Surviving Studenthood

How to Get Good Grades in University

If you are in university, this is probably right around the time you feel like hell, with exams, papers and a million readings that you put off, even though you swore this was the year you would keep up. Don’t fear, you are not alone.


This post is a tough-love post: it is for those students who have been cruising through university, and have suddenly realized their grades are not high enough – whether it is for professional school or grad school, for graduation, for your parents, or just for yourself.

1. Stop Skipping Class: I make it a rule never to skip class unless it is an emergency. Sometimes, you have a big midterm or paper due, and you've fallen behind and every minute counts – and then it is an emergency. But skipping because you feel too lazy to walk to class, or because your relaxing day was so wonderful that you can’t seem to muster enough brains to attend, or because the commute is just too damn long – those are not excuses that will increase your grades. It isn't rocket science: class is important; and your perception that missing a class or two is not a big deal is just plain stupid.

2. Adjust your Attitude: Can I confess something to you? The majority of university students go through university with the perception that fun and freedom are as equal in the “university” experience as studying. But in essence – that’s basically it: if you intend to get good grades, or to improve the ones you have, get your head out of you ass and realize that study and fun are not a 50-50 concept. Sorry to disappoint you!

3. Never Hand Something In Late: It is one of the biggest mistakes students can make – you lose marks for absolutely no reason other than you can’t afford a calendar to mark a correct due date.

Get an agenda! And at the beginning of the term, write in all of your important due dates. When you see a week where there four papers due, you don’t  go out clubbing the night before your paper is due and decide to miss class the next day to hand in your paper late. Even if that is an incredibly stupid example (I know people who have done it!), there are still other common mistakes students make. For example: It is not enough to start working on four papers the week before week they are due. Part of having an agenda is that it allows you to look ahead into the future (yup, it’s a crystal ball) to due dates weeks in advance. When you see four papers coming up, or a very heavy week, start a few weeks early so you aren't swamped with work the week or night before.

This also goes with …

4. Get the Readings Done on Time: this one is an obvious one – despite the fact that doing readings in advance will assist you in class and make life easier, when it comes to exam crunch time, you won’t be cursing yourself for leaving it all to the last minute.

5. Talk to the T.A.s: If I could give a person one piece of advice to succeed in university, it would be to talk in advance to the person who marks your work. It is so important – its like guessing what kind of present someone wants as opposed to just asking them!

Always schedule an appointment with your T.A., come prepared with some ideas/questions, and you will find them to be a resource of great help. Consider your meeting with your T.A. a permanent appointment rather than something you can cancel, otherwise it will be easy to change your mind because you couldn't come up with anything to discuss. The purpose of the appointment is to force you to think about the paper in advance.

6. Consider a Study Group: Although planning/putting a study group together can be work, they can be incredibly beneficial. Working with like-minded, hardworking people can help you connect with the readings and lectures better, and can ensure you don’t miss any concepts – or better, learn a new way to approach the concepts – so that everything is clear at the end. If you know someone who can help you in a study group, really use that time effectively: students often comment that they retain more from the study group than memorizing on their own, and that when it comes to discussion/essay questions (rather than multiple choice or short answer), the study group helps to better critically analyze ideas.

7. Use your Weekends More Effectively: Students often let their weekends dwindle away – particularly a day off like Friday or Monday. Your weekend should always be a catch-up time rather than a party time. While you may have commitments you can’t avoid, remember that if your fun time adds up to more than 15% of your weekend time, then you can mentally decrease your paper or exam mark by 25%. I know it sounds harsh (you would think I would say 40% fun time is too much), but it isn't. Unless you are a genius – or even naturally smart and school comes easily for you, expect to work hard if you want 80+ in all your courses.  In a three-day weekend (with Friday or Monday off), I would say an evening off would be fine, but any more than that, and I think it becomes easy to let the whole weekend slip away.

8. Stop Fooling Around: We thought we ought to hammer it home a little more than tip two of getting an attitude face-lift:

STOP FOOLING AROUND!!!

