NEISSERIA GONORRHEAE (GONORRHEA)

MORPHOLOGY AND CULTURE: Gonococci are Gram-negative, coffee-bean-shaped cocci that are usually paired. Attachment pili on the bacterial cell surface are responsible for their adhesion to mucosal cells. Gonococci can be grown on moist culture mediums enriched with protein (blood). The atmosphere for primary culturing must contain 5–10% CO2.

PATHOGENESIS AND CLINICAL PICTURE: Gonorrhea is a sexually transmitted disease. The pathogens penetrate into the urogenital mucosa, causing a local purulent infection. In men, the prostate and epididymis can also become infected. In women, the gonococci can also cause salpingitis, oophoritis, or even peritonitis. Gonococci reaching the conjunctival membrane may cause a purulent conjunctivitis, seen mainly in newborn children. Gonococci can also infect the rectal or pharyngeal mucosa. Hematogenously disseminated gonococci may also cause arthritis or even endocarditis.

DETERMINANTS OF THE PATHOGENICITY OF GONOCOCCI: Attachment pili on the surface and the outer membrane protein are responsible for adhesion to cells of the urogenital tract. It also directs the invasion process by means of endocytosis. Immune defenses against granulocytes are based on the outer membrane porin that prevents the phagosome from fusing with lysosomes, resulting in the survival, and proliferation of phagocytosed gonococci in granulocytes. 

The lipo-oligosaccharide (LOS) in the outer membrane is responsible for resistance to complement (serum resistance) as well as for the inflammatory tissue reaction in a manner analogous to the more complexly structured LPS of enterobacteria.

Gonococci can capture iron from the siderophilic proteins lactoferrin and transferrin, accumulating it inside the bacterial cells to facilitate their rapid proliferation.

An IgA1 protease produced by the gonococci hydrolyzes secretory antibodies in the mucosal secretions. The pronounced antigen variability of the attachment pili and the Opa protein make it possible for gonococci to thwart specific immune defense mechanisms repeatedly.

DIAGNOSIS: The method of choice is detection of the pathogens by means of methylene blue and gram staining and culturing. Gonococci are sensitive in cultures and the material must be used immediately after they are obtained to inoculate. Thayer-Martin blood agar with antibiotics added to eliminate accompanying flora, on which medium the cultures are then transported to the laboratory. The identification procedure involves both morphology and biochemical characteristics. Techniques developed recently utilize immunofluorescence or coagglutination methods utilizing monoclonal antibodies to the main protein of the outer membrane, Por. Direct detection in pus and secretion samples is possible using an enzymatic immunosorbence test or detection of gonococcus-specific DNA sequences coding for rRNA using a gene probe.

THERAPY: The agent of choice used to be penicillin G. In recent years, however, the percentage of penicillinase-producing strains has increased considerably all over the world. For this reason, third-generation cephalosporins are now used to treat uncomplicated cases of gonorrhea. They are applied in a single dose (e.g., ceftriaxone, 250–500 mg I.M.). Good results have also been reported with single-dose oral application of fluorinated 4-quinolones (e.g., 0.5 g ciprofloxacin or 0.4 g ofloxacin).

RELATED;

1. Neisseria

2. Antimicrobial drug resistance

3. Penicillin

4. Cephalosporins

5. Medical microbiology

6. Pharmacology and therapeutics

References

VITAMINS AND MINERALS

 

INTRODUCTION: Vitamins are organic molecules needed in very small amounts for normal body functioning. Some vitamins are coenzymes; that is, they are necessary for the functioning of certain enzymes. Others are antioxidant vitamins, including vitamins C, E, and betacarotene, which is a precursor for the synthesis of vitamin A. Antioxidants prevent damage from free radicals, which are molecules that contain an unpaired electron and are highly reactive. The reactions of free radicals can damage DNA, cell membranes, and the cell organelles.

FORMATION OF FREE RADICALS: Free radicals are formed during some normal body reactions, but smoking and exposure to pollution will increase their formation. Antioxidant vitamins combine with free radicals before they can react with cellular components. Plant foods are good sources of these vitamins.

DEFICIENCY OF VITAMINS: Deficiencies of vitamins often result in diseases including but not limited to: vitamin C deficiency and scurvy, for example. Other deficiency diseases that have been known for decades include pellagra which is due to lack of niacin, beri-beri which is due to lack of riboflavin, pernicious anemia for lack of vitamin B12, and rickets for lack of vitamin D. More recently the importance of folic acid (folacin) for the development of the fetal central nervous system has been recognized. Adequate folic acid during pregnancy can significantly decrease the chance of spina bifida also known as, open spinal column and anencephaly which is the absence of the cerebrum and always fatal in a fetus. All women should be aware of the need for extra folic acid during pregnancy.

