic therapy may include urokinase, streptokinase, and alteplase. Bleeding is a significant side effect; nonessential invasive procedures are avoided.

SURGICAL MANAGEMENT: A surgical embolectomy is rarely performed but may be indicated if the patient has a massive PE.

RELATED;

2. PNEUMONIA

3. DEEP VEIN THROMBOSIS