These are NOT the best years of your life, so please, celebrating these years like the next 50 will be a disaster. University is prepping you for life – and doing poorly in school, or being on academic probation/dropping out isn't going to help. If you want to be  treated like a grown-up, you have to act like one. It is hard for people to take you seriously when you spend a lot of time fooling around. When you have a busy week ahead, do not waste your time going on dates or lounging about – put a clamp on your libido, and recognize that your brain should always take precedence over your nether-regions. In the end, a little sacrificed fun time can make up big during crunch-time.
Get started early! Okay, not as early as childhood, but you get our point!

8. Hang Out with the Right Crowd and Learn From Others: Ask yourself – how many of my friends are partying it up, and how many are working hard?  Am I surrounding myself with people I want to be like, or people I have a good time with but who don’t motivate me to study?
It is so fabulous to have friends from all walks of life and I encourage that highly; but when you are in school, you need to be around people who are working hard. It rubs off on you a little easier, and you can learn from others. If you have a friend who seems to be doing well in school, ask them for some tips, and emulate their example. Think of it this way: Studying can be a bit like dieting – it is a little hard to commit to initially, but having a buddy makes it 100 times easier. If you really want to change your ways, it is about making a commitment, and being around others who make it easier, rather than harder, to keep that commitment.

9. Remember it is never too late: Somehow, when people get close to graduating, they kind of give up in frustration. Never give up: learning proper study skills will not only help you this year – still 25% of your university career left! – but it will provide you with skills for graduate school, and life.

Well, that’s some tough love from Surviving Student-hood (it comes from a good place!). We welcome all your other suggestions on helping people do better in school!

Cheers!

25 Year-Old Secondary School Dropout Arrested for Impersonating a Doctor at University of Uyo Teaching Hospital

Has it become so easy for someone to impersonate a doctor for two months without going unnoticed? That is the sad reality of what happened at the University of Uyo Teaching Hospital (UUTH), Akwa-Ibom state.

A 25-year-old man, Usen Effiong, was recently arrested for posing as a medical doctor and consulting for the Teaching Hospital for more than two months. The State Police Command Public Relations Officer,Etim Dickson confirmed the arrest to Punch, adding that Effiong was caught based on intelligence report from the UUTH.

The Chairman, Nigerian Medical Association, Akwa Ibom State branch, Dr. John Udobang denied ever knowing the man saying that he is not a member of the association. He told Punch that he received a call from the Dean of the Faculty of Clinical Sciences, UUTH, Dr. Sunday Udo on the activities of Effiong. When he went to interview the suspect, he found him with stethoscope and sphygmomanometer (blood pressure apparatus).

“Udo told me that they caught someone who has not finished secondary school parading himself as a consultant in the teaching hospital as a medical doctor. We also found some prescriptions and forms that he wanted to fill to become a member of the association of resident doctors.

“Later, when they went to look for him, he was found in the doctor’s consulting room eating. He has confessed that he is not a doctor, and has not finished his school certificate, and has been coming there to consult in the last two months.”

When Punch asked how it was possible for an SS II dropout to be consulting in a teaching hospital, Udobang replied that people used to see him but did not know his intention.

“The Dean whose table he was sitting on used to see him and thought he was a medical student or a newly employed doctor that he has not known. It was after one of the younger doctors saw him and asked the Dean who he was that they started investigating him.”

***
For some people, the action of this young man can be described as criminal, whereas others see him as ambitious and say he should be given a chance to study medicine and prove himself. However, if an unqualified person can impersonate a medical doctor in a teaching hospital for as long as two months, then it sadly exposes the porousness of our medical institutions.

Culled from Bella Naija

INDOMETHACIN: THE RAT POISON, HUMAN NSAID

I for a person seems to ramble a lot naturally, I explain history when allowed to. Hence, this blog has to be about my ramblings. To my readers, I really have been trying not to make the write ups too long but for now it seem to elude positivism.