MINERALS IN THE HUMAN BODY: Minerals are simple inorganic chemicals and have a variety of functions, many of which you are already familiar with. Among some of the most important minerals we have Sodium and potassium which are very important in the normal functioning of the nervous system and the heart, Calcium important in bone formation, Magnesium and phosphorous as we shall be discussing them in details later.

RELATED;

1. VITAMIN A

2.  VITAMIN C

3.  MAGNESIUM

4.  DYNAMICS OF THE HUMAN BODY

REFERENCES

CANCER

 

INTRODUCTION: Cancer is a disease process that begins when an abnormal cell is transformed by the genetic mutation of the cellular DNA. The abnormal cell forms a clone and begins to proliferate abnormally, ignoring growth-regulating signals in the environment surrounding the cell. The cells acquire invasive characteristics, and changes occur in surrounding tissues. The cells infiltrate these tissues and gain access to lymph and blood vessels, which carry the cells to other areas of the body. This phenomenon is called metastasis. In otherwards the cancer spread to other parts of the body.

DESCRIPTION OF CANCER: Cancerous cells are described as malignant neoplasms and are classified and named by tissue of origin. The failure of the immune system to promptly destroy abnormal cells permits these cells to grow too large to be managed by normal immune mechanisms. Certain categories of agents or factors implicated in carcinogenesis include viruses and bacteria, physical agents, chemical agents, genetic or familial factors, dietary factors, and hormonal agents.

CLINICAL MANIFESTATIONS: Cancerous cells spread from one organ or body part to another by invasion and metastasis; therefore, manifestations are related to the system affected and degree of disruption. Generally, cancer causes anemia, weakness, weight loss, and pain which is often in late stages. Symptoms are from tissue destruction and replacement with nonfunctional cancer tissue or overproductive cancer tissue such as, bone marrow disruption and anemia or excess adrenal steroid production; pressure on surrounding structures; increased metabolic demands; and disruption of production of blood cells.

ASSESSMENT AND DIAGNOSTIC METHODS: Screening to detect early cancer usually focuses on cancers with the highest incidence or those that have improved survival rates if diagnosed early. Examples of these cancers include breast, colorectal, cervical, endometrial, testicular, skin, and oropharyngeal cancers. Patients with suspected cancer undergo extensive testing to;

1) Determine the presence and extent of tumor.

2) Identify possible spread (metastasis) of disease or invasion of other body tissues.

3) Evaluate the function of involved and uninvolved body systems and organs.

4) Obtain tissue and cells for analysis, including evaluation of tumor stage and grade.

Diagnostic tests may include tumor marker identification, genetic profiling, imaging studies (mammography, magnetic resonance imaging [MRI], computed tomography [CT], fluoroscopy, ultrasonography, endoscopy, nuclear medicine imaging, positron emission tomography [PET], PET fusion, radioimmunoconjugates), and biopsy.

RELATED;

1.  THE ORIGIN OF CANCER

2.  PATHOLOGY

REFERENCES

COLLOIDS

 

INTRODUCTION: Colloids are proteins, starches, or other large molecules that remain in the blood for a long time because they are too large to easily cross the capillary membranes.

EFFECTS OF COLLOIDS: While circulating, they have the same effect as hypertonic solutions, drawing water molecules from the cells and tissues into the plasma through their ability to increase plasma osmolality and osmotic pressure. Sometimes called plasma volume expanders, these solutions are particularly important in treating hypovolemic shock due to burns, hemorrhage, or surgery

EXAMPLES OF COLLOIDS: The most commonly used colloid is normal serum albumin, which is featured as a prototype drug for shock. Several colloid products contain dextran, a synthetic polysaccharide. Dextran infusions can double the plasma volume within a few minutes, although its effects last only about 12 hours.

Plasma protein fraction is a natural volume expander that contains 83% albumin and 17% plasma globulins. Plasma protein fraction and albumin are also indicated in patients with hypoproteinemia. Hetastarch is a synthetic colloid with properties similar to those of 5% albumin, but with an extended duration of action.

RELATED;

1.  INTRAVENOUS INFUSION OF FLUIDS

2.  PLASMA VOLUME EXPANDERS

3.  ANATOMY AND PHYSIOLOGY

REFERENCES

DIGESTION OF LIPIDS

 

INTRODUCTION: The major dietary lipids are triacyl glycerol, cholesterol and phospholipids. The average normal diet contains about 20-30 g of lipids per day. Western diet generally contains two or three times more than this quantity.

DIGESTION IN STOMACH: The lingual lipase from the mouth enters stomach along with the food. It has an optimum pH of 2.5-5. The enzyme, therefore, continues to be active in the stomach. It acts on short chain triglycerides (SCT). SCTs are present in milk, butter and ghee. The action of lingual lipase is observed to be more significant in the newborn infants. Gastric lipase is acid stable, with an optimum pH around 5.4. It is secreted by chief cells, the secretion is stimulated by gastrin. Up to 30% digestion of triglycerides occurs in stomach.

