Contact Us

Use the form on the right to contact us.

You can edit the text in this area, and change where the contact form on the right submits to, by entering edit mode using the modes on the bottom right. 

14893 Northwest Purvis Drive
Portland, OR, 97229
United States

971-208-5909

Reliable source for medical, health and beauty products, medical review articles and business medicine services.

MEDICAL CONTENT ARTICLES (Republishable)

Quality medical content articles that can be republished in full without permission.

Why Older Women Break Their Hip Bones So Easily

Drotumdi O

display.jpg

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Fifty five percent of all Americans aged over 50 years have osteoporosis or thin spongy bone, that is highly susceptible to compression and breakage. One out of every two white women in US will fracture a bone in her lifetime. Although all long bones and vertebral bones are vulnerable, the most common fractures affect the hip bones. About 20% of post-menopausal women who fracture their hip bone die within a year of the fracture, while 20% of these women often have a second fracture one year down the road. 

 

The cost of treatment and nursing home rehabilitation of hip bone fracture patients runs into about one billion dollars a year. Currently about 10 million Americans have mild bone thinning or osteopenia. Another 34 million people have severe bone thinning or osteoporosis. This number is expected to increase in the years ahead with many more US citizens growing older. 

 

 Osteoporosis is mostly attributable to bone thinning usually after the age of 35 years, for various reasons. The normal rate of bone thinning due to age is 0-3% to 0,5% per year. Bone density usually peaks at the age 25 and remains there for another 10 years. Genes (family history), environment, sex, ethnicity, hormones, and medications influence bone density. 

 

 Men tend to have heavier bones than women, even as African Americans tend to have heavier bones than Caucasians and Asian Americans. The short supply of sunshine in North America reduces the availability of Vitamin D, which normally helps the absorption of dietary calcium. 

 

 Women are particularly vulnerable to osteoporosis because of the progressive decrease in the level of estrogen needed to support bone density after the menopausal age of 45 years. Bone thinning is accelerated to 2% - 4% with up 25 % to 30% loss of bone density by age 55. The spongy nature of the bone is produced by normal formation of protein structure (collagen) of the bone without adequate calcification. 

 

 Cigarette smoking, alcohol consumption, low protein and low calcium diets, as well as malabsorption from celiac sprue or biliary cirrhosis can all contribute to low bone density and easy bone fracture in older women. Diseases like hyperthyroidism, anorexia nervosa or vigorous exercises (common among teenagers) can eventually cause amenorrhea (cessation of menses) with secondary bone thinning. 

 

 Stroke and chronic arthritis, which cause immobility, also lead to loss of bone density. Abnormally high level of parathyrioid hormone, which normally maintains the normal level of blood calcium ends up stripping the bones of calcium, with marked reduction in density. High level of parathyroid hormone is often found in some forms of lung cancer as a paraneoplastic syndrome. Long-term use of heparin (blood thinner), phenythoin (anticonvulsant) and prednisolone (steroid) may also lead to loss of bone density. 

 

 Based on the what has been discussed so far it becomes necessary for every woman above 45 years to be aware of the high risk of bone fracture from osteoporosis and seek to be on a physician-prescribed preventive program. This includes X-ray and DEXA scan monitoring (T score of - 2.5 of or higher), adequate moderate outdoor exercises, and preventive medications like Alendronate (Fosamax) and estrogen replacement therapy (ERT).  See more of similar articles and product recommendations. 

Snoring and Obstructive Sleep Apnea

Drotumdi O

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Snoring is a noisy and often embarrassing behavior that deprives the snorer and his/her sleep partner of adequate sleep, causing them to have day time sleepiness and/or fatigue, plus other medical problems including heart attacks, strokes, diabetes, hypertension, etc. 

 

§ It may be an indication of night time breathing obstruction or obstuctve sleep apnea (OSA) 

 

§ 45% of normal adults snore occasionally while 25 % are chronic snorers 

 

§ Men have more problem with snoring than women 

 

§ Snoring is more common in overweight people and tends to worsen with age. 

 

§ It requires the expensive attention of an otolaryngologist or ear, nose and throat specialist 

 

§ A documentation of sleep study is required for health insurance coverage 

 

Causes of Snoring 

 

Obstruction to the free flow of air through the paharyngeal and laryngeal passages at the back of the mouth and nose.Snoring sound is produced when the tongue, upper throat, soft palate and uvula meet, strike each other and vibrate during breathingUnduely long soft palate, uvula or tongue produces fluttering noise in the throat during relaxed breathingMay be caused by enlarged tonsils and adenoids in chilren, or tumors (rarely)May also be caused by excessive relaxation of tongue and throat muscles during sleep, with the tongue falling back and the throat muscles sagging in from the sidesCould be worsened by muscle relaxant drugs including alcohol and sedativStrong vacuum effect needed to breath through a stuffy nose could suck in the side walls of the throat during relaxed sleep causing seasonal snoringNarrowing of one of the nostrils by the deviation of the partitioning nasal septum, may also have the same effect all year roundExcessive tissue in the throat of obese people tends to narrow down their airways 

 

Causes of Obstuctive Sleep Apnea (OSA) 

 

History of repeated episodes (30 –300) of occlusion of the airway for more than ten seconds may occur during deep sleep to produce obstructive sleep apnea.Once the patient startles up as a result of low oxygen supply to the brain, and changes position, the airway reopens and normal breathing resumesThe respiratory center could also momentarily cease firing from the mid brain,  for a few seconds, for different reasons, with resultant sleep apneaWith increased frequency over time, OSA causes disruption of sleep cycle, chronic fatigue, and overworks the heart, which has to beat faster to meet the oxygen demant of the whole body tissues 

 

Diagnosis of Obstructive Sleep Apnea 

 

§ Loud and disturbing snooring calls for a consult with an ear, nose, and throat specialist or otolaryngologist to identify the cause(s) and rule out obstructive sleep apnea 

 

§ Fiberoptic rhinophryngolaryngoscopy is done to examine the upper respiratory tract for possible cause of snoring 

 

§ Sleep study is conducted in sleep labs or at home to document the existence and frequency of sleep apnea, especially for insurance purposes 

 

Treatment of Snooring and OSA 

 

§ Depends on the cause and the level of the airway narrowing or 

 

§ The first step is usually to provide a continuous positive airway pressure (CPAP) machine which supplies minimal air pressure through a nasal caterher to the throat region to maintain a positive pressure, which prevents the airway from closing completely at any time. 

 

§ Where that is no help, uvulopalatopharyngoplasty (UPPP) surgery is done by the otolaryngologist to remove redundant soft palate tisue and widen the airway. 

 

§ The healing process after surgery stiffens the tissues and prevents undue vibrations 

 

§ Repeated thermal ablation procedures using bipolar cautery, laser, and radiofrequency are also employed to surgically burn away obstructive polyps and redundant tisues in the nose and back of the mouth 

 

§ Palate stiffening injections are also given to patients near the uvular to reduce the  vibrations that cause the snoring sound 

 

§ Pillar implants or stiffening rods may also be surgically inserted to reduce the vibrations that cause snoring 

 

§ Genioglossus and hyoid advancement procedure surgically opens the obstructed airway bjy pulling the tongue muscles forward 

 

§ Custom fit oral night guards, that reposition the lower jaw forward, are also being used for certain patients with snoring and/or OSA. This requires an experienced otolaryngologist, dentist, or oral surgeon to fit it safely and acurately 

 

§ Weight loss through athletic lifestyle can improve snoring and OSA without the need for surgery 

 

§ Elevating the bed head four inches is advised 

 

§ Avoiding alcohol and tranquilizers can prevent excessive throat muscle relaation 

 

§ Sleeping on the side rather than the back reduces snoring 

 

§ OTC (over-the-counter) devices approved by FDA have their own claims toward the relief of snoring and OSA. Choosing the best from over 300 approved brands is the main challenge. 

Alcohol Abuse: Fast Facts

Drotumdi O

display.jpg

Otumdi Omekara, MD. MPAHA - Member of Society of Physician Entrepreneurs 

 

Alcohol abuse, also known as alcohol use disorder or alcoholism, is the consumption of alcohol in such a way and to such an extent that it causes distress or harm to individuals and people around them. It makes people incapable of fulfilling their major responsibilities at home, school or work. They drink in dangerous situations like while driving and or operating machinery. Their lives are complicated by alcohol related legal problems like arrests for DUI or physical assaults while intoxicated, or frequent family frictions. 

 

Ethyl alcohol (ethanol) is the main form of alcohol in wines, beer, and liquor, derived from the fermentation of sugars and starches with yeast. 

 

Alcohol affects every organ in the body. It depresses the central nervous system after it is rapidly absorbed through the stomach and small intestines into the blood stream. The liver enzymes metabolize only small amounts of alcohol at a time leaving a high level of alcohol circulating through the whole body most of the time. Thus rapidly consuming large quantities of alcohol overwhelms the liver and exposes body organs to alcoholic toxicity. 

 

According to Dietary Guideline for Americans, moderate drinking means that women should take only 1 drink a day while men take only 2 drinks a day. 

 

All the 50 states in USA agree on 0.08% (80mg/100ml) as the legal blood alcohol limit for adults over 21 to drive motor vehicles. Below this level no amount of alcohol is allowed while driving. Blood alcohol levels (BAC) are checked on the spot with breathalyzers whenever a driver is pulled over for possible DUI. 

 

Alcohol abuse is a treatable chronic disease that prevents the patient from living a productive economy life because of the amount time spent in treatment, recovery and incarceration. 

 

Global alcohol consumption of alcohol in 2005 was 6.13 liters of pure alcohol per person 15 years and older (55% of global population and 3.8% of all global death). Fatal alcohol consumption occurs more among young people. 

 

Alcohol is the 3rd largest risk factor for untimely death, disability and illness worldwide. It is the leading factor in Europe and North America. 

 

People drink because it helps them with socialization, celebration and relaxation. But alcohol overpowers heavy drinkers when the blood alcohol (BAC) level exceeds the normal range of ( ). 

 

It makes them lose count of how many drinks they have had and to drink excessively. 

 

As their blood alcohol levels rise, they go from tipsy to drunk, to stupor to coma and even to death. They also experience memory loss and inability to concentrate. 

 

At the tipsy stage people are disinhibited, talkative, highly sociable, flirtatious and vulnerable to risky behaviors like unprotected sex and violence. 

 

When people get drunk they become drowsy, disoriented, incapable of maintaining balance, weak and slow in both movement and speech. 

 

During the stupor stage the person is semiconscious or delurious, drifting in and out of consciousness. 

 

At the coma stage, the person passes out completely, and unable to respond to painful stimuli. 

 

At death there is no heart, lung or brain activity detectable by a physician. 

 

Alcohol abuse manifests in the following ways: troubled relationships, frequent social frictions, abnormal thoughts and feelings. 

 

The rate at which drinkers progress downhill varies with the rate and type of alcoholic drink, body constitution, body size, time of last meal, age, health status, current medication intake, race, gender, and family history (genes). 

 

Current research studies indicate that heavy drinking or alcohol abuse involves craving sensation created by a complex interaction of genes, hormones and other biochemical substances, inside the body cells. This accounts also for physical and psychological alcohol dependence 

 

Alcohol affects every organ of the body. It is a central nervous system depressant that is rapidly absorbed from the stomach and small intestine into the blood stream. 

 

Alcohol is metabolized in the liver by enzymes; however, the liver can only metabolize a small amount of alcohol at a time, leaving the excess alcohol to circulate throughout the body. The toxic effect of the excess alcohol depends on the amount consumed and the rate of consumption. 

 

This new insight has led to the discovery of drugs other than antabuse, now used to disrupt the Intracellular craving mechanism at different points. The two new drugs are naltrexone and acamprose. 

 

Moderate alcohol consumption has its benefits including protection against coronary heart disease, but the consequences of too much alcohol drinking far outweighs them all. It destroys not only an individual’s physical and social wellbeing, but also that of people close to them and the society at large. 