Once when I was young I took a popular rat poison known as indocide (a yellow capsule) for pain during an ailment treatment, the spelling is according to pronunciation i knew then. It was an opportunity for me then because i have asked my dad why i had to take it and he had explained that humans could take it and not die. In my house, those days we also used it for rats disturbing the household's peace by loosening the capsule pack and pouring the powdered  content on foods like garri or dried fish and placing in corners for the rats to eat and die.

About a decade from the occurrence of the above narrated story, i have learnt about the mechanism of action of  the drug INDOMETHACIN. It is a Non-steroidal Anti-Inflammatory drug (NSAID), with anti-inflammatory, anti-pyre tic, analgesic/ anti-pain and anti-coagulant effects. The anti- coagulant effect is what makes it usable as a rat poison.

Vitamin K is a very important component in blood clotting, its necessary for synthesis of clotting factors VII,IX,X and prothrombin. Indomethacin does kills the rat is by suppressing the growth of Vitamin K in the intestinal tract, where much of it is produced. With the Vitamin K production halted, it is only a matter of days until the rodent's Vitamin K stores are completely depleted. 4-hydroxycoumarin and indandione are also anticoagulants that have effect on rats. These chemicals cause trauma to the blood vessel walls, increasing the risk for damage and internal bleeding. When the rodents begin to bleed internally, there is no Vitamin K available to aid the  clotting process. The rodents die, usually within one to two days, from internal hemorrhaging. 

This is the preferred type of rat bait, as the antidote to ingestion by animals or humans is Vitamin K and i guess this explains why some rats do not die even after eating the poisoned food if they could find themselves foods rich in vitamin K to eat .

And then we have the annoying odour arising from their decay disturbing our peace again till they are either found and disposed off or dried completely if we can't find them. Then happy times again......

And now I would say knowledge is power. Lets search for it. Peace

Mitochondrial Quality Control Researchers define how a gene mutated in Parkinson’s disease may normally function to ensure neuronal health

The VDAC3 mitochondrial pore is ubiquitylated on 3 lysine residues, shown in red, on the cytoplasmic surface on mitocohndria. The membrane protein makes a channel through which molecules can be transported. Ubiquitylation could potentially affect this trafficking. Image courtesy of the Harper Lab.

Cell biologists studying Parkinson’s disease are training their sights on mitochondria, the energy source of the cell, whose activity in neurons appears to go awry in this devastating neurodegenerative illness. A neuron needs its mitochondria to be healthy and mobile, particularly during their continual cycles of fission and fusion in which damaged bits are removed and healthy mitochondria are renewed.

A particular gene that is mutated in early-onset Parkinson's—a subset of the disease that can strike people in their 30s—has opened a window into a mechanism called mitophagy, an important component in this form of cellular housekeeping. When mitochondria are damaged, they must first be identified and then cleared away so they don’t fuse with and poison “good” mitochondria. In mitophagy, an unwanted mitochondrion is engulfed and degraded.

Fundamental biochemical pathway

The gene PARKIN and its regulatory companion PINK1 work together in this process, one that involves multiple proteins on the mitochondrial outer membrane that may ultimately serve as potential targets for treatments in Parkinson’s. PARKIN was discovered a dozen years ago, but only within the last couple of years have scientists pinpointed its role in mitochondrial quality control.

Wade Harper, the Bert and Natalie Vallee Professor of Molecular Pathology, together with his collaborator Steven Gygi, HMS professor of cell biology, led an HMS Department of Cell Biology team that has identified a fundamental biochemical pathway in which PARKIN resculpts the mitochondrial proteome—the full complement of mitochondrial proteins produced—to promote mitophagy. Harper and his colleagues published their results in Nature this week and share a web portal with a wealth of information about the proteins in this pathway.