DIGESTION IN INTESTINES: Emulsification is a prerequisite for digestion of lipids. The lipids are dispersed into smaller droplets; surface tension is reduced; and surface area of droplets is increased. This process is favored by:

1. Bile salts also known as detergent action

2. Peristalsis which provides mechanical mixing

3. Phospholipids

ENZYMES IN INTESTINES:

1. Pancreatic lipase with Co-lipase

2. Cholesterol esterase

3.Phospholipase A2.

The bile (pH 7.7) entering the duodenum serves to neutralise the acid chyme from the stomach and provides a pH favorable for the action of pancreatic enzymes.

DIGESTION OF TRIGLYCERIDES: 1. Pancreatic lipase can easily hydrolyse the fatty acids esterified to the 1^st and 3^rd carbon atoms of glycerol forming 2-monoacylglycerol and two molecules of fatty acid.

2. Then an isomerase shifts the ester bond from position 2 to 1. The bond in the 1st position is then hydrolysed by the lipase to form free glycerol and fatty acid.

3. The major end products of the digestion of TAG are 2-MAG (78%), 1-MAG (6%), glycerol and fatty acids (14%). Thus digestion of TAG is partial (incomplete).

4. Cholesterol ester may be hydrolysed to free cholesterol and fatty acid. The action of phospholipase A2 produces lysophospholipid and a fatty acid.

Co-lipase: The binding of co-lipase to the triacyl glycerol molecules at the oil water interface is obligatory for the action of lipase. The co-lipase is secreted by the pancreas as an inactive zymogen. It is activated by trypsin.

RELATED;

1.  PHASES OF METABOLISM

2.  METABOLISM OF PROTEINS

3.  METABOLISM AND METABOLIC DISORDERS

REFERENCES

METABOLISM DURING STARVATION

 

INTRODUCTION: In early fasting the effect of short term regulation by altering the activity of existing enzymes also known as, fine control, is more significant. When starvation is prolonged foe example for more than 2 days, long term adaptation sets in. For example, the brain starts metabolising ketone bodies deriving about 30% energy from ketone bodies.

FIRST STAGE: Glycogenolysis: During fasting, at first, blood glucose level is maintained by hepatic glycogenolysis. The glycogen stores are sufficient for about 18 hours. The primary requirement for glucose is to meet the demands of the brain.

SECOND STAGE: Gluconeogenesis: Even before the glycogen stores are depleted, gluconeogenesis is accelerated. The amino acids released from muscle form the major substrate for gluconeogenesis. The amino nitrogen is transferred from other amino acids to pyruvate to form alanine. Thus the amino group reaches the liver as alanine where it is transaminated to give pyruvate for gluconeogenesis. This glucose alanine cycle serves to transport the amino nitrogen of other amino acids to liver in a harmless form. Glutamic acid also serves as an important mode of transport of amino acids to liver. The branched chain amino acids liberated by muscle protein catabolism especially leucine and isoleucine are utilized by the muscle to give energy. Brain can preferentially take up the glucogenic valine from the blood stream.

THIRD STAGE: Lipolysis: The prevailing state of high glucagon-insulin ratio stimulates cAMP mediated lipolysis by increasing the activity of hormone sensitive lipase. Then skeletal muscle, heart and kidney will shut down their glucose utilization; and will depend mainly on fatty acids for energy needs (glucose-fatty acid cycle). Inactivation of pyruvate dehydrogenase by phosphorylation is the basis of this change. The stimulation of the activity of CAT by glucagon favors increased rate of beta oxidation. The increased rate of lipolysis and beta oxidation provides an alternate source of fuel as acetyl CoA and subsequently ketone bodies. Ketone bodies provide fuel for tissues like heart muscle, skeletal muscle and to some extent the brain. It is seen that brain starts utilizing ketone bodies from 3rd day of starvation. By 10th day of starvation about 60% of energy for brain is derived from ketone bodies.

FOURTH STAGE: Acidosis: However, this state cannot continue indefinitely since excessive production of ketone bodies leads to metabolic acidosis. When the bicarbonate buffering capacity is exceeded, the pH falls and hyperventilation occurs as a compensatory mechanism. 

FIFTH STAGE: Death from Starvation: Metabolic acidosis and dehydration, unless corrected efficiently, will lead to death. A normal person has fuel reserves to live up to 45–60 days.

RELATED;

1.  Glycolysis

2.  Gluconeogenesis

3.  BIOCHEMISTRY

REFERENCES

INTRAVENOUS INFUSION OF FLUIDS

 

INTRODUCTION: When fluid output exceeds fluid intake, volume deficits may result. Shock, dehydration, or electrolyte loss may occur; large deficits are fatal, unless treated. The following are some common reasons for fluid depletion: 

1) Loss of gastrointestinal (GI) fluids due to vomiting, diarrhea, chronic laxative use, or GI suctioning. 