 

Alcohol abuse causes many serious social and developmental problems, including violence, child neglect and abuse, work absenteeism, family, friends, coworker, and stranger violence and injury. 

 

Driving while intoxicated (DWI) or driving under the influence of alcohol (DUI) causes up to 2.5 million deaths a year worldwide from vehicle and other injurious accidents. It also causes increased violence, suicide attempts, and homicide. 

 

Other health problems attributable to alcohol abuse include alcoholic withdrawal syndrome, liver fibrosis and cirrhosis, fetal alcoholic spectrum disorders, sudden infant death syndrome pancreatitis, hepatitis, fatty liver, dilated cardiomyopathy, cardiac arrhythmias, hypertension, stroke, and cancers of the live (hepatoma), mouth, esophagus, throat, and breast. 

 

Alcohol weakens the immune system after a long period of heavy drinking because it weakens the liver, which produces immunoglobulins. This makes chronic alcoholics vulnerable to HIV/AIDS, tuberculosis, and sexually transmitted diseases. 

 

5,000 people < 21 years die from underage drinking yearly. See more of similar articles andproduct recommendations. 

Living Well With Diabetes Mellitus

Drotumdi O

display.jpg

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

The idea of living with diabetes mellitus may not sound very plausible when one considers the ravaging nature of uncontrolled diabetes. But it has been reported by the American Diabetes Association (ADA) that life style changes alone can reduce the risk of diabetes by up to 91 %. A diabetic patient’s quality of life is not usually significantly altered until the disease gets complicated. 

Neither does diabetes get complicated until it is left uncontrolled. The tricky thing about uncontrolled diabetes is that it shortens life expectancy by up to 13 years; takes the lives of 300,000 Americans yearly (NIH); claims $130 billion from US health care budget yearly (a quarter of Medicare budget). A lot of the cost goes into the treatment and rehabilitation of patients with eye, heart, brain, peripheral nerve fiber, kidney and limb complications of diabetes. 

Currently the United States has a diabetes epidemic, with over 23.1 million Americans having diabetes, and probably another 23.1 million remaining undiagnosed (NIH). Ninety percent (21 million adults) of these diabetics have Type 2, while the rest (10 %) are children with Type 1 diabetes. 

Type 1 diabetics have no insulin production from their pancreas and are therefore insulin dependent. The pancreatic beta cells are commonly destroyed early in life by viral infections or autoimmune diseases. As a result, they easily build up blood glucose levels high enough to put them into ketoacidotic coma if they miss their insulin injections    

Type 2 diabetics either produce insufficient insulin or normal quantity that the body tissues respond poorly to (resistance). This usually happens after age 45 when the aging pancreatic beta cells are no longer able to meet the normal insulin demand of the body. Adults also tend to become less active at this stage, too busy to manage their diets. 

The leading cause of insulin resistance today, in the United States, is obesity among both adults and children. Unfortunately diabetes produces no early dramatic symptoms. It requires a high index of suspicion to start monitoring a patient as a potential diabetic. 

Diabetic screening of the general population starts once any of the criteria laid down by ADA is met. A primary care practitioner is encouraged to become suspicious of any patient who: 

§Has a family history of diabetes 

§Has a body mass index of greater than 25 (obesity) 

§Has an inactive or sedentary lifestyle 

§Has African American, Asian American, Hispanic American, Native American, or Pacific Islander ethnicity 

§Has had diabetes in pregnancy or given birth to a 9lb baby; 

§Has blood pressure of 140/90 mmHg or more 

§Has good cholesterol (HDL) equal to or less than 35mg/dL or bad cholesterol (LDL) equal to or higher than 250 mg/dL 

§Has had a fasting blood glucose (FBG) test result of 100 mg/dL – 125mg/dL 

§Has had a history of vascular problems or has a polycystic ovary syndrome. 

Blood glucose monitoring is a key surveillance factor in the US diabetes epidemic control. ADA recommends that people who are 45 years and above should have their blood glucose checked every three years, while only obese younger people with additional risk factors should be tested every year. Pre-diabetic patients (FBS of 100mg/dL – 125mg/dL) are taught how to test their own blood sugar and blood pressure at home with various brands of electronic glucometers and sphygmomanometers supplied free of charge by their health Medicare through their insurance companies. They are followed up every three months for a laboratory fasting blood glucose (FBG) test and hemoglobin A1C check. Normally the blood glucose level rises after food and drops back to normal after  

The HbA1C test is used to monitor compliance because it documents what the steady plasma glucose level has been over the last 90 – 120 days. The steady plasma glucose level over that period is reflected in the percentage glucose of the population of HbA1C, which has been shown to increase with persistent high level of blood glucose.   

The FBS testing goal is to monitor lifestyle (workout) and dietary habits in such a way as to keep the fasting (pre-breakfast) blood glucose level below 100mg/dL. Only when the FBS rises above 125mg/dL despite active lifestyle and good diet, is oral diabetic medication option considered. 

The goal of HbA1C testing is to keep it at or below 5%. HbA1C levels between 5.7% and 6.4% correspond to the prediabetic stage. From 6.5% and above the patient is considered for oral diabetic medication. 

Oral diabetic medications are generally used at stimulate a weak pancreas, reduce insulin resistance or reduce intestinal absorption of glucose. The choice of oral diabetics pills will depend on the diagnosis. Because some adults are both obese and above 45 years, combination of pills are frequently use to both stimulate the pancreas and combat insulin resistance caused by the obesity. Down the road, some adult diabetics end up depending on insulin injections like young diabetics because the oral drugs have stopped working for them. 

Preventive management of diabetic complications involves 

§Monitoring the blood pressure with PCP supervision to keep it at or below 130/80 

§Keeping bad cholesterol below 400mg/dL with lifestyle changes, diabetic dieting, and prescription medications 

§Monitoring the kidneys for the slightest hint of protein in urine. 

§Monitoring vision, with eye care providers for the earliest signs of diabetic retinopathy 

§Protection of feet against painless injuries due to numbness of extremities. Medicare mostly covers podiatric visits for diabetic patients. 

CONCLUSION: 

Understanding that diabetes hardly gives any warning symptoms until it gets complicated helps every person at risk to appreciate the need to watch his/her blood glucose jealously. Once the complications set in, they tend to show up in virtually every organ of the body. Compliance with all the monitoring schedules just discussed has been shown to make living well with diabetes mellitus a very achievable goal. 

Ear Infections: Types, Causes, Diagnosis, Treatment, Prevention

Drotumdi O

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

The two common types of otitis are otitis externa and otitis media 

Otitis Externa or Swimmer's Ear 

 -Infection of ear lobe, external ear canal, and ear drum 

 - Caused by bacteria and viruses that enter the ear during swimming 

-  Surface cells of the external ear are inflamed, swollen, itchy, and painful to touched 

- Makes kids irritable, cry a lot, and pull frequently on their ears 

- Kids may have fever, runny nose or stuffy nose 

- Adults may have no complaints other than ear irritation and mild ear ache or stuffiness 

- Earache usually controlled with mild analgesics like Tylenol and Ibuprofen 

- Tends to clear spontaneously, but some may need antibiotic ointment prescription by a care provide 

  

Otitis Media or Labrynthitis 

  - May be purulent or exudative 

Purulent otitis media 

- Results from either heavy external ear infections that rupture the eardrum and invade the middle ear 

- Or from the extension of upper respiratory tract infections through the eusthacian tube which connects the oral cavity to the ear 

- Infection affects the eardrum, ossicles, and labrynth 

- Offensive pus drains out of the external ear canal 

- Pus is cultured to determine the right antibiotic treatment 

- Stronger pain pills like vicodin may be needed to control the pain 

Exudative otitis media 

- Causes a sterile fluid to accumulate in the middle ear due to swelling and blockage of the eusthacian tube during an upper respiratory tract infection 

- Complete resolution of recurrent ear infections requires the expertise of an otolaryngologist (ear nose and throat specialist 

DIAGNOSIS 

- Made through focused history taking, and physical exam 

- Otoscope is used to light up the ear canal and middle ear 

- May reveal inflammation, discharge, tympanic membrane rupture, or foreign body 

- Tuning fork is used to test for hearing by bone conduction, where there is the possibility of nerve deafness 

-  Audiometry (hearing evaluation) may be done if there is evidence of poor response to tuning fork test 

 TREATMENT 

-         Spontaneous resolution of ear infection is common once the source of infection is identified and avoided 

-         Some cases of chronic otitis externa and otitis media require antibiotic ointments or drops 

-         Hydrogen peroxide drops have also been used to clean out was and debris from the external ear canal.  

-          ENT specialists also do eusthacian tube irrigation or insert plastic tubes to help keep the eusthacian tube    open 

-         Supportive treatments include pain pills and warm compress 

PREVENTION 

-    Avoiding dirty swimming pools 

-         Wearing ear plugs during swimming 

-         Avoiding ear picking with fingers of unsterile sticks 

-         Reporting ear symptoms early to the health care providers 

display.jpg

The two common types are otitis externa and otitis media 

Otitis Externa or Swimmer's Ear 

 -Infection of ear lobe, external ear canal, and ear drum 

 - Caused by bacteria and viruses that enter the ear during swimming 

-  Surface cells of the external ear are inflamed, swollen, itchy, and painful to touched 

- Makes kids irritable, cry a lot, and pull frequently on their ears 

- Kids may have fever, runny nose or stuffy nose 

- Adults may have no complaints other than ear irritation and mild ear ache or stuffiness 

- Earache usually controlled with mild analgesics like Tylenol and Ibuprofen 

- Tends to clear spontaneously, but some may need antibiotic ointment prescription by a care provide 

  

Otitis Media or Labrynthitis 

  - May be purulent or exudative 

Purulent otitis media 

- Results from either heavy external ear infections that rupture the eardrum and invade the middle ear 

- Or from the extension of upper respiratory tract infections through the eusthacian tube which connects the oral cavity to the ear 

- Infection affects the eardrum, ossicles, and labrynth 

- Offensive pus drains out of the external ear canal 

- Pus is cultured to determine the right antibiotic treatment 

- Stronger pain pills like vicodin may be needed to control the pain 

Exudative otitis media 

- Causes a sterile fluid to accumulate in the middle ear due to swelling and blockage of the eusthacian tube during an upper respiratory tract infection 

- Complete resolution of recurrent ear infections requires the expertise of an otolaryngologist (ear nose and throat specialist 

DIAGNOSIS 

- Made through focused history taking, and physical exam 

- Otoscope is used to light up the ear canal and middle ear 

- May reveal inflammation, discharge, tympanic membrane rupture, or foreign body 

- Tuning fork is used to test for hearing by bone conduction, where there is the possibility of nerve deafness 

-  Audiometry (hearing evaluation) may be done if there is evidence of poor response to tuning fork test 

 TREATMENT 

-         Spontaneous resolution of ear infection is common once the source of infection is identified and avoided 

-         Some cases of chronic otitis externa and otitis media require antibiotic ointments or drops 

-         Hydrogen peroxide drops have also been used to clean out was and debris from the external ear canal.  

-          ENT specialists also do eusthacian tube irrigation or insert plastic tubes to help keep the eusthacian tube    open 

-         Supportive treatments include pain pills and warm compress 

PREVENTION 

-    Avoiding dirty swimming pools 

-         Wearing ear plugs during swimming 

-         Avoiding ear picking with fingers of unsterile sticks 

-         Reporting ear symptoms early to the health care providers 

Complications of Uncontrolled Hypertension

Drotumdi O

display.jpg

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Blood Pressure Ranges 

 Normal – Systolic BP < 120 / Diastolic BP < 80 mmHg 

 Prehypertension – Systolic BP 120 – 139 / Diastolic BP 80 – 89 mmHg 

 Stage 1 Hypertension – Systolic BP 140 – 159 / Diastolic BP 90 – 99 mmHg 

 Stage 2 Hypertension – Systolic BP > 160 / Diastolic BP > 100 mmHg 

 Hypertensive Crisis – Systolic BP > 210 / Diastolic BP > 120 mmHg 

Complications of uncontrolled hypertension affect almost all the major organs of the body, especially when it graduates to hypertensive crisis. 