The pathway that eradicates damaged mitochondria begins with a process called ubiquitylation. Ubiquitin is a small protein that modifies other proteins in many aspects of biology, including the response to damage that ultimately ends in ridding the cell of such waste. Understanding the sites of modification in target proteins is a key step in elucidating the role of ubiquitin in specific pathways, but this has been a technically challenging area of research. The Gygi and Harper labs recently developed a mass spectrometry-based proteomic methodology to identify ubiquitylation sites in target proteins, potentially on a global scale, and in the current study extended this to the PARKIN system.

Resculpting the mitochondrial proteome

“Identifying actual sites of ubiquitylation provides us not only a visual way to look at the structure and mechanisms of how the PARKIN system works, but it also gives you the potential in the future to make reagents that will let you look in tissue of the brain, for example, and determine whether the pathway is on or off,” said Harper.

In defining the near complete repertoire of PARKIN substrates—which they call the PARKIN-dependent ubiquitylome—the researchers reveal how the structure and function of the mitochondrial proteome is resculpted byPARKIN. Indeed, their work identified hundreds of ubiquitylation sites on dozens of proteins.

While this contribution does not have immediate clinical implications, it does serve as a key steppingstone toward a greater understanding of Parkinson’s and perhaps other neurodegenerative diseases involving mitochondrial quality control. This challenging work is necessary before contemplating ways to somehow overcome defects in genes such as PARKIN.

“We want to be able to use the data to understand in more detail howPARKIN is regulated and how it is activated and how it is capable of ubiquitylating a dizzying array of proteins on the mitochondrial surface,” Harper said. “In addition, we also want to try to test the hypothesis that ubiquitylation of specific mitochondrial proteins is critical for mitophagy.”

Dr Ben Carson

Wow, just wow! Dr. Ben Carson — who criticized some of President Obama’s economic policies during his speech at America's National Prayer Breakfast that held today,  — hinted that he might be interested in a 2016 presidential run.

The 62-year-old Carson says he is retiring from surgery within roughly the next three to four months. He said his immediate focus will be on “educating the next generation,” then “once we get that taken care of who knows.”
Carson, raised in poverty, returned to his concerns including the decline of education in America, Washington overspending and the importance of God in American life.
“We continue to spend ourselves into oblivion,” said Carson, adding the country’s younger generations have become “uniformed” and “ignorant.”----very true!

NEUROSURGERY REPORT:Stenting Alters Flow Impingement Zone

Background: Self-expanding intracranial stent-assisted coiling of bifurcation aneurysms has recently been shown to straighten target cerebral vessels, a phenomenon with unknown hemodynamic effect.

Objective: To investigate the impact of angular remodeling in aneurysms treated with single stent-assisted coiling using computational fluid dynamic (CFD) techniques.

Methods: Fourteen patients (7 women, mean age 55) who underwent stent-coiling of 14 wide-necked bifurcation aneurysms were included based on availability of high-resolution three-dimensional rotational angiography. Pre-treatment datasets underwent virtual aneurysm removal to isolate the effect of stenting. Wall shear stress (WSS) and pressure profiles obtained from constant flow input CFD analysis were analyzed for apical hemodynamic changes.

Results: Stenting increased bifurcation angle with significant straightening immediately after treatment and at follow-up (107.3[degrees] vs. 144.9[degrees], P<.0001). The increased stented angle at follow-up led to decreased pressure drop at the bifurcation apex (12.2 vs. 9.9 Pa, P<.003) and migration of the flow impingement zone (FIZ) towards the contralateral non-stented daughter branch by a mean of 1.48+/-0.2 mm. Stent-induced angular remodeling decreased FIZ width (WFIZ) separating peak apical WSS (3.4 vs. 2.5 mm, P<.004). Analysis of FIZ distance (DFIZ) measured from parent vessel centerline showed it to be linearly (r=.58, P<.002) and WFIZ inversely correlated (r=.46, P<.02) to vessel bifurcation angle.

Conclusion: Stent-induced angular remodeling significantly altered bifurcation apex hemodynamics in a favorable direction by blunting apical pressure, and inducing narrowing and migration of the flow impingement zone, a novel response to intracranial stenting which should be added to intimal hyperplasia and flow diversion.