2) Excessive sweating during hot weather, athletic activity, or prolonged fever. 

3) Severe burns. 

4) Hemorrhage. 

5) Excessive diuresis due to diuretic therapy or uncontrolled diabetic ketoacidosis.

PURPOSE OF ADMINISTERING IV FLUIDS: The immediate goal in treating a volume deficit disorder is to replace the depleted fluid. In non-acute circumstances, this may be achieved by drinking more liquids or by administering fluids via a feeding tube. In acute situations, IV fluid therapy is indicated. Regardless of the route, careful attention must be paid to restoring normal levels of blood elements and electrolytes as well as fluid volume. IV replacement fluids are of two basic types namely; crystalloids and colloids.

CRYSTALLOIDS: Crystalloids are IV solutions that contain electrolytes and other substances that closely mimic the body’s ECF. They are used to replace depleted fluids and to promote urine output. Crystalloid solutions are capable of quickly diffusing across membranes, leaving the plasma and entering the interstitial fluid and ICF. It is estimated that two thirds of infused crystalloids will distribute in the interstitial space.

COMPONENTS OF IV FLUIDS: Isotonic, hypotonic, and hypertonic solutions are available for that purpose. Sodium is the most common crystalloid added to solutions. Some crystalloids contain dextrose, a form of glucose, commonly in concentrations of 2.5%, 5%, or 10%. Dextrose is added to provide nutritional value: 1 L of 5% dextrose supplies 170 calories. In addition, water is formed during the metabolism of dextrose, enhancing the rehydration of the patient. When dextrose is infused, it is metabolized, and the solution becomes hypotonic.

EFFECTS OF IV FLUIDS: Infusion of crystalloids will increase total fluid volume in the body, but the compartment that is most expanded depends on the solute in this case, sodium, concentration of the fluid administered. Isotonic crystalloids can expand the circulating intravascular (plasma) fluid volume without causing major fluid shifts between compartments. Isotonic crystalloids such as normal saline are often used to treat fluid loss due to vomiting, diarrhea, or surgical procedures, especially when the blood pressure is low.

Because isotonic crystalloids can rapidly expand circulating blood volume, care must be taken not to cause fluid overload in the patient. Infusion of hypertonic crystalloids expands plasma volume by drawing water away from the cells and tissues.

RELATED;

1.  PLASMA VOLUME EXPANDERS

2.  BODY FLUIDS

3.  ANATOMY AND PHYSIOLOGY

REFERENCES

DATA COLLECTION

 

INTRODUCTION: Data collection is one of the most exciting parts of research. After all the planning, writing, and negotiating that precede it, the researcher is eager for this active part of research. However, before beginning, the researcher must spend time carefully preparing for this endeavor and double-checking each step.

DATA FOR QUANTITATIVE RESEARCH: For quantitative research, preparation begins with clarifying exactly which data will be collected, how they will be collected, and how they will be recorded. The data to be collected are determined by the variables' operational definitions.

THE PROCESS OF DATA COLLECTION: Data collection is the process of selecting subjects and gathering data from them. The actual steps of collecting data are specific to each study and depend on both research design and measurement methods. Data may be collected from subjects by observing, testing, measuring, questioning, recording, or any combination of these methods, either conducted by the research team or retrieved from data sources.

The researcher is actively involved in this process either by collecting data or by supervising data collectors.

RELATED;

1.  Data collection tools

2.  Data analysis

3.  Research methodology

4.  How to write a research proposal

5.  Analysis and presentation of data

REFERENCES

INFECTIVE ENDOCARDITIS

 

INTRODUCTION: Infective endocarditis is a microbial infection of the endothelial surface of the heart. A deformity or injury of the endocardium leads to accumulation on the endocardium of fibrin and platelets involving clot formation. Infectious organisms, usually staphylococci, streptococci, enterococci, pneumococci, or chlamydia invade the clot and endocardial lesion. Other causative microorganisms include fungi such as, Candida, Aspergillus and rickettsiae

RISK FACTORS: Prosthetic heart valves or structural cardiac defects such as, valve disorders, hypertrophic cardiomyopathy

Age: More common in older people, who are more likely to have degenerative or calcific valve lesions, reduced immunologic response to infection, and the metabolic alterations associated with aging.

Intravenous (IV) drug use: There is a high incidence of staphylococcal endocarditis among IV drug users.

Hospitalization: Hospital-acquired endocarditis occurs most often in patients with debilitating disease or indwelling catheters and in those receiving hemodialysis or prolonged IV fluid or antibiotic therapy.

Immunosuppression: Patients taking immunosuppressive medications or corticosteroids are more susceptible to fungal endocarditis.