 Head and Neck 

 - Rupture of cerebral blood vessels (cerebrovascular accidents) usually involving berry aneurysms at the base of the brain 

 - Stroke from bleeding or ischemia (insufficient blood supply) 

 - Aortic Dissection – separation of the innermost and middle layers of the aorta by the influx of blood under high   

pressure, through a tear or ulceration of the endothelial plaque 

 - Papilledema – swelling of the optic disk in the eyes due to raised intracranial pressure, with the potential to cause sudden blindness 

Heart 

 - Heart Attack (Acute Coronary Syndrome) due to the narrowing of the coronary arteries supplying blood to the heart as a consequence of aortic dissection 

 - Congestive Heart Failure (CHF) occurs as the heart becomes unable to pump blood adequately against the very high pressure build up 

 Kidneys 

 - Kidney failure occurs especially with the dissection of abdominal aorta in the area of the exit of the renal artery 

 - Mild leakage of protein (proteinuria) and blood (hematuria) into the urine occurs with mild narrowing of the renal arteries 

 - Acute renal failure occurs with moderate narrowing of the renal arteries 

 - Renal crisis occurs with complete occlusion of the renal arteries 

 - Encephalopathy (brain toxicity) occurs from the accumulation of ammonia and its intermediate products in the blood circulating in the brain 

 Skin and Blood 

 Skin damage (scleroderma) and 

 – Acute anemia due to red blood cell damage with thin the blood vessels (microangiopathic hemolysis) also occurs during hypertensive crisis 

These complications all call for urgent or emergency care at the ER. Regular BP monitoring at home and during provider visits helps to prevent hypertension from reaching the crisis point. ER doctors have effective drugs like nitroprusside; nitroglycerine, labetalol, hydrallazine and phentolamine that combine very well to quickly knock down BP below the crisis point. Take the regular BP medications as instructed is very important to keep it under to control after it has been stabilized. 

Otumdi Omekara, MD., MPAHA

Blood Pressure Ranges 

 Normal – Systolic BP < 120 / Diastolic BP < 80 mmHg 

 Prehypertension – Systolic BP 120 – 139 / Diastolic BP 80 – 89 mmHg 

 Stage 1 Hypertension – Systolic BP 140 – 159 / Diastolic BP 90 – 99 mmHg 

 Stage 2 Hypertension – Systolic BP > 160 / Diastolic BP > 100 mmHg 

 Hypertensive Crisis – Systolic BP > 210 / Diastolic BP > 120 mmHg 

Complications of uncontrolled hypertension affect almost all the major organs of the body, especially when it graduates to hypertensive crisis. 

 Head and Neck 

 - Rupture of cerebral blood vessels (cerebrovascular accidents) usually involving berry aneurysms at the base of the brain 

 - Stroke from bleeding or ischemia (insufficient blood supply) 

 - Aortic Dissection – separation of the innermost and middle layers of the aorta by the influx of blood under high   

pressure, through a tear or ulceration of the endothelial plaque 

 - Papilledema – swelling of the optic disk in the eyes due to raised intracranial pressure, with the potential to cause sudden blindness 

Heart 

 - Heart Attack (Acute Coronary Syndrome) due to the narrowing of the coronary arteries supplying blood to the heart as a consequence of aortic dissection 

 - Congestive Heart Failure (CHF) occurs as the heart becomes unable to pump blood adequately against the very high pressure build up 

 Kidneys 

 - Kidney failure occurs especially with the dissection of abdominal aorta in the area of the exit of the renal artery 

 - Mild leakage of protein (proteinuria) and blood (hematuria) into the urine occurs with mild narrowing of the renal arteries 

 - Acute renal failure occurs with moderate narrowing of the renal arteries 

 - Renal crisis occurs with complete occlusion of the renal arteries 

 - Encephalopathy (brain toxicity) occurs from the accumulation of ammonia and its intermediate products in the blood circulating in the brain 

 Skin and Blood 

 Skin damage (scleroderma) and 

 – Acute anemia due to red blood cell damage with thin the blood vessels (microangiopathic hemolysis) also occurs during hypertensive crisis 

These complications all call for urgent or emergency care at the ER. Regular BP monitoring at home and during provider visits helps to prevent hypertension from reaching the crisis point. ER doctors have effective drugs like nitroprusside; nitroglycerine, labetalol, hydrallazine and phentolamine that combine very well to quickly knock down BP below the crisis point. Take the regular BP medications as instructed is very important to keep it under to control after it has been stabilized. 

Eight Possible Reasons for A Fainting Attack

Drotumdi O

Otumdi Omekara, MD., Member of Society of Physician Entrepreneurs

Syncope or fainting attack is a short-term loss of consciousness and balance, which occurs when the brain temporarily shuts down due to inadequate blood supply. There may be a short spell of seizure and after-faint confusion. The longer the fainting episode and the more convulsive the seizure, the more likely it is an epileptic attack. Having a sense of which it could be in emergency could make the difference between life and death. 

While a cube of sugar may be put under the tongue of a fainted person not having a seizure, no intervention is encouraged in a patient having seizure, other than making sure the person is breathing and the pulse can be felt. Although fainting may be more common among teenagers and seniors, the average person has a 40-50% lifetime chance of having a fainting spell. 

There are at least eight possible reasons why a person may faint. Knowing about these potential causes of fainting or syncope helps us to be pro active in preventing it. It will inform our First Aid and CPR intervention limits in an emergency It will also enhance our telephone reporting to the 911 operator when a person suddenly slumps to the ground. Some patients experience dizziness, palpitations, transient vision or hearing loss, or cold sweats, before they pass out. Quickly loosening neckties or laying down on a couch may abort an at attack at this presyncopal stage. 

Neurogenic Syncope or Fainting of Nervous Origin 

The most frequent reason why people faint is neurogenic syncope caused by the failure of the peripheral nervous system reflex that controls blood pressure. Physicians diagnose about 24 % of syncope as neural in origin. This usually happens in people with marginally low blood volume due to low sodium intake or high sodium loss through diuretics. Under stressful situations like very hot environment, the sympathetic nervous system reflexly dilates the veins to increase sweating and heat loss. 

The dilating of veins suddenly drops the venous return to the heart. The heart responds via the carotid sinus by pumping faster (tachycardia). It is the exaggerated attempt of the vagal parasympathic nervous system to control this tachycardia that slows the heart to the point of under-perfusion of heart muscles. Under-perfused heart then pumps inadequate blood supply to the brain, leading to the fainting experience. Once flat on the ground the patient soon gets increased blood supply to the brain and quickly recovers consciousness in a simple fainting episode. 

Idiopathic Syncope or Fainting of Unknown Origin 

Unfortunately, about another 24 % of fainting attacks end up with unknown diagnosis even after a full work up. Such fainting incidents are managed mainly by supportive treatment. 

Cardiovascular Syncope or Fainting from Circulatory Failure 

About 18 % of fainting attacks fall into this category. It may be due to structural abnormalities in the heart or blood vessels leading to under-perfusion of the heart and brain (ischemia). In other situations it may be due to abnormal heart rhythm (arrhythmia)   

Hypotensive Syncope or Postural Fainting 

About 11 % of fainting attacks are postural in origin. A sudden rise from lying to standing position drops the blood pressure faster the sympathetic nervous reflex can compensate for it. By the time the patient is flat on the ground more blood reaches the brain and he/she soon regains consciousness. 

Metabolic Syncope or High/Low Blood Sugar Fainting 

May be ketoacidotic or hypoglycemic. Fasting or over dosage of diabetic medication may lead to drastically low blood sugar level and fainting attack. Lack of insulin in Type 1 diabetes may lead to very high blood glucose level and secondary high level of ketone bodies (keto acids). This leads to a more serious type of syncope where the patient may lapse into coma if not seen fast enough at the ER. 

Neuropathologic Syncope or Fainting from CNS Disease 

May be due to pressure from tumors or bleeding inside the brain (hematoma) 

Psychiatric Syncope or Fainting from Mental Illness 

Mostly hysteria and anxiety. 

Vasovagal Syncope or Situational Fainting 

Frequently emotional situations (like fear or anxiety) lead to heart racing, which triggers an oversized vagal parasympathetic response, which virtually grinds the heart to a halt. Inadequate blood output from the heart then causes the brain to respond with a fainting incident. 

display.jpg

Syncope or fainting attack is a short-term loss of consciousness and balance, which occurs when the brain temporarily shuts down due to inadequate blood supply. There may be a short spell of seizure and after-faint confusion. The longer the fainting episode and the more convulsive the seizure, the more likely it is an epileptic attack. Having a sense of which it could be in emergency could make the difference between life and death. 

While a cube of sugar may be put under the tongue of a fainted person not having a seizure, no intervention is encouraged in a patient having seizure, other than making sure the person is breathing and the pulse can be felt. Although fainting may be more common among teenagers and seniors, the average person has a 40-50% lifetime chance of having a fainting spell. 

There are at least eight possible reasons why a person may faint. Knowing about these potential causes of fainting or syncope helps us to be pro active in preventing it. It will inform our First Aid and CPR intervention limits in an emergency It will also enhance our telephone reporting to the 911 operator when a person suddenly slumps to the ground. Some patients experience dizziness, palpitations, transient vision or hearing loss, or cold sweats, before they pass out. Quickly loosening neckties or laying down on a couch may abort an at attack at this presyncopal stage. 

Neurogenic Syncope or Fainting of Nervous Origin 

The most frequent reason why people faint is neurogenic syncope caused by the failure of the peripheral nervous system reflex that controls blood pressure. Physicians diagnose about 24 % of syncope as neural in origin. This usually happens in people with marginally low blood volume due to low sodium intake or high sodium loss through diuretics. Under stressful situations like very hot environment, the sympathetic nervous system reflexly dilates the veins to increase sweating and heat loss. 

The dilating of veins suddenly drops the venous return to the heart. The heart responds via the carotid sinus by pumping faster (tachycardia). It is the exaggerated attempt of the vagal parasympathic nervous system to control this tachycardia that slows the heart to the point of under-perfusion of heart muscles. Under-perfused heart then pumps inadequate blood supply to the brain, leading to the fainting experience. Once flat on the ground the patient soon gets increased blood supply to the brain and quickly recovers consciousness in a simple fainting episode. 

Idiopathic Syncope or Fainting of Unknown Origin 

Unfortunately, about another 24 % of fainting attacks end up with unknown diagnosis even after a full work up. Such fainting incidents are managed mainly by supportive treatment. 

Cardiovascular Syncope or Fainting from Circulatory Failure 

About 18 % of fainting attacks fall into this category. It may be due to structural abnormalities in the heart or blood vessels leading to under-perfusion of the heart and brain (ischemia). In other situations it may be due to abnormal heart rhythm (arrhythmia)   

Hypotensive Syncope or Postural Fainting 

About 11 % of fainting attacks are postural in origin. A sudden rise from lying to standing position drops the blood pressure faster the sympathetic nervous reflex can compensate for it. By the time the patient is flat on the ground more blood reaches the brain and he/she soon regains consciousness. 

Metabolic Syncope or High/Low Blood Sugar Fainting 

May be ketoacidotic or hypoglycemic. Fasting or over dosage of diabetic medication may lead to drastically low blood sugar level and fainting attack. Lack of insulin in Type 1 diabetes may lead to very high blood glucose level and secondary high level of ketone bodies (keto acids). This leads to a more serious type of syncope where the patient may lapse into coma if not seen fast enough at the ER. 

Neuropathologic Syncope or Fainting from CNS Disease 

May be due to pressure from tumors or bleeding inside the brain (hematoma) 

Psychiatric Syncope or Fainting from Mental Illness 

Mostly hysteria and anxiety. 

Vasovagal Syncope or Situational Fainting 

Frequently emotional situations (like fear or anxiety) lead to heart racing, which triggers an oversized vagal parasympathetic response, which virtually grinds the heart to a halt. Inadequate blood output from the heart then causes the brain to respond with a fainting incident. 