From: Angular Remodeling In Single Stent-Assisted Coiling Displaces and Attenuates The Flow Impingement Zone At The Neck Of Intracranial Bifurcation Aneurysms by Gao et al.

HYDROPS OF LABYRINTH

                                                    MENIERE' DISEASE

ETIOLOGY:The exact cause of the disease is still being investigated and likewise the pathogenesis but known triggers include Viral illness, Autoimmune reactions, Endocrinopathies, Allergies, Stress, Sodium and Water retention, Trauma of Head, Alcohol intoxication, Side effect of drugs e.g ototoxic antibiotic; Aminoglycosides

CLINICS:
 Main Signs: Hearing loss/Deafness,Dizziness/Vertigo,Tinnitus, Nystagmus, Aural Fullness
 Minors: Headache,change in heart activity during attacks, pale skin, cold sweat.

There is always a period of remission and exacerbation. The patient due to aural fullness can feel when the wave of attack is about to start. Attack period ranges from hour to several weeks. Based on this, patient has stages of disease;
First stage---- 1-2hours twice or thrice a year
Second stage--- 2-4hrs once a month
Third stage-----9-12hrs daily

Note that during remission, symptoms are not seen in patient except for Deafness that remains always.
Diagnostics:
Neurological examination
ENT examination;
Tuning fork test
Audiometry(subjective and objective form and this includes impedometry),
Vestibulometry
Electrocochleography (ECOG)
Electronystagmography (ENG) or videonystagmography (VNG)
Head MRI scan
Glycerol Test must be positive

Treatment
There is no known cure for this disease but it can be managed,Treatment is basically symptomatic,
Treat other diseases present in patient
Manage patient with Diuretics, Diet, Lifestyle changes and Physiotherapy.
Note that Labyrinthectomy is indicated in uncontrollable vertigo thou it doesn't cure illness but takes care of vertigo.
Prognosis in every patient can be determined by how well a doctor can manage the symptoms in patient and the course of illness in individual patient.

MOUTH SORES

Different types of sores can appear anywhere in the mouth. Some of the places mouth sores can occur are:
Bottom of the mouth
Inner cheeks
Gums
Lips
Tongue
Causes

Mouth sores may be caused by irritation from:
A sharp or broken tooth or poorly fitting dentures
Biting your cheek, tongue, or lip
Burning your mouth from hot food or drinks
Braces
Chewing tobacco

Cold sores are caused by the herpes simplex virus . They are very contagious. Usually, you will have tenderness, tingling, or burning before the actual sore appears. Cold sores usually begin as blisters and then crust over. The herpes virus can live in your body for years. It only appears as a mouth sore when something triggers it, such as:
Another illness, especially if there is a fever
Hormone changes (such as menstruation)
Stress
Sun exposure

Canker sores are not contagious. They may look like a pale or yellow ulcer with a red outer ring. You may have one, or a group of them. Women seem to get them more than men. The cause of canker sores is not clear. It may be due to:
A weakness in your immune system (for example, from the cold or flu)
Hormone changes
Stress
Lack of certain vitamins and minerals in the diet, including vitamin B12 or folate

Less commonly, mouth sores can be a sign of an illness, tumor, or reaction to a medication. This can include:
Autoimmune disorders (including systemic lupus erythematosus)
Bleeding disorders
Cancer of the mouth
Infections such as hand-foot-mouth disease
Weakened immune system -- for example, if you have AIDS or are taking medication after a transplant

Drugs that may cause mouth sores include aspirin, beta-blockers, chemotherapy medicines, penicillamine, sulfa drugs, and phenytoin.

Home Care

Mouth sores often go away in 10 to 14 days, even if you don't do anything. They sometimes last up to 6 weeks. The following steps can make you feel better:
Avoid hot beverages and foods, spicy and salty foods, and citrus.
Gargle with salt water or cool water.
Eat popsicles. This is helpful if you have a mouth burn.
Take pain relievers like acetaminophen.