CLINICAL MANIFESTATIONS: Primary presenting symptoms are fever and a heart murmur: Fever may be intermittent or absent, especially in elderly patients, patients receiving antibiotics or corticosteroids, or those who have heart failure or renal failure. Vague complaints of malaise, anorexia, weight loss, cough, and back and joint pain.

A heart murmur may be absent initially but develops in almost all patients. Small, painful nodules (Osler nodes) may be present in the pads of fingers or toes. Irregular, red or purple, painless, flat macules may be present on the palms, fingers, hands, soles, and toes. Hemorrhages with pale centers (Roth spots) caused by emboli may be observed in the fundi of the eyes. Splinter hemorrhages (ie, reddish brown lines and streaks) may be seen under the fingernails and toenails. Petechiae may appear in the conjunctiva and mucous membranes. Cardiomegaly, heart failure, tachycardia, or splenomegaly may occur.

ASSESSMENT AND DIAGNOSTIC METHODS: A diagnosis of acute infective endocarditis is made when the onset of infection and resulting valvular destruction are rapid, occurring within days to weeks. Blood cultures Doppler or transesophageal echocardiography.

COMPLICATIONS: Complications include heart failure, cerebral vascular complications, valve stenosis or regurgitation, myocardial damage, and mycotic aneurysms.

MEDICAL MANAGEMENT: Objectives of treatment are to eradicate the invading organism through adequate doses of an appropriate antimicrobial agent (continuous IV infusion for 2 to 6 weeks at home). Treatment measures include the following:

1) Isolating causative organism through serial blood cultures. Blood cultures are taken to monitor the course of therapy.

2) Monitoring patient’s temperature for effectiveness of the treatment. After recovery from the infectious process, seriously damaged valves may require debridement or replacement. For example, surgical valve replacement is required if heart failure develops, if patient has more than one serious systemic embolic episode, if infection cannot be controlled or is recurrent, or if infection is caused by a fungus.

REFERENCES;

1. HEART MURMURS

2. HEART FAILURE

3.  ANGINA PECTORIS

REFERENCES

GLYCOLYSIS

 

INTRODUCTION: In the pathway of glycolysis, glucose is split into two 3-carbon pyruvate molecules under aerobic conditions; or lactate under anaerobic conditions, along with production of a small quantity of energy. All the reaction steps take place in the cytoplasm. Pyruvate: Lactate 

SIGNIFICANCE OF THE GLYCOLYSIS PATHWAY:

1) It is the only pathway that is taking place in all the cells of the body.

2) Glycolysis is the only source of energy in erythrocytes.

3) In strenuous exercise, when muscle tissue lacks enough oxygen, anaerobic glycolysis forms the major source of energy for muscles.

4) The glycolytic pathway may be considered as the preliminary step before complete oxidation.

5) The glycolytic pathway provides carbon skeletons for synthesis of non-essential amino acids as well as glycerol part of fat.

6) Most of the reactions of the glycolytic pathway are reversible, which are also used for gluconeogenesis.

GLUCOSE ENTRY INTO CELLS: Glucose transporter-4 (GluT4) transports glucose from the extracellular fluid to muscle cells and adipocytes. This translocase is under the influence of insulin. Insulin  In diabetes mellitus, insulin deficiency hinders the entry of glucose into the peripheral cells. Diabetes Mellitus  But GluT2 is the transporter in liver cells; it is not under the control of insulin.

STEPS OF GLYCOLYTIC PATHWAY

STEP 1 OF GLYCOLYSIS: Glucose is phosphorylated to glucose-6-phosphate. The enzyme is hexokinase (HK), which splits the ATP into ADP, and the Pi is added on to the glucose. The energy released by the hydrolysis of ATP is utilized for the forward reaction. Hexokinase is a key glycolytic enzyme. Hexokinase catalyses a regulatory step in glycolysis that is irreversible. But this irreversibility is circumvented by another enzyme glucose-6-phosphatase. The phosphorylation of glucose traps it within the cells. Once phosphorylated, glucose-6-phosphate is trapped within the cell and has to be metabolized.

STEP 2 OF GLYCOLYSIS: Glucose-6-phosphate is isomerised to fructose-6-phosphate by phosphohexose isomerase. This is readily reversible.

STEP 3 OF GLYCOLYSIS: Fructose-6-phosphate is further phosphorylated to fructose1,6-bisphosphate. The enzyme is phosphofructokinase. PFK is an allosteric, inducible, regulatory enzyme. It is an important key enzyme of this pathway. This is again an activation process, the energy being derived by hydrolysis of yet another molecule of ATP. This irreversible step is the rate limiting reaction in glycolysis. However, during gluconeogenesis, this step is circumvented by fructose-1,6-bisphosphatase. The steps 1,2 and 3 together are called as the preparatory phase.