Signs of Asthma In Kids

Drotumdi O

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Asthma is the most important chronic disease in US children. It accounts for up to 48,% of ER visits and 34% of hospitalizations per year. Seventy five percent of childhood asthma is allergic with onset mostly before the age of five. After obtaining clinical history that is suggestive of acute asthmatic attack, the physician proceeds to physically examine the child for confirmatory signs. 

  It is hard to miss the symptoms and signs of an acute asthmatic attack. The expiratory wheeze is audible without a stethoscope, except when the airflow is almost down to zero. Breathlessness or shortness of breath is noticeable with intercostal recessions on expiration. The sound of coughing is also quite evident. Sputum production may be noticeable in an older child, while infants tend to drool or sound croaky.   

The trapped air in the lungs gives the child's chest a barrel or bloated shape due to increased lung volume. The desperate look and irritability are noticeable. An infant will pause frequently while breastfeeding, with soft and short cries. Poor feeding results from the frequent interruptions. There might be weight loss from poor feeding, rapid breathing,; and labored breathing. There might be flaring of the nasal opening (alae nasi). In very severe asthmatic attacks, with drastic reduction in oxygen content of blood, the patient may turn blue in the face and limbs (blue bloater)  

 If the attack was triggered by infection, the body temperature may be higher than normal. Depending on the type of infection, there might be white spots or whiting coating inside the mouth. The erythrocyte sedimentation rate (ESR) may also be raised because of the infection. A throat swab culture and sensitivity could grow some bacterial. The oxygen saturation test result will also be lower than normal at about 70-85%. Chest shows increased anterior-posterior diameter of the chest due to the increased lung volume. 

 A child who is able to blow into a spirometer for lung function test will record an abnormal Q/V (ventilation perfusion) and FEV1/FVC (Forced Expiratory Volume/Forced Vital Capacity) ratios. The Forced Expiratory Volume in the first minute (FEV1) is measured by having the patient take a normal breath and blow with normal effort into a spirometer for a minute. The forced vital capacity is measured by having the patient take a deep breath and forcefully blow into a spirometer.  

Sorting through these signs to make a diagnosis could be tricky in children who tend to have attacks at night and look well during the day. Such kids are the ones the doctor has to depend a lot on the test results to determine their risk of an imminent flare-up attack that calls for preventive measures. Otherwise there are so many signs and symptoms for the diagnosis of asthma in children that it can hardly be missed. For more of similar articles visit

display.jpg

Asthma is the most important chronic disease in US children. It accounts for up to 48,% of ER visits and 34% of hospitalizations per year. Seventy five percent of childhood asthma is allergic with onset mostly before the age of five. After obtaining clinical history that is suggestive of acute asthmatic attack, the physician proceeds to physically examine the child for confirmatory signs. 

  It is hard to miss the symptoms and signs of an acute asthmatic attack. The expiratory wheeze is audible without a stethoscope, except when the airflow is almost down to zero. Breathlessness or shortness of breath is noticeable with intercostal recessions on expiration. The sound of coughing is also quite evident. Sputum production may be noticeable in an older child, while infants tend to drool or sound croaky.   

The trapped air in the lungs gives the child's chest a barrel or bloated shape due to increased lung volume. The desperate look and irritability are noticeable. An infant will pause frequently while breastfeeding, with soft and short cries. Poor feeding results from the frequent interruptions. There might be weight loss from poor feeding, rapid breathing,; and labored breathing. There might be flaring of the nasal opening (alae nasi). In very severe asthmatic attacks, with drastic reduction in oxygen content of blood, the patient may turn blue in the face and limbs (blue bloater)  

 If the attack was triggered by infection, the body temperature may be higher than normal. Depending on the type of infection, there might be white spots or whiting coating inside the mouth. The erythrocyte sedimentation rate (ESR) may also be raised because of the infection. A throat swab culture and sensitivity could grow some bacterial. The oxygen saturation test result will also be lower than normal at about 70-85%. Chest shows increased anterior-posterior diameter of the chest due to the increased lung volume. 

 A child who is able to blow into a spirometer for lung function test will record an abnormal Q/V (ventilation perfusion) and FEV1/FVC (Forced Expiratory Volume/Forced Vital Capacity) ratios. The Forced Expiratory Volume in the first minute (FEV1) is measured by having the patient take a normal breath and blow with normal effort into a spirometer for a minute. The forced vital capacity is measured by having the patient take a deep breath and forcefully blow into a spirometer.  

Sorting through these signs to make a diagnosis could be tricky in children who tend to have attacks at night and look well during the day. Such kids are the ones the doctor has to depend a lot on the test results to determine their risk of an imminent flare-up attack that calls for preventive measures. Otherwise there are so many signs and symptoms for the diagnosis of asthma in children that it can hardly be missed. For more of similar articles visit

Treatment of Asthma Without Inhaler

Drotumdi O

display.jpg

Otumdi Omekara, MD., MPAHA MD., MPAHA - Member of Society of Physician Entrepreneurs

Once the diagnosis of bronchial asthma has been made, the physician then has to decide on the most appropriate treatment option based on the specific cause(s). There are at least nine treatment options for bronchial asthma without inhaler:1) IV/IM short-acting beta agonist for quick rescue of mild intermittent attacks; 2) IV/IM low-dose synthetic steroids for quick rescue; 3) IV/IM long-acting beta agonists; 4) mast cell stabilizers; 5) anti-leukotriene or IV low dose long-acting steroids for moderate persistent attacks; 6) IV/IM low to moderate dose long-acting steroids and long-acting beta agonists for moderate persistent attacks; 7) IV/IM high dose long acting steroids with long-acting beta agonists for severe persistent attacks; 8) Trigger identification and elimination through behavior therapy and allergic desensitization through immunotherapy; 9) Antibiotic or antifungal or antiviral therapy to control trigger infections. 

 Under certain circumstances, it may not be possible for an asthmatic patient to use an inhaler: for instance in a patient with throat cancer or a semi-conscious patient. The choice of medication route under such conditions will be intravenous (IV), intramuscular (IM) or subcutaneous (SC) injection. The second consideration will be which component of the airway targeted.

Most inhalers used to rescue patients from acute exacerbation of asthma, usually target the constricted bronchial muscles to relax them in a matter of minutes. The third consideration will be the classification of the asthmatic attack, whether it is mild intermittent, mild persistent, moderate persistent or severe persistent. 

 Mild intermittent asthmatic attacks occurring less than twice a week, with less than two night attacks a month, will be treated with IV quick-acting rescuer beta agonist drugs like salmeterol, pirbuterol, or terbutaline. Instead of the usually ipratropium inhaler used to improve the delivery of beta agonist drugs, intravenous anticholinergics like atropine could be administered. IV low dose steroids like hydrocortisone will then complete the quick rescue treatment. 

 Mild persistent asthmatic attacks occurring more than two to six times a week, with less than two night attacks per month, will be treated with IM low dose steroids like prednisolone, or mast cell stabilizers like cromolyn sodium or, anti-leukotrienes like montelukast and zafirlukast. 

 Moderate persistent asthma occurring daily with more than one night attack per week will need low to medium dose IM steroids like prednisolone, plus long acting beta agonist drugs like salmeterol and theophylline 

 For the severe persistent asthma with flares and frequent nighttime symptoms per week, long-acting beta agonist drugs like salmeterol or theophylline is given. IV or IM to keep the bronchi dilated. IV/IM long-acting steroids like prednisolone, to control airway swelling, follow the beta agonist treatment. 

 For the asthma treatment to be effective, the triggers must be identified and avoided through behavior modification. Aspirin or exercise or cold or dust or smoke sensitive asthmatics must avoid those triggers in their homes of work sites. Allergic desensitization through immunotherapy is needed in allergic asthma. Antibiotics or anti-fungal treatments are added if the trigger is infection. 

The Benefits of Adopting An Anti-depressive Mindset

Drotumdi O

  .  &nbsp;

. 

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

The average person in the United States has a one in seven chance of suffering a major depression during his or her lifetime (NIMH). Anybody can come down with mood depression with or without warning at any time. All it takes is a sudden major personal loss of something valuable, be it a spouse, a child, a sibling, a close friend, job, business, or property. About 33 per cent of bereaved people may also be depressed one month after the loss, and up to 15 per cent may remain depressed one year after the loss.

The immediate reaction to such acute loss, disappointment, or traumatic stress is called a normal acute grief reaction. According to Elizabeth Kubler-Ross, stage one of this reaction is denial; stage two is anger; stage three is bargaining; stage four is depression; while stage 5 is acceptance. The most critical stage of acute grief reaction is the depression stage. If one gets stagnated at this stage, a major depression could set in without being noticed. 

The normal adaptive behavior of a bereaved person, for instance, is to be sad, sob at length, lose appetite, lose sleep, and still be willing to talk about the circumstances surrounding the loss of his/her spouse. When the person becomes too preoccupied with guilt feelings about the sad event to move on to the acceptance stage that is the first indication that a major depression might be setting in. But by definition a diagnosis of major depression can only be made after two weeks following the trigger event.

There must be depressed mood or severely diminished interest in or pleasure from previously pleasurable activities. In addition, there has to be at least four out of the following seven symptoms: 1) 5% change in body weight in one month or significant appetite change with weight loss, 2) lack of sleep or excessive sleep, 3) fatigue or loss of energy, 4) Reduced or excessive physical activity, 5) Impaired thinking, concentration, or decision-making, 6) diminished self-esteem with feeling of worthlessness and undue guilt, and 7) repeated thoughts of death and suicide.  

Moderate exercise, supportive relationships, and positive life experiences are all useful in depression as in other illnesses, if only the depressed person can muster the courage to get them started. This is why the proactive anti-depressive lifestyle is preferable. It targets the core symptoms of major depression. It prepares the individual to see that self worth does not have to depend entirely on any single aspect of life. It exposes the person to similar occurrences in that past despite adequate provisions, which takes away the guilt feelings. It enables the person to understand the normal time frame of four to six weeks for normal grief. It also teaches the person to make advance decisions should they find they become grief-stricken. It restores hope by exposing people to survivors of catastrophic events. 

The first benefit of an anti-depressive mindset is that it takes out the surprise element from the sad events that trigger acute grief reactions. In essence it puts a person in the mindset of always being prepared for the unexpected or for the worst. To develop this mindset the person will deliberately flood his/her mind with thoughts of very ugly events that could happen to anyone, and figure out what he/she might do under those circumstances. The natural approach to this “what if” style of thinking is to try to empathize with people close to us when they experience the never expected losses or disappointments that put them into grief. 

 The second benefit of this mindset is that it encourages an individual to talk openly about similar sad events and how they were resolved with grieving people. It might just be a matter of sharing one’s knowledge of some the symptoms of depression manifested by other bereaved people in the past and how quickly they got resolved..  

The third benefit is that it encourages people to research the available resources for treating depression in the community even when they are not depressed.  An easy place to start would be during a visit to a primary care physician for routine medical examination. Where possible, a visit to a psychotherapist just to see exactly what they do for depressed patients and what symptoms would warrant a consult, could be very helpful. This is particularly important because a chronically moody people hardly knows when to talk to a friend, a doctor or a therapist about it.  

The fourth benefit is that it gives people reason to stay socially connected with people who share similar concerns or interest, know them by their first names, and are ready to telephone them or knock on their doors when they go off the radar. It is very easy nowadays to go online or page through church directories and find a group that shares the same concern about how to prepare for unexpected personal losses of life. It might not be totally out of place to attend group meetings for the unemployed, divorced, handicapped, cancer survivors, blind, etc. Seeing how members of these different groups are coping with their circumstances, quietly prepares an individual to face similar situations should they come their way. 

The fifth benefit of ant-depressive mindset is that it gets people interested in the various medications advertised in the electronic and print media for the treatment of depression. The share number of brand name drugs alone begins to suggest that depression is a treatable disease. Once a depressed person comes to term with the fact that depression is a treatable illness, seeking help for it becomes a lot easier. Most cases of major depression that present early for diagnosis and treatment usually get resolved in about six months. See more of similar articles and product recommendations . 