For canker sores:

Mix 1 part hydrogen peroxide with 1 part water and apply this mixture to the sores using a cotton swab.
For more severe cases, treatments include fluocinonide gel (Lidex), anti-inflammatory amlexanox paste (Aphthasol), or chlorhexidine gluconate (Peridex) mouthwash.

Over-the-counter medications, such as Orabase, can protect a sore inside the lip and on the gums. Blistex or Campho-Phenique may provide some relief of canker sores and fever blisters, especially if applied when the sore first appears.
To help cold sores or fever blisters, you can also apply ice to the sore.

When to Contact a Medical Professional

Call your doctor if:
The sore begins soon after you start a new medication
You have large white patches on the roof of your mouth or your tongue (this may be thrush or another type of infection)
Your mouth sore lasts longer than 2 weeks
You have a weakened immune system (for example, from HIV or cancer)
You have other symptoms like fever, skin rash, drooling, or difficulty swallowing
What to Expect at Your Office Visit

The doctor or nurse will examine you, and closely check your mouth and tongue. You will be asked questions about your medical history and symptoms.

Treatment may include:
A medicine that numbs the area such as lidocaine to ease pain. (Do not use in children.)
An antiviral medication to treat herpes sores. (However, some experts do not think medicine makes the sores go away sooner.)
Steroid gel that you put on the sore.
A paste that reduces swelling or inflammation (such as Aphthasol).
A special type of mouthwash such as chlorhexidine gluconate (such as Peridex).

Prevention
You may reduce your chance of getting common mouth sores by:
Avoiding very hot foods or beverages
Reducing stress and practicing relaxation techniques like yoga or meditation
Chewing slowly
Using a soft-bristle toothbrush
Visiting your dentist right away if you have a sharp or broken tooth or misfitting dentures

If you seem to get canker sores often, talk to your doctor about taking folate and vitamin B12 to prevent outbreaks.

To prevent cancer of the mouth:
Do not smoke or use tobacco.
Limit alcohol to two drinks per day.
Wear a wide-brimmed hat to shade your lips. Wear a lip balm with SPF 15 at all times.

Free CME Article: Long-term Outcomes of PLIF

Background: Although posterior lumbar interbody fusion (PLIF) is regarded as an effective treatment for spondylolisthesis, few studies have reported comprehensive, long-term outcome data, and none has investigated the incidence of deterioration of outcomes.

Objective: To determine and compare the success rates and long-term stability of outcomes of open PLIF and minimal-access PLIF in the treatment of radicular pain and back pain in patients with spondylolisthesis.

Methods: Forty-three patients were followed for a minimum of 3 years. They completed a Short-Form Health Survey and visual analog scores for back pain and leg pain and underwent lumbar spine radiography. Outcomes were compared with baseline data and 12-month data.

Results: Surgery succeeded in reducing listhesis and increasing disc height, but had little effect on lumbar lordosis or the angulation of the segment treated. At 12 months after surgery, listhesis was reduced, disc height was increased, leg pain was reduced or eliminated, and physical functioning restored. Back pain was less often relieved. These outcomes were largely maintained over the ensuing 2 years. Only 5% to 10% of patients reported deterioration in their relief of pain. Depending on the definition adopted for success, the long-term success rate of PLIF may be as high as 70%.

Conclusion: For the relief of leg pain, the success rates of open PLIF (70%) and minimal-access PLIF (67%) for spondylolisthesis are high and durable in the long-term. PLIF is less often successful in relieving back pain, but the outcomes are maintained. The outcomes of open PLIF and minimal-access PLIF were statistically indistinguishable.

DBS in Lateral Habenular Complex

Background: Deep brain stimulation (DBS) has recently been discussed as a promising treatment option for severe cases of major depression. Experimental data have suggested that the lateral habenular complex (LHb-c) is a central region of depression-related neuronal circuits. Due to its location close to the midline, stereotactic targeting of the LHb-c confronts surgeons with distinct challenges.