STEP 4 OF GLYCOLYSIS: The 6 carbon fructose-1,6-bisphosphate is cleaved into two 3 carbon units; one glyceraldehyde-3-phosphate and another molecule of dihydroxyacetone phosphate (DHAP). Since the backward reaction is an aldol condensation, the enzyme is called aldolase. This reaction is reversible.

STEP 4-A OF GLYCOLYSIS: Dihydroxy acetone phosphate is isomerised to glyceraldehyde-3-phosphate by the enzyme phosphotriose isomerase. Thus net result is that glucose is now cleaved into 2 molecules of glyceraldehyde-3-phosphate. The steps 4 and 4-A are together called the splitting phase. Glycerol portion of the neutral fat can enter into glycolytic or gluconeogenic pathways at this point. Similarly for neutral fat synthesis, glycerol is required which can be derived from glucose through DHAP.

STEP 5 OF GLYCOLYSIS: Glyceraldehyde-3-phosphate is dehydrogenated and simultaneously phosphorylated to 1,3-bisphosphoglycerate (1,3-BPG) with the help of NAD+. The enzyme is glyceraldehyde-3-phosphate dehydrogenase. The product contains a high energy bond. This is a reversible reaction.

STEP 6 OF GLYCOLYSIS: The energy of 1,3-BPG is trapped to synthesize one ATP molecule with the help of bisphosphoglycerate kinase. This is an example of substrate level phosphorylation, where energy is trapped directly from the substrate, without the help of the complicated electron transport chain reactions. When energy is trapped by oxidation of reducing equivalents such as NADH, it is called oxidative phosphorylation. Step 6 is reversible.

STEP 7 OF GLYCOLYSIS: 3-phospho glycerate is isomerized to 2-phosphoglycerate by shifting the phosphate group from 3^rd to 2^nd carbon atom. The enzyme is phosphogluco mutase. This is a readily reversible reaction.

STEP 8 OF GLYCOLYSIS: 2-phosphoglycerate is converted to phosphoenol pyruvate by the enzyme enolase. One water molecule is removed. A high energy phosphate bond is produced. The reaction is reversible. Enolase requires Mg++, and by removing magnesium ions, fluoride will irreversibly inhibit this enzyme. Thus, fluoride will stop the whole glycolysis. So when taking blood for sugar estimation, fluoride is added to blood. If not, glucose is metabolized by the blood cells, so that lower blood glucose values are obtained.

STEP 9 OF GLYCOLYSIS: Phosphoenol pyruvate (PEP) is dephosphorylated to pyruvate, by pyruvate kinase. First PEP is made into a transient intermediary of enol pyruvate; which is spontaneously isomerized into keto pyruvate, the stable form of pyruvate. One mole of ATP is generated during this reaction. This is again an example of substrate level phosphorylation. The pyruvate kinase is a key glycolytic enzyme. This step is irreversible.

STEP 10 OF GLYCOLYSIS: In anaerobic condition, pyruvate is reduced to lactate by lactate dehydrogenase (LDH).

RELATED;

1.  GLUCONEOGENESIS  

2.  GLUCAGON  

3.  GLYCOGEN

4.  PYRUVATE  

5.  LACTATE

6.  METABOLISM AND METABOLIC DISORDERS

REFERENCES

SPINAL CORD INJURIES

 

INTRODUCTION: Spinal cord injuries (SCIs) are a major health problem. Most SCIs result from motor vehicle crashes. Other causes include falls, violence especially primarily from gunshot wounds, and recreational sporting activities. Half of the victims are between 16 and 30 years of age; most are males. Another risk factor is substance abuse (alcohol and drugs). There is a high frequency of associated injuries and medical complications. The vertebrae most frequently involved in SCIs are the fifth, sixth, and seventh cervical vertebrae (C5–C7), the 12th thoracic vertebra (T12), and the first lumbar vertebra (L1). These vertebrae are the most susceptible because there is a greater range of mobility in the vertebral column in these areas. 

Damage to the spinal cord ranges from transient concussion (patient recovers fully), to contusion, laceration, and compression of the cord substance (either alone or in combination), to complete transection of the cord (paralysis below the level of injury). Injury can be categorized as primary (usually permanent) or secondary (nerve fibers swell and disintegrate as a result of ischemia, hypoxia, edema, and hemorrhagic lesions). Whereas a primary injury is permanent, a secondary injury may be reversible if treated within 4 to 6 hours of the initial injury. The type of injury refers to the extent of injury to the spinal cord itself. Incomplete spinal cord lesions are classified according to the area of spinal cord damage: central, lateral, anterior, or peripheral. A complete SCI can result in paraplegia (paralysis of the lower body) or tetraplegia (formerly quadriplegia— paralysis of all four extremities).

CLINICAL MANIFESTATIONS: The consequences of SCI depend on the type and level of injury of the cord.