How to Treat Someone Who Complains of Chest Pain

Drotumdi O

 Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

How a patient who complains of chest pain is treated will depend on the diagnosis. To make a diagnosis of chest pain, a health care provider will first get a detailed history of the exact location of the pain, where it radiates to, how long it has been on, how it started, any associated symptoms, any previous episodes and how it was resolved. The clinician will also ask about history of high blood pressure, peripheral vascular disease, stroke, high cholesterol, high triglyceride, pneumonia, pulmonary embolism, pneumothorax, diabetes, kidney disease, stomach ulcer, reflux disease, gall bladder disease, liver disease, pancreatitis, chest injury, family history or heart attack, medication history especially aspirin and nitroglycerine use, etc.

Based on the outcome of this history, the clinician will conduct a general physical examination, followed by a focused chest examination. He/she will inspect, palpate, auscultate (with a stethoscope), for tender spots, swelling, heaves, fractures, abnormal heart sounds, abnormal breath sounds, abdominal tenderness, gall bladder tenderness, kidney and pancreatic tenderness etc. The arms and legs will be examined for signs of stroke, while the eyes are examined for signs of internal bleeding in the head.

Next the patient will be hooked unto the ECG machine for an electrocardiographic recording to rule out ischemic heart disease or heart attack, which is the biggest threat. Blood is also collected for cardiac enzyme and coagulation tests to further double-check for heart attack. If there is a suggestion of heart attack, the patient is quickly admitted into the ICU. Portable chest x-ray is done in ICU to rule out pulmonary embolism, pneumonia and pneumothorax. A CT scan of the head and chest is also done to rule out stroke and pulmonary embolism.

Immediate anticoagulation treatments including aspirin are started if there is any suggestion of vascular obstruction in the heart or brain by a blood clot. Nitroglycerin and selective beta blockers are initiated to increase blood supply to the hear muscles, if there is a high suspicion of heart attack. Meanwhile the patient is put on oxygen mask and electronic heart and lung monitor. The oxygen saturation, blood pressure, pulse, and respiratory rates are monitored for any negative changes. Emergency resuscitation is kept handy for possible cardiac arrest or arrythmias (irregular hear beats). The AED machine is kept handy in case the heart stops beating or starts beating irregularly or too fast.

By this time is would have become fairly clear where the chest pain is coming from. If so the specific treatment is continued according to normal schedules. Otherwise explorations of abdominal diagnostic options are commenced, to rule out gastric ulcer, PUD, esophageal reflux, all bladder disease and pancreatitis. Detailed investigations are usually conducted when the patient is stabilized in ICU and transferred to the ward. The rest of the treatment will then depend on subsequent findings and final diagnosis.

 

Some Insight On What It Is Like To Be A Medical Writer And What Skills Are Needed

Drotumdi O

Otumdi-Omekara_1234667.jpg

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Do you find medicine and healthcare subjects interesting?

· Do you enjoy writing in general, and have a good control of written English up to high school level?

· Then you may find medical writing a challenging but rewarding career.

· A a medical writer you may choose to work as a:

- Health columnist for a newspaper, magazine or website

- Publisher of e-books, news letters, pamphlet, brochures, technical manuals or inserts for healthcare industries

- Healthcare research producer

- Health education material and text book writer

- Medical textbook writer and publisher

- Medical Review book writer and publisher

- A medical education website editor and content provider

The list can go on and on.

· As a medical technical writer, you may choose to go free lance or accept an employment position in healthcare organizations

· The freelance option is for those who have some savings to depend on while growing their clientele. Otherwise the startup period could be very stressful financially.

· The information to be put in writing is usually in the form of medical manuscripts from individuals or research organizations in a disorganized manner.

· The information will need to be organized and formatted to meet the standards of various journal or magazine publishing companies.

· An experienced medical writer will be familiar with formats of big organizations like the American Medical Journal.

· When attending interviews a medical writer would need to present a portfolio of properly formatted writings, whether published or unpublished, in hard copy or electronic copy.

· A medical writer must double check content information with the author, and verify spellings and punctuations with quality word processing software, since there is almost zero tolerance for typos or misinformation in medical writing

· Over time a non-medical medical copy writer may take courses in basic medical sciences to qualify them to write original articles or books in hard copy or online

· How much a medical writer makes annually depends on level of education, experience, output quality, and the organization he/she works for. The pharmaceutical companies tend to pay more and, of course, are most demanding.

Medical writers can earn from as low as $35, 000 per year to as high as 80, 000 per year depending of the above factors

· A freelance medical writer may need only high school education and healthcare work experience.

· But employers tend to prefer medical writers who have college degrees in medical writing, technical writing, basic medical sciences, or English language.

· There are many universities and community colleges now offering courses geared toward medical writing. For more information visit http://www.amwa.org

For more information visit: http://www.amwa.org



Article Source: http://EzineArticles.com/7067152

Ebola: Fast Facts

Drotumdi O

 Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

The current Ebola hemorrhagic fever outbreak has been described as the largest in history and the first of its kind in West Africa. The disease is related to but distinct from Lasa fever which had an outbreak in Nigeria in th 1980s. Four types affecting human beings include: Ebola Zaire, Ebola Sudan, Ebola Ivory Cost and Ebola Bundibugyo.

Ebola hemorrhagic fever affects both animals (primates like monkeys) and human beings and can be transmitted between the two species. Transmission is mainly through body fluids entering broken skins or mucosa membranes. Ebola virus causes severe damages to the major organs of the body and often causes blood clotting failure with massive internal bleeding; hence the name hemorrhagic fever. It is a deadly disease without intensive supportive treatment.

The current FDA approved antiviral drugs are ineffective against Ebola virus, hence the death rate from Ebola infection is up to 95%. Researchers have noticed a continuous change in the genetic make up of Ebola virus between 2014 and 2024, as it switches human hosts. The current outbreak has been traced to an initial animal to human transmission in Central Africa, with human to human spread to West Africa.

As of October 14, 2014, over 2470 people have been infected and over 1300 people have been killed by Ebola virus in West Africa. These numbers are said to be increasing exponentially. Only one death has been reported in Dallas Texas in the US, of a Liberian male who contracted the disease before leaving for US. One of the nurses who attended to the dead patient has just been diagnosed with Ebola infection, is not in critical condition.

Failure of personal protective equipment (PPE) protocol has been suggested, and US healthcare workers are getting actively prepared to handle potential outbreaks in their institutions. All healthcare workers presented with patients with high fever must ask about their travel history and instantly commence universal precautionary measures.

The National Institute of Health (NIH) has warned the US Congress about possible Ebola epidemic and even pandemic without aggressive national and international Ebola infection preventive measures. Some legislators are calling for restriction of inbound flights from Liberia, Sierra Leone, or Guinea. However, the US Congress is yet to have a debate on that call.

The US Congress has approved mandatory screening of all passengers from West Africa for high fever and other symptoms at the international airports. All travellers entering the US with symptoms of Ebola infection must be observed in isolation for a specified period before they can enter the country.

If Ebola symptoms presented after visitors have made contact with US residents, their contacts must also be traced and observed in isolation, The homes and surroundings of their hosts are also actively disinfected by specially equipped CDC crew. The same precaution was taken for the first US patient recently diagnosed with Ebola hemorrhagic fever in Texas. Contact with potential Ebola patients must be avoided without adequate personal protective wears.

A $50 Billion dollar public health aid package for the affected countries has also been approved by US congress, along with over 1000 military personnel to help with Ebola epidemic containment efforts. An Ebola Response Team has also been established in the US by the Center for Disease Prevention (CDC) to step in immediately the diagnosis of the Ebola is confirmed in any part the country. The team is to help with patient management expertise, provision and supervision of proper use of personal protective equipment (PPE), transportation, environmental disinfection, and more.

New vaccine testing on US Ebola patients brought back from West Africa is providing modest hope of arresting the speed of Ebola infection. Ebola virus is not airborne, so there is no need for panic among unexposed individuals, who have made no direct contacts with infected patients. Ebola virus produces symptoms after up to 21 days, when and only when it becomes infectious

The symptoms of Ebola hemorrhagic fever include: fever of up to 103°F, flu-like symptoms, stomach upset, general body ache, muscle weakness, loss of appetite, diarrhea, nausea, vomiting, malaise, and mild headache, skin rashes, sore throat, and gastrointestinal bleeding. In severe cases coma and death may follow hypotensive shock.

These symptoms are produced by viral invasion of the blood, liver, kidneys, and other vital organs, including the central nervous system. Toxic pyrogens disrupt the hypothalamic thermoregulatory system, allowing the body temperature to rise up to 103°F. Severe damage to the liver cuts off production of clotting factors leading to generalized bleeding disorder.

In general, epithelial cells lining the skin and mucous membranes normally release interferon - alpha (IFN-alpha) from CD4 T lymphocytes and immunoglobulin-M (IgM) from CD8 B- lymphocytes immediately invading viruses are detected. IFN-alpha activates natural killer (NK) cells which destroy the viruses. About 24 hours later activated CD4 T-Helper lymphocytes switch immunoglobulin production from IgM to IgA which protects secretory surfaces from bacterial invasion. When the viral load overwhelms this natural defense mechanism, symptoms of the disease begin to manifest. Vaccine development is aimed at stimulating increased production of natural killer cells specifically targeted at Ebola virus genome.

From what is happening in West Africa, the World Health Organization (WHO) has warned that without aggressive preventive measures and logistic supports, there might soon be up to 10,000 new Ebola hemorrhagic fever patients daily. The US president has also called on those nations who have some resources to offer to step up to the plate and send aid packages to Sierra Leone, Liberia and Guinea.

http://www.nih.gov

 

Breast Cancer Cure Research - Some Promising Breakthroughs (I)

Drotumdi O

 Otumdi Omekara, MD., MPAHA Member of Society of Physician Entrepreneurs

Otumdi Omekara, MD., MPAHA Member of Society of Physician Entrepreneurs

A lot of research has been conducted and continues to be conducted into finding a cure for breast cancer. The various clinical research efforts have focused on various factors that improve the chances of a cure. How to detect the disease as early as possible is still getting a lot attention among researchers. Screening for early cases has gone beyond regular breast-exam and mammography to magnetic resonance imaging (MRI) and blood circulating tumor cell (CTC) count.

Diagnostic techniques have gone beyond total excision lymph node biopsy to sentinel lymph node biopsy, microwave breast tissue density measurement, and oncotype DX genomic testing. Risk factor identification has gone beyond age, gender and hormone sensitivity to intracellular receptor proteins and specific breast cancer genes like BRCA1 and BRCA2.

Similar strides have also been made in the treatment modalities. The broad treatment options have expanded beyond surgical excision, radiotherapy and chemotherapy to include biotherapy, and genetic engineering of T-lymphocytes. Breast cancer surgery now starts with a minimally invasive surgery to excise little breast tissue and one or two sentinel axillary lymph nodes. A radical surgery to remove the breast(s) and dissect all axillary lymph nodes is now only indicated by a high risk rating or a lymph node biopsy test suggesting disseminated disease.

Radiotherapy has advanced from non-selective irradiation of both cancerous and non-cancerous tissues to selectively focused radiation delivery techniques including radioactive breast tissue implants. Chemotherapy has also gone beyond non-selective cytotoxic (cancer-killing) drugs to highly tissue/cell specific cytotoxic drugs..Such tissue specific cytotoxic drugs (ADCs) are now tagged onto monoclonal antibodies to the proteins expressed on the cancer cells via stable linkers. The ADCs are then engulfed by endocytosis into the cancer cell lysosomes, where they are discharged to destroy the cells.

Biotherapy now targets the biochemical pathways that lead to the overexpression of the various cancer tissue growth factors to inhibit them, or induce the expression of genes that suppress the growth of cancer cells. It is also targeting energy supply pathways to disrupt them. Genetic engineering is currently being used to redirect T-lymphocytes that have the natural ability to destroy viruses toward cancer cells with encoded instructions to destroy them from the inside.