Objective: To define the obstacles of DBS surgery for stimulation of the LHb-c and thus establish safe trajectories.

Methods: Stereotactic MRI datasets of 54 hemispheres originating from 27 DBS patients were taken for analysis on a stereotactic planning workstation. After alignment of images according to the ACPC-definition, analyses focused on vessels and enlarged ventricles interfering with trajectories.

Results: As major trajectory obstacles, (1) enlarged ventricles and (2) an interfering superior thalamic vein were found. A standard frontal trajectory (angle >40[degrees] relative to the ACPC in sagittal images) for bilateral stimulation was safely applicable in 48% of patients, whereas a steeper frontal-trajectory (angle <40[degrees] relative to ACPC in sagittal images) for bilateral stimulation was possible in 96%. Taken together, safe bilateral targeting of the LHb-c was possible in 98% of all patients.

Conclusion: Targeting LHb-c is a feasible and safe technique in the majority of patients undergoing surgery for DBS. However, meticulous individual planning to avoid interference with ventricles and thalamus-related veins is mandatory, as an alternative steep frontal entry point has to be considered in about half of the patients.

On Diabetes.

November is Diabetes awareness month and with just few days to its end I decided to write on it. Moreover, it seems to be one of the leading reason for hospital visits.

Diabetes itself means plenty urination(polyuria) and increased thirst(polydipsia). Diabetes could be Mellitus i.e related to insulin or Insipidus related to vasopressin.
The most common one is Diabetes Mellitus. Insulin is a hormone secreted in the pancreas by the beta cells of langerhans. Its secretion is stimulated by glucose in blood when we eat and hence it functions at driving glucose into cells and ensuring its usage in energy production and building up energy stores. As discussed by most recent studies by WHO, it can be classified into 4 based on its causes(Etiological)
1. Insulin Dependent Diabetes mellitus, popularly known as type 1, its know to be of juvenile onset appearing in childhood though few related cases of adult after immune stimulation has been recorded LADA. This form of DM has been related to genetics, chromosome 6 and is known to be aggravated by childhood diseases not well treated like measles, chicken pox, parotitis etc The body generate immune body T cells and B cells against this disease causing microbes but in the process generate autoimmune bodies against the insulin secreting cells in pancreas causing their death hence reduced insulin secretion.
2.NON INSULIN DEPENDENT DM: this is of adult onset thou children are been recorded to having it now. its the types most of our parents have. Its genetically related to changes in chromosome 11 and its aggravated by Obesity(most especially abdominal form of obesity). Life style has a lot to do with this, the food we eat, the drinks we take, lack of physical activities etc. What happens here is that due to excessive fat in our body, we develop resistance to insulin and then Tolerance to Glucose.
3. DM RELATED TO OTHER DISORDERS: This includes; DM associated with endocrinopathies like cushing disease, Addisons etc;genetic defects of Beta cells of pancreas, pathology of exocrine gland of pancreas, drug induced Diabetics e.g unregulated use of Beta-adrenoblockers
4.DM ASSOCIATED WITH PREGNANCY: Due to changes that occurs in woman during pregnancy, she develops resistance to insulin thou its slight in healthy pregnancy and in women who visits antenatal clinics. Hence not all pregnant women have DM thou they are a risk group during pregnancy and post delivery if not well taken care of. 

Prediabetes is an elevated blood glucose level that is not quite high enough to be diagnosed as diabetes, but is higher than normal. Most do not even know they have it. Many people with prediabetes who do not lose weight or do moderate physical activity will develop type 2 diabetes within 3 years.Diabetes can cause serious health complications including heart disease, blindness, kidney failure, and amputations of the foot, toe or leg. Diabetes is the seventh leading cause of death

Symptoms:
frequent urinations
Increased thirst
Increased Appetite
loss of weight over time
Dizziness
sleeping in day and restless at night,visual problem, itching of skin.

Treatment:
its best to Visit a doctor and not do self medication so i will not mention specific drugs.
In DM1: mild form we only regulate patient