Neurologic Level: The neurologic level refers to the lowest level at which sensory and motor functions are normal. Signs and symptoms include the following: Total sensory and motor paralysis below the neurologic level. Loss of bladder and bowel control (usually with urinary retention and bladder distention). Loss of sweating and vasomotor tone. Marked reduction of BP from loss of peripheral vascular resistance. If conscious, patient reports acute pain in back or neck; patient may speak of fear that the neck or back is broken.

Respiratory Problems: Related to compromised respiratory function; severity depends on level of injury. Acute respiratory failure is the leading cause of death in high cervical cord injury.

ASSESSMENT AND DIAGNOSTIC METHODS: Detailed neurologic examination, x-ray examinations (lateral cervical spine x-rays), computed tomography (CT), magnetic resonance imaging (MRI), and ECG (bradycardia and asystole are common in acute spinal injuries) are common assessment and diagnostic methods.

COMPLICATIONS: Spinal shock, a serious complication of SCI, is a sudden depression of reflex activity in the spinal cord (areflexia) below the level of injury. The muscles innervated by the part of the cord segment situated below the level of the lesion become completely paralyzed and flaccid, and the reflexes are absent. BP and heart rate fall as vital organs are affected. Parts of the body below the level of the cord lesion are paralyzed and without sensation.

EMERGENCY MANAGEMENT: Immediate patient management at the accident scene is crucial. Improper handling can cause further damage and loss of neurologic function. Consider any victim of a motor vehicle crash, a diving or contact sports injury, a fall, or any direct trauma to the head and neck as having an SCI until ruled out. Initial care includes rapid assessment, immobilization, extrication, stabilization or control of life-threatening injuries, and transportation to an appropriate medical facility. Maintain patient in an extended position (not sitting); no body part should be twisted or turned. The standard of care is referral to a regional spinal injury center or trauma center for treatment in first 24 hours.

MEDICAL MANAGEMENT: Acute Phase Goals of management are to prevent further SCI and to observe for symptoms of progressive neurologic deficits. The patient is resuscitated as necessary, and oxygenation and cardiovascular stability are maintained. High-dose corticosteroids (methylprednisolone) may be administered to counteract spinal cord edema. Oxygen is administered to maintain a high arterial PaO2. Extreme care is taken to avoid flexing or extending the neck if endotracheal intubation is necessary. Diaphragm pacing (electrical stimulation of the phrenic nerve) may be considered for patients with high cervical spine injuries. SCI requires immobilization, reduction of dislocations, and stabilization of the vertebral column. The cervical fracture is reduced and the cervical spine aligned with a form of skeletal traction (using skeletal tongs or calipers or the halo-vest technique). Weights are hung freely so as not to interfere with the traction. Early surgery reduces the need for traction. The goals of surgical treatment are to preserve neurologic function by removing pressure from the spinal cord and to provide stability.

MANAGEMENT OF COMPLICATIONS:

Spinal and Neurogenic Shock: Intestinal decompression is used to treat bowel distention and paralytic ileus caused by depression of reflexes. This loss of sympathetic innervation causes a variety of other clinical manifestations, including neurogenic shock signaled by decreased cardiac output, venous pooling in the extremities, and peripheral vasodilation. Patient who does not perspire on paralyzed portion of body requires close observation for early detection of an abrupt onset of fever. Body defenses are maintained and supported until the spinal shock abates and the system has recovered from the traumatic insult (up to 4 months).

RELATED;

1. THE CENTRAL NERVOUS SYSTEM  

2. THE ENTERIC NERVOUS SYSTEM  

3. ACTIVATION OF A NERVE IMPULSE

4.  BACK PAIN

REFERENCES

LACTATE

 

Introduction: During power exercises such as sprinting, when the rate of demand for energy is high, glucose is broken down and oxidized to pyruvate, and lactate is then produced from the pyruvate faster than the body can process it, causing lactate concentrations to rise. The production of lactate is beneficial because it regenerates NAD+ (pyruvate is reduced to lactate while NADH is oxidized to NAD+), which is used up in oxidation of glyceraldehyde 3-phosphate during production of pyruvate from glucose, and this ensures that energy production is maintained and exercise can continue.  

During intense exercise, the respiratory chain cannot keep up with the amount of hydrogen atoms that join to form NADH, and cannot regenerate NAD+ quickly enough. The resulting lactate can be used in these ways: 

(1) Oxidation back to pyruvate by well-oxygenated muscle cells, heart cells, and brain cells. 

(2) Pyruvate is then directly used to fuel the citric acid cycle. 

(3) Conversion to glucose via gluconeogenesis in the liver and release back into circulation via the Cori cycle If blood glucose concentrations are high, the glucose can be used to build up the liver's glycogen stores. 

RELATED.