Excess Human Epidermal Growth Factor Receptor 2 protein (HER2) has been found in up to 30% of breast cancer patients, thereby making it a major risk factor and a negative survival indicator. It has been understood that ER (Estrogen Receptor) and PR (Progesterone Receptor), which tend to be increased along with HER2, are not as reliable as the latter for risk estimation. HER2 status measurement has become mandatory for proper diagnosis and treatment planning. (continued in Part II).



Article Source: http://EzineArticles.com/7178656

Breast Cancer Cure Research - Some Promising Breakthroughs (II)

Drotumdi O

 Otumdi Omekar, MD., MPAHA- Member of Society of Physician Entrepreneurs

Otumdi Omekar, MD., MPAHA- Member of Society of Physician Entrepreneurs

Genetic engineering is currently being used to direct the natural ability of some T-lymphocytes to destroy viruses toward the destruction of breast cancer cells. The drug CX 5461 has been shown to block ribosome biogenesis and protein production. Excess Human Epidermal Growth Factor Receptor 2 protein (HER2) has been found in up to 30% of breast cancer patients, thereby making it a major risk factor and a negative survival indicator. It has been understood that ER (Estrogen Receptor) and PR (Progesterone Receptor), which tend to be increased along with HER2, are not as reliable as the latter for risk estimation. HER2 status measurement has become mandatory for proper diagnosis and treatment planning.

Women who have positive for HER2 protein have also been found to have a lot of female hormone receptors that make them very sensitive to estrogen and progesterone. These hormone sensitive breast tumors have been found to have the tendency to be the lobular type. Breast tumors that are not hormone-sensitive are known to have a greater tendency to spread, and therefore prove more difficult to treat. Tumors that test negative for HER2, ER and PR, have been identified and designated 'triple negative'.

HER2-negative tumors have been shown to be mostly ductal carcinomas and very hard to treat. It has been understood that only the 15% to 20% of breast malignancies caught in their very early (carcinoma-in-situ) stage prior to spreading to lymph nodes can be surgically eradicated. Ductal carcinoma-in-situ (DCIS) is now known to be the precursor (preceding stage) for invasive carcinoma. Lobular carcinoma-in-situ (LCIS), on the other hand, is now known to be just an indicator of high risk for breast cancer development.

Tamoxifen, an aromatase inhibitor (AI) that blocks the conversion of other hormones to estrogen has been successfully used to limit their growth. Researchers in London have shown that the drug AT 13148 can block multiple breast cancer targets - HER2 positive and PIK3CA-mutated BT474 receptors. Researchers at Cinergy Health in New York have shown that the drug poly adenosine diphosphate ribose polymerase (PARP) enzyme inhibitors can shrink BRCA gene mutation positive tumors. The drug CX 5461 has also been shown to block ribosomal biogenesis and protein synthesis in cancer cells. The drug herceptin (trastuzumab) has been successfully used to inhibit the overproduction of HER2 in some patients.

Given this rapid explosion of the understanding of how these tumors develop, the various possible intervention targets, and potential drug treatment options, there is good reason to look forward to an imminent final breakthrough in the search for a cure for breast cancer. (See Part I)

 

Why Older Women Break Their Hip Bones So Easily

Drotumdi O

 Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Fifty five percent of all Americans aged over 50 years have osteoporosis or thin spongy bone, that is highly susceptible to compression and breakage. One out of every two white women in US will fracture a bone in her lifetime. Although all long bones and vertebral bones are vulnerable, the most common fractures affect the hip bones. About 20% of post-menopausal women who fracture their hip bone die within a year of the fracture, while 20% of these women often have a second fracture one year down the road. The cost of treatment and nursing home rehabilitation of hip bone fracture patients runs into about one billion dollars a year. Currently about 10 million Americans have mild bone thinning or osteopenia. Another 34 million people have severe bone thinning or osteoporosis. This number is expected to increase in the years ahead with many more US citizens growing older.

Osteoporosis is mostly attributable to bone thinning usually after the age of 35 years, for various reasons. The normal rate of bone thinning due to age is 0-3% to 0,5% per year. Bone density usually peaks at the age 25 and remains there for another 10 years. Genes (family history), environment, sex, ethnicity, hormones, and medications influence bone density. Men tend to have heavier bones than women, even as African Americans tend to have heavier bones than Caucasians and Asian Americans. The short supply of sunshine in North America reduces the availability of Vitamin D, which normally helps the absorption of dietary calcium.

Women are particularly vulnerable to osteoporosis because of the progressive decrease in the level of estrogen needed to support bone density after the menopausal age of 45 years. Bone thinning is accelerated to 2% - 4% with up 25 % to 30% loss of bone density by age 55. The spongy nature of the bone is produced by normal formation of protein structure (collagen) of the bone without adequate calcification. Cigarette smoking, alcohol consumption, low protein and low calcium diets, as well as malabsorption from celiac sprue or biliary cirrhosis can all contribute to low bone density and easy bone fracture in older women.

Diseases like hyperthyroidism, anorexia nervosa or vigorous exercises (common among teenagers) can eventually cause amenorrhea (cessation of menses) with secondary bone thinning. Stroke and chronic arthritis, which cause immobility, also lead to loss of bone density. Abnormally high level of parathyrioid hormone, which normally maintains the normal level of blood calcium ends up stripping the bones of calcium, with marked reduction in density. High level of parathyroid hormone is often found in some forms of lung cancer as a paraneoplastic syndrome. Long-term use of heparin (blood thinner), phenythoin (anticonvulsant) and prednisolone (steroid) may also lead to loss of bone density.

Based on the what has been discussed so far it becomes necessary for every woman above 45 years to be aware of the high risk of bone fracture from osteoporosis and seek to be on a physician-prescribed preventive program. This includes X-ray and DEXA scan monitoring (T score of - 2.5 of or higher), adequate moderate outdoor exercises, and preventive medications like Alendronate (Fosamax) and estrogen replacement therapy (ERT).

 

Autism Spectrum Diseases - The Importance of Early Diagnosis - II

Drotumdi O

 Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

When neutral proteins are produced, mild ASD will occur due to inadequate production of synaptic adhesion proteins (neuroligin, neurexin, MDGA1 and MDGA2) needed for normal mood, speech and behavior. When a toxic protein results it would destroy the target sites, and impaIr their functions.

On rare occasions, a mutant synaptic adhesion protein may have an enhancing protein may lead to a super-functioning ASD patient. Synaptic protein abnormalities have been associate with autism and schizophrenia. In order to easily recognize an abnormal pattern of child development, one needs to have a sense of what is normal.

After having two normal kids a mom might get a sense of what is normal in child development. But a new mom will need help knowing what to expect. She needs to know that at birth, a newborn baby will have a grabbing and reaching behavior or the startle reflex. The newborn is also able to initiate facial grimace, as well as cry and cling for attachment.

As early as 1 week a newborn can distinguish mom's smell from dad's smell. A normal newborn, in the first couple of months is attracted to bright, colorful, moving objects, and can distinguish voice sound from ordinary noise. Prior to the 8th week, the baby exhibits reflex (endogenous) smile. But by week 8, the baby responds to faces with a smile (exogenous or social smile). By week 12, the smile becomes selective for familiar faces only (preferential social smile). The newborn quickly learns to draw attention to personal needs by crying aloud.

The loud cry usually builds up from unhappy face to grunting to sobbing to cry outburst with tear stream. As the child grows older he/she learns to kick off bed covers in protest and roll into ready to crawl position with head lifted up and eyes scanning for parents. In general the manifestations of autism are related to the child's tendency to be disinterested in the environment, to be inflexible with habits and mannerisms, and to be emotionally numb. Two early sign of inflexibility often overlooked in a newborn are the selective feeding on only one breast and selective sleeping in only one position.

The autistic newborn may also only fall asleep when the room is pitch dark or clutching a specific part of his/her body. Some may insist on having their thumb in their mouth before they can fall asleep. One of the earliest obvious suggestions that something may be wrong is the absence social smile between three to four months after birth.

There may also be absence of eye contacts or tracking eye movements. It becomes more obvious that something is wrong between ages 6 and 12, when a child fails to develop normal emotional, speech and play patterns, and makes only repetitive sounds and hand movements.

Synaptic failures between primary cortical sensory areas (visual, auditory, and somatosennsory) and association cortex, prevents learning and memory formation that occurs through the association of particular emotions with specific stimuli, place and objects. Normally, the smiley face of a mom breastfeeding her baby stimulates increased dopamine release in the pleasure center (nucleus accumbens), and causes the baby to return a smile whenever a physiologic need is met.

The pleasure of social interaction by itself may directly create a positive memory in a normal child through the hippocampus without nuerotransmitter surge in nucleus accombens. The script recorded in the hypocampus is played over and over by the autistic kid for every emotional situation, until there occurs a strong intrusive override by way of teaching.

This accounts for the repetitive and non-interactive, domineering style of communication exhibited by autistic individuals. A negative emotion creates a diminished desire for the stimulus, by reducing the level of dopamine, which normally causes a craving for the stimulus. This association of negative emotion with withdrawal occurs in the amygdala, the limbic nucleus for harm avoidance.

Dopamine reduction is produced by a surge of serotonin into the synapses, which creates the feeling of satisfaction and switches off the stimulus. Two other neurotransmitters, mGluR2 and mGluR3, inhibit the opening of dopamine receptors, thereby further reducing its craving effect and increasing the harm avoidance response. The craving response and harm avoidance response are modulated by the ventromedial prefrontal cortical association area, which is the center for problem solving reward with a strong kink to the limbic system.

 

Dr. Otumdi Omekara is a preventive/business medicine specialist and medical publisher with over two decades of clinical practice experience and over a decade of provider management experience. His passion for patient education drives his medical content article writing and publishing. He was a health educator at Oregon DHS Center for Disease Control from 2001 to 2002. Prior to that he volunteered at NE Portland Neighborhood Clinic as a health educator from 1997 to 2002. Since 2002 he has been the Medical Publisher at Drotumdio Health Publications (dHp). He can be reached at PO Box 91221 Portland Oregon 97291, drotumdi.o@health-pub.com or 9712085909

Autism Spectrum Diseases - The Importance of Early Diagnosis - I

Drotumdi O

Otumdi-Omekara_1234667.jpg

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

The ability of parents to suspect that their baby may have autism is very critical to early diagnosis and intervention. This article is aimed at getting parents to the point where they are able to ask: Is this autism or what? How early this question is answered in a child's life, goes a long way to determine whether he/she will live a dependent or independent life. A high index of suspicion is so important because having had previous normal children does not exclude the possibility of having an autistic baby.

The risk of having autism is highest (90%) for a concordant twin of a known autistic kid. Other siblings have only 35% risk of being diagnosed with autism. Autism usually presents enough symptoms and signs for accurate diagnosis by the age of two. As such many federal and state government programs for supporting autistic children require that it is diagnosed before his/her second birth day for them to qualify.

In response to the growth of autism as a source of disability in the US, Congress passed the Children's Health Act in 2000, mandating several activities that included the establishment of a new autism research network. This legislation led to the birth of five NIH institutes charged with the responsibility of researching into the causes, diagnosis, early detection, prevention and treatment of autism.

Yet a CDC autism survey in 2009 showed that 1 in 110 US kids was at risk of developing autism, with boys being four to five times more likely to be affected than girls. A significant number of high-functioning autistic kids diagnosed in 2000 are now in their early twenties and need vocational employments as people with liability. There are many federal, state and county programs currently available to assist higher functioning autistic adults with independent living, job procurement, community inclusion, speech therapy and mental health care.

Since 2000 a lot has been learned about autism neurobiology, diagnosis, intervention genetics, and services. The number of autism support resources have also grown dramatically. One key knowledge that has emerged from the various research efforts is that autism is a broad spectrum disorder including several members of a group of disorder known as pervasive developmental disorders (PDDs).

Autism is therefore presently classified in the Diagnostic and Statistical Manual of Mental Disorders, 4th Edition. (DSMV--IV-TR) as Autism Spectrum Disorder (ASD). The DSMV-IV describes ASD as a group of five pervasive brain. disorders (AD, AS, PDD-NOS, RD, and PCDD) which variably impair a child's ability to communicate, socialize, behave normally. and reason at age-appropriate levels. AD is the classic autism disorder. AS is Asperger's Syndrome. PDD-NOS is Pervasive Developmental disorders Not Otherwise Specified. RS IS Rett Syndrome while CDD is Childhood Disintegrative Disorder.

The classic ASD is a neuro-psychiatric developmental disorder affecting the brain in such a way that an individual's communication, socialization, behavioral, cognitive (reasoning) abilities are compromised to various extents. It is the extent to which these adaptive skills are compromised that differentiates one PDD from the other. It also accounts for the spectral nature of autism. In severe ASD the IQ is substantially reduced adding the fourth component, cognitive (reasoning) impairment to the picture.

This same compromise accounts for the highly variable levels of disability observed among individuals diagnosed with ASD. Some autism patients are so minimally affected as in Rett disorder that they live independently without supervision. Others are so severely affected, as in classic ASD, that they need 24/7 residential care, as well as assistance with activities of daily living (ADL).

The rest of the PDDs then fit in at various levels between these two extremes. How ASD selectively targets and alters the areas of the brain responsible for emotions, speech, behavior and reasoning is still being actively researched. These target areas include the limbic system (amygdala and nucleus accombens), and the ventromedial prefrontal cortex and the frontal lobe.

The understanding of how these areas have been genetically altered by other disorders affecting them, coupled with observations in traumatic or surgical lobotomy, have both provided some insight into the possible risk factors for autism. What is known so far is that ASD is triggered by multiple and random gene alterations (frame shift mutation or gene duplication, or deletion), on chromosomes 15 and 16. Gene deletion or duplication leads to a frame shift mutation, which in turn leads to the production of a neutral protein, a destructive protein, or an enhancing protein in the target areas of the brain

 

Dr. Otumdi Omekara is a preventive/business medicine specialist and medical publisher with over two decades of clinical practice experience and over a decade of provider management experience. His passion for patient education drives his medical content article writing and publishing. He was a health educator at Oregon DHS Center for Disease Control from 2001 to 2002. Prior to that he volunteered at NE Portland Neighborhood Clinic as a health educator from 1997 to 2002. Since 2002 he has been the Medical Publisher at Drotumdio Health Publications (dHp). He can be reached at PO Box 91221 Portland Oregon 97291, drotumdi.o@health-pub.com or 9712085909

Antioxidants, Acids, Alkali and Cancer

Drotumdi O

 Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

In my previous articles on cancer, I did not discuss the role of acids, bases and antioxidants in detail. But with the current hype about the miraculous nature of basic water, antioxidant foods and drugs, I feel compelled to step in and set the records straight with currently available medical literature.

The efficacy of acids, bases and antioxidants in cancer therapy is not a myth. It has biochemical basis informed by modern research (SS Kim et al, 2004; Ian F. Robey & Lance A. Nesbit, 2013). The apparent controversy surrounding this subject emanates from poor coordination of research findings.

I have read articles (Bradley A. Web et al, 2011; Shi Q. et al, 2001; Silver M. et al, PubMed 2011) supporting systemic alkalosis or systemic hyperacidosis as the dominant toxic factor in cancer development. I have also watched video presentations claiming that cancer development is just a natural cellular adaptation to toxic environment, which is corrected by normalizing the environment.

These claims are to say the least, unbalanced truths. By the end of this discussion it would have become obvious that there is no basis for undue generalizations in the management of cancer. There still remains the need for expert judgement in formulating a cancer treatment protocol.

BEFORE CANCER

First, let me state that the human body will literally rust away like a nail left under the rain over time without inbuilt natural protective mechanisms. To prevent rust or oxidation, most macromolecules essential for human existence are shielded from molecular oxygen or oxygen equivalents with hydrogen molecules (reduction). Oxygen equivalents are those compounds that remove these protective hydrogen molecules from other compounds.

They are also called oxidizing agents. Compounds that restore these hydrogen molecules are called reducing agents. The two most important organic reducing agents in human body are glutathione and ubiquinone, while the two most important oxidizing agents are molecular oxygen and free oxygen radicals.

APOPTOSIS AND GROWTH SUPPRESSOR GENES

The human body cells are normally continuously moving from resting phase, to growth phase and then multiplication phase. This continuous state of growth and multiplication means that any organ can potentially grow to any size, depending on its natural growth rate. By inference all human beings may also grow into giants. It even suggests immortality of human beings.

Thankfully, every cell has an inbuilt apoptotic clock that ensures that it dies after a specified number of days, making room for incoming cells. Thus red blood cells, for instance, are recycled every 120 days. The size and shape of the cells of individual organs are equally limited prior to their date of apoptosis, by growth suppressor genes (notably p53, AP1, NF-kB) located in the nucleus.

Anything that hinders the functions of apoptosis and growth suppressor genes would obviously be expected to unleash uncontrolled growth and multiplication of cells in any organ of the body. This rapid growth of disorganized and poorly differentiated cells is called cancer.

All anti-growth suppression and anti-apoptosis agents are called carcinogens. They may be chemicals, radiations, biochemical molecules, acids, bases, free radicals, heat, cold, etc. But they all exert their effect by in activating apoptosis gene or growth suppressor gene. They accomplish this by corrupting the gene coding system in such a way that the codes are wrong (missense) or mean nothing (nonsense).

The code is corrupted due to the insertion of the wrong amino acid code into a gene sequence or the excision of the right amino acid code from the sequence. Consequently the t-RNA misreads or miss-senses the expression of the right apoptosis or growth suppressor protein.

TOXINS, FREE RADICALS AND CARCINOGENS

Toxins are basically those compounds whose activities will directly or indirectly lead to human rust and death by causing catabolic or destructive oxidative reactions in body tissues. The high powered toxic tissue oxidizing agents are called free radicals (ROS and RNS), which are basically free ionized oxygen or Nitrogen atoms (O2- and N2- )

When a toxin causes a gene altering damage in the nuclear region of a cell (oxidative nuclear damage) it is then known as a carcinogen. As such not all toxins are carcinogen. Aflatoxin (from mold) is not only toxic to liver cells, but ultimately causes liver cancer, making it a carcinogen.

The detoxification process mainly converts lipid soluble toxins into excretable water soluble glucuronides in three steps. In step one the toxins are aggregated and isolated in the specific organs that neutralize them.

Then glucuronic acid is attached to them in the presence of glutathione which the protective hydrogen molecules. (Note that in fighting oxidants hydrogen (non-ionized) carried by reduced NADPH is a friend, while in acid-base balance ionized hydrogen is the enemy).

Free radicals can also contribute to cancer development by inducing genetic mutation through oxidative nuclear damage, or suppress cancer growth by promoting apoptosis. Step three is the excretion of the toxins.

ANTIOXIDANTS

Compounds use to replenish hydrogen molecules in glutathione and other endogenous reductase enzymes are called antioxidants. A lot of these reducing agents occur naturally in fruits and vegetables. Others are available as drug extracts from plants and animals.

Individual antioxidants target different steps of the detox process. This is why balanced nutrition by itself goes a long way to keep our bodies toxin free. The air we breathe, the food we eat, the water we drink, and the environments we live in are all full of toxins, including heavy metals. To survive as human beings, an extensive detoxification mechanism has to exist.

Every body tissue has detox ability, but the liver, gut, and lymphoid tissues and kidneys play the dominant role. Thus most toxins are trapped, neutralized and excreted through feces, urine or bile. Stagnation or obstruction of flow in any of these three organs, generally leads to a toxic state.

Stressors and nutritional insufficiencies that weaken the immune system also contribute to toxic states allowing micro-organisms to multiply and generate additional toxic substances that must be removed.

Successful detoxification requires a lot of energy, which comes from glucose metabolism. Biochemical energy is not measured in Joules, but in ATPs (Adenosine Triphosphate). The metabolic process for converting glucose to ATP is called glycolsis.

During aerobic glycolysis one molecule of glucose combines with two molecules of ADP3- (Adenosine Diphosphate) and two ionic phosphoric acid molecules to yield two ionic ATP4- molecules and two lactate molecules. The ionic ATP4- molecule gives up one Hydrogen proton (H+) to yield one molecule of ionic ADP3-, which is reused in glycolysis.

Under anaerobic (low oxygen) conditions, ATP is generated differently. One molecule, each, of ADP3- and ionic phosphoric acid accumulated from aerobic glycolysis recombine without glucose to form one molecule of ATP4+ and one hydroxyl molecule. Two hydrogen protons combine with two bicarbonates to end up as carbonic acid inside body cells.

TOXIC ACIDOSIS

Glycolsis can be aerobic when it consumes molecular oxygen, or anaerobic when it consumes oxidizing agents. Both the detox reactions and glycolsis are driven or catalyzed by enzymes, which depend on the availability of specific micro-molecules, proteins, amino acids and vitamins as cofactors for their functions.

By the time enough ATP is generated to keep the body toxin safe, enough carbonic acid hydration of respiratory carbon dioxide (CO2) has accumulated to keep the inside of every cell perpetually acidic. In a highly toxic state, which includes rapid proliferation of cells, this intracellular acid builds up exponentially beyond survivable limits.

Cancer cells are known to rapidly outgrow their blood supplies and go into severe hypoxic states. This is why the cancer cell nucleus has to rapidly increase the expression of sodium driven proton extruding proteins and enzyme proteins through nuclear sensing of sharp rise in HIF.

Thus, by default, the Intracellular fluid (ECF) of every cell is acidic (low pH) while that of the extracellular fluid (ECF) is alkaline (high pH). It is important to note at this point that while intracellular fluids exist in compartments inside the cells, extracellular fluids coalesce to form a pool in which all body cells submerged.

This ECF pool is represented by intercellular fluid, lymph, blood, and glandular secretions, all of which feed into the circulatory system of the body. ECF acid or base build up in any part of the body is ultimately dissipated into the circulatory system, which centrally maintains a mildly basic pH of 7.20 -7.40.

In addition to mobilizing ammonium and bicarbonate ions the central buffer system has the ability to move chloride ions in and out cells (chloride shift) to maintain acid-base balance.

MEMBRANE SENSORS AND TRANSPORTERS

To keep intracellular acidity below lethal level, the inner surface of the cell membrane has acid sensors and transporters that detect abnormal rise in intracellular acidity and trigger increased extrusion of hydrogen and retention of alkaline bicarbonate ions.

This trigger is mediated by the rise in the blood level of hypoxia induced factors (HIF) and probably acidosis induced factors (AIF). On detecting this rise in HIF, the nucleus temporarily increases the expression of Na-driven proton transport proteins and histidine rich basic proteins.

The ammonium radicals on the amino acids of these basic proteins (especially histidine) serve as physiologic buffers for organic acids.

"Protonation and de-protonation has been experimentally shown to change protein structure and thus, alter protein-protein binding affinity, change protein stability, modify protein function, and alter subcellular localization (Schonichen et al., 2013b).

Evolutionarily, histidines must confer some selective advantage for cancers, as 15% of the 2000 identified somatic mutations in cancer involve histidine substitutions, with Arg-to-His being the most frequent (Kan et al., 2010)".

The nucleus also temporarily steps up the expression of important enzyme proteins that catalyze the buffer reactions, namely mono-carboxylate, carbonic anhydrase, and aminotransferase enzymes.

In a similar manner the external surface of the cell also has alkaline sensors made up of G-protein coupled surface receptors, which also communicate with the nucleus to increase or decrease the expression of relevant proteins and enzymes. As tissue hypoxia decreases, the level of HIF decreases along with nuclear expression of proton extrusion proteins and enzymes.

Failure of this return to normalcy has been observed as one of the hallmarks of early cancer. What started out as a normal adaptive change becomes persistent because of irreversible genetic modifications that triggered it.

CELLULAR SURFACE ACID/BASE REVERSAL

The central physiological buffer system has a maximum capacity to neutralize up to 30 micromoles of acid/gram tissue/min in systemic acidosis or 5-10 micromoles of base in alkalosis.