1.  Glycogen

2.  Insulin

3.  Glycolysis

4.  Biochemistry

DIVISIONS OF THE NERVOUS SYSTEM

INTRODUCTION: The nervous system can also be divided on the basis of its functions, but anatomical divisions and functional divisions are different. The CNS and the PNS both contribute to the same functions, but those functions can be attributed to different regions of the brain (such as the cerebral cortex or the hypothalamus) or to different ganglia in the periphery. The problem with trying to fit functional differences into anatomical divisions is that sometimes the same structure can be part of several functions. For example, the optic nerve carries signals from the retina that are either used for the conscious perception of visual stimuli, which takes place in the cerebral cortex, or for the reflexive responses of smooth muscle tissue that are processed through the hypothalamus. There are two ways to consider how the nervous system is divided functionally. First, the basic functions of the nervous system are sensation, integration, and response. Secondly, control of the body can be somatic or autonomic divisions that are largely defined by the structures that are involved in the response.

There is also a region of the peripheral nervous system that is called the enteric nervous system that is responsible for a specific set of the functions within the realm of autonomic control related to gastrointestinal functions.

BASIC FUNCTIONS: The nervous system is involved in receiving information about the environment around us (sensation) and generating responses to that information (motor responses). The nervous system can be divided into regions that are responsible for sensation (sensory functions) and for the response (motor functions). But there is a third function that needs to be included. Sensory input needs to be integrated with other sensations, as well as with memories, emotional state, or learning (cognition). Some regions of the nervous system are termed integration or association areas. The process of integration combines sensory perceptions and higher cognitive functions such as memories, learning, and emotion to produce a response.

Sensation: The first major function of the nervous system is sensation, receiving information about the environment to gain input about what is happening outside the body (or, sometimes, within the body). The sensory functions of the nervous system register the presence of a change from homeostasis or a particular event in the environment, known as a stimulus. The senses we think of most are the “big five”: taste, smell, touch, sight, and hearing. The stimuli for taste and smell are both chemical substances (molecules, compounds, ions, etc.), touch is physical or mechanical stimuli that interact with the skin, sight is light stimuli, and hearing is the perception of sound, which is a physical stimulus similar to some aspects of touch. There are actually more senses than just those, but that list represents the major senses. Those five are all senses that receive stimuli from the outside world, and of which there is conscious perception. Additional sensory stimuli might be from the internal environment (inside the body), such as the stretch of an organ wall or the concentration of certain ions in the blood. 

Response: The nervous system produces a response on the basis of the stimuli perceived by sensory structures. An obvious response would be the movement of muscles, such as withdrawing a hand from a hot stove, but there are broader uses of the term. The nervous system can cause the contraction of all three types of muscle tissue. For example, skeletal muscle contracts to move the skeleton, cardiac muscle is influenced as heart rate increases during exercise, and smooth muscle contracts as the digestive system moves food along the digestive tract. Responses also include the neural control of glands in the body as well, such as the production and secretion of sweat by the eccrine and merocrine sweat glands found in the skin to lower body temperature. Responses can be divided into those that are voluntary or conscious (contraction of skeletal muscle) and those that are involuntary (contraction of smooth muscles, regulation of cardiac muscle, activation of glands). Voluntary responses are governed by the somatic nervous system and involuntary responses are governed by the autonomic nervous system.

Integration: Stimuli that are received by sensory structures are communicated to the nervous system where that information is processed. This is called integration. Stimuli are compared with, or integrated with, other stimuli, memories of previous stimuli, or the state of a person at a particular time. This leads to the specific response that will be generated. Seeing a baseball pitched to a batter will not automatically cause the batter to swing. The trajectory of the ball and its speed will need to be considered. Maybe the count is three balls and one strike, and the batter wants to let this pitch go by in the hope of getting a walk to first base. Or maybe the batter’s team is so far ahead, it would be fun to just swing away.

RELATED;

1.  ENTERIC NERVOUS SYSTEM  2.  PROPAGATION OF A NERVE IMPULSE

REFERENCES

SPECIAL DIET IN MY COUNTRY

SPECIAL DIET IN MY COUNTRY:  When we talk about nutrition and diet, our emphasis goes to the basic body requirements such as energy or high calories food supplements, proteins, fats, fiber and vitamins.  And although that is our initial and common goal we also tend to face a challenge of nice looking and cheaply available food stuffs that sometimes does not meet our daily nutritional requirements.  There are many diet in my country that are special in their own way and on this page, we are going to look at some of the most commonly available, cheap and nutritious.

1.  The roasted maize:  I don't know whether in many countries maize is available especially those cold countries but here in the tropics this is one of our staple foods.  And although in most case we harvest maize for posho and porridge, roasted maize is also always available especially for travelers.  Our immediate glimpse may focus on the appearance but to be on the nutrition side, maize is very rich in some of most body's immediate requirements as we are going to look at them;.....................

RELATED;

1.  METABOLISM AND HOMEOSTASIS