Beyond these levels, normal body cells are unable to continue their buffer functions because the enzymes are deactivated. At this point there is a reversal of the normal acid-base distribution on either side of the cell membrane, which is lethal to normal issues. In some critical situations, chloride ions are shifted massively into all body cells (chloride shift) to urgently dilute the extracellular acidity.

But the gastric cells have the natural ability to survive in the presence of high extracellular acidity (HCl at pH of 6.6). How they manage this high extracellular acidity then becomes very important in understanding how cancer cells survive high extracellular acidity with normal intracellular acidity for their survival and proliferation. Some cancer cells are known to have accumulated genetic adaptations that enable them to survive extreme pH conditions (carbonic acid at pH of 6.6).

Gastric cells are shielded from concentrated HCl secreted into the stomach mainly by structural barriers (thick basement membrane, thick mucosal layer and thick mucous layer). There are no natural inhibitors of hydrogen potassium ATPase enzyme that catalyzes the final phase of acid excretion.

In severe cases of Peptic Ulcer Disease (PUD), Gastro-esophageal reflux (GERD), or Zollinger-Ellison Syndrome, when this natural barrier is ulcerated by concentrated HCl, some gastric lining cells undergo goblet intestinal metaplasia (transformation into ectopic intestinal epithelium in the stomach) to secrete neutralizing alkaline fluids into the stomach.

While there is no natural attempt to control the hydrogen potassium ATPase enzymes, pharmacological intervention with proton pump inhibitors (PPIs) like omeprazole has been successful in reducing gastric secretion in severe cases of chronic gastric hyperacidity.

Similarly some esophageal epithelial cells undergo gastric metaplasia to become gastric cells in the face of chronic exposure to reflux gastric acid (Barrett's Esophagus). Acquisition of this missing ability to control hydrogen potassium ATPase and sodium driven proton extrusion by monocarboxylate enzyme appear to be critical to the survival of cancer cells

IN EARLY CANCER

It is important to note that the natural response to extracellular hyperacidity in the GIT depends on the stage and localization of the acidity. Both goblet metaplasia and gastric metaplasia have been recognized as precancerous lesions (carcinoma in situs). At the early stage of Barret esophagus, the response is only structural to prevent cell wall damage.

But when the barrier has failed in the stomach, the response is alkaline secretion. A person on preventive alkaline water will be helping to neutralize the added hypoxic acidity of early cancer in Barret's Esophagus and chronic PUD, but not in any way preventing the occurrence of cancer itself, since proton extrusion in cancer is irreversible.

Any cancer caught at the in situ stage is usually best treated with surgical excision and radiotherapy, rather than alkaline water.The question then is: "Why did prophylactic alkaline water not prevent the metaplasia?"

The answer to that is that while oral alkali intake may cap out at micromoles of alkali per gram tissue, cancer proton extrusion acid build up ranges in nanomoles per gram tissue (a thousand times more). Also intracellular hypoxia and hyperacidity are not the only risk factors for cancer.

Radiations are known to be commonly responsible for skin cancers, even as HPV is known to be responsible for cervical cancer. Prophylactic alkalosis has not been reported to prevent any of them. Sticking to the hype that alkaline water is the best way to prevent and even cure cancer, puts people at risk of missing early opportunities to truly cure cancer.

Alkaline water intake will help the body maximize the physiological adaptive response acidosis. Unfortunately, even at maximum physiological capacity, extracellular buffers are no match for cancer intracellular proton extruders.

As the well adapted cancer cells grow and multiply freely their neighboring non-cancerous cells are rapidly destroyed by ECF hyperacidity creating more space for them to occupy. Thus cancer invasiveness has been shown to correlate with the degree of acid-base reversal across the cancer cell membrane.

At the advanced stage of cancer with ECF acidity readings in nanomols compared to orally boosted alkalinity readings in micromoles, buffer therapy has been shown to be resisted by cancer cells. One such reported example is the inefficacy of a basic drug doxorubicin used in the treatment of Leukemias and lymphomas.

Going by what has been discussed so far, it is obvious that externally sourced acids and alkali cannot be safely loaded to outweigh tumor generated levels in ECF and ICF. It is also understandable that no single pH balancing agent, can be used to treat both acid sensing and alkaline sensing cancers.

Preventive or prophylactic intake of acidic or alkaline liquids or foods remain relevant only within the physiological buffering range, when adaptive changes are still reversible. Unfortunately at that point the tumor generated acidity would have risen to resistant levels. Preventive alkaline water intake in a person with undiagnosed acid sensing cancer is not likely to retard the growth of the tumor.

Similarly preventive intake of alkaline water in a patient with undiagnosed alkaline sensing cancer will encourage it to grow and establish faster. Patients receiving treatment for emesis gravid arum (vomiting in pregnancy) for instance, cannot be on preventive alkaline regimens in the face of systemic alkalosis from heavy loss of gastric acid through vomiting.

However, it is possible that some people are unable to fully optimize the natural buffer system, due to genetic predisposition or problems related to amino acid metabolism. In such situations, preventive acid or base intake supplements the patients effort to achieve maximum physiological buffering. This can easily account for some of the spectacular results observed in some patients whose cancers were caught early.

In conclusion, the management of cancer remains complicated. When there is a strong family history or occupational predisposition for cancer, cancer screening needs to be done early to search for risk factors and genetic markers.

Where there are suggestions of cancer predisposition, full blood tests, scans, biopsies, endocrinological tests, and radiological test should be done by a primary care provider and reviewed by a team of experts in radiology, hematology, pathology, oncology surgical oncology, gastroenterology, and international medicine.

References:

Ian F. Robey and Lance A. Nesbit, Investigating Mechanisms of Alkalinization for Reducing Primary Breast Tumor Invasion

Bradley A. Webb, Michael Chimenti, Matthew P. Jacobson & Diane L. Barber, Dysregulated pH: a perfect storm for cancer progression

Silvia M. Titan1, Otávio C.E. Gebara2, Silvia H.V. Callas2, Ana O. Hoff3, Paulo M. Hoff2 and P.C.A. Galvão2, Case report: a rare cause of metabolic alkalosis, 2011

SS Kim, HW Yang, HG Kang, HH Lee, HC Lee, DS Ko... - Fertility and sterility, Quantitative assessment of ischemic tissue damage in ovarian cortical tissue with or without antioxidant (ascorbic acid) treatment, 2004 - Elsevier

M Valko, CJ Rhodes, J Moncol, MM Izakovic... - Chemico-biological... , Free radicals, metals and antioxidants in oxidative stress-induced cancer, 2006 - Elsevier

Rofstad EK, Mathiesen B, Kindem K, Galappathi K. Acidic extracellular pH promotes experimental metastasis of human melanoma cells in athymic nude mice. Cancer Res. 2006;66(13):6699-6707. doi: 10.1158/0008-5472.CAN-06-0983.

Gillies R. J. (2002). In vivo molecular imaging. J. Cell Biochem. Suppl. 39, 231-238 10.1002/jcb.10450 (monocarboxylate transporters and Na-driven proton extrusion)

Shi Q, Le X, Wang B, Abbruzzese JL, Xiong Q, He Y, Xie K. Regulation of vascular endothelial growth factor expression by acidosis in human cancer cells. Oncogene. 2001;20(28):3751-3756. doi: 10.1038/sj.onc.1204500.

Gallagher F. A., Kettunen M. I., Day S. E., Hu D. E., Ardenkjaer-Larsen J. H., Zandt R., et al. (2008). Magnetic resonance imaging of pH in vivo using hyperpolarized 13C-labelled bicarbonate. Nature 45

Gatenby R. A., Gillies R. J. (2004). Why do cancers have high aerobic glycolysis? Nat. Rev. Cancer 4, 891-899 10.1038/nrc1478 (Pasteur Effect)

Otumdi Omekara is a physician web publisher of health and fitness articles that keep consumers well informed. They also help webmasters speed up their website traffic, as satisfied readers keep returning for more articles. He can be reached at 971-208-5909, drotumdi.o@health-pub.com, or [https://www.health-pub.com].

 

 

Outdoor Treatment for SAD Time Blues

Drotumdi O

 Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Otumdi Omekara, MD., MPAHA - Member of Society of Physician Entrepreneurs

Sad feelings come and go following bad news, disappointments, financial losses, rejections, health failures, job losses, relationship failures, etc. But when we get SAD during the fall and winter months, we are diagnosed with seasonal affective disorder or SAD Time Blues. This is one of the six recognized types of clinical depression, differing mainly in its timing. It has been associated with the sudden switch from longer summer days to shorter fall and winter days in temperate regions of the world.

Day light entering the eyes helps the hypothalamus in the brain to maintain the normal sleep - wake cycle or circadian rhythm. The light stimulates the pituitary, and pineal glands to release hormones that stimulate the ascending reticulated activating system (ARAS) to keep us awake. The same light normally suppresses the release of serotonin from the enterochromaffine cells of the raffle nuclei of the brain. Thus with sudden drop of light supply during the fall and winter months, the blood level of serotonin rises dramatically causing increased sleepiness, tiredness, irritability and ultimately depression. Severe depression may lead to suicidal thoughts and suicide attempts, which also generally increase during the winter months.

Like other major depressions, SAD may present with, sadness and irritability, loss of interest in previously exciting activities, feeling of hopelessness, social isolation, excessive sleep, increased appetite and weight gain. The diagnosis is mostly clinical and therapeutic. Hormonal assays are mainly used to confirm the diagnosis and track clinical progress. With or without treatment, seasonal affective disorders tend to improve by the onset of spring season. This is what differentiates it from the other five forms of major depression.

Treatment modalities include, light therapy, cognitive therapy and antidepressants (when severe). Light therapy substitutes 10,000 Lux light for day light for the short fall in normal day light (Danilenko K. V.V et al). Cognitive therapy helps patients to actively substitute optimism for hopelessness, social involvement for social withdrawal, and thoughts of living for suicidal thoughts (Melrose Sherri, 2015). Both light therapy and cognitive therapy have been shown to be effective in the treatment of SAD (Rohan, K. J. et all, 2015). But patients treated with cognitive therapy have been also been shown to have lower recurrence rate in subsequent seasons because they have thought through their conditions and adopted positive interpretations (Sitnikov L. et al, 2013).

Social integration or outdoor treatment has the advantage of combining light therapy and cognitive therapy. 'Outdoor' here is relative to a patient's seclusion environment. Since most social environments like the malls tend to be well lit up, the SAD patient gets supplemental light while socializing. The outdoor patient also sees how other people are coping with shorter days and finds hope for making it through another winter. Seeing less privileged people in the community actively striving to survive also helps the SAD patient to switch from death wish to life wish. Volunteering in social recreational activities away from their homes may, therefore, be the easiest way for patients to take advantage of the outdoor Treatment for SAD.

References:

Danilenko, K. V., and I. A. Ivanova. "Dawn simulation Vs. bright light in seasonal affective disorder: Treatment effects and subjective preference." Journal of affective disorders 180 (2015): 87-89.

Melrose, Sherri. "Seasonal affective disorder: an overview of assessment and treatment approaches." Depression research and treatment 2015 (2015).

Rohan, K. J., et al. "Randomized Trial of Cognitive-Behavioral Therapy Versus Light Therapy for Seasonal Affective Disorder: Acute Outcomes." The American journal of psychiatry (2015): appiajp, 201514101293.

Sitnikov L, Rohan K. J, Evans M, Mahon J. N, Nillni Y. I."Winter depression recurrence one year after cognitive-behavioral therapy, light therapy, or combination treatment." Behav Res Ther. 2013 Dec;51(12):872-81. doi: 10.1016/j.brat.2013.09.010. Epub 2013 Oct 17. PMID: 24211338

Dr. Otumdi Omekara is preventive medicine specialist and medical publisher based in Portland Oregon. He publishes health & Fitness articles for consumer information and webmaster republication to boost traffic on their websites. He also features selected well priced medical products. He can be reached at PO Box 91221, Portland OR 97291, drotumdi.o@health-pub.com, or 971-208-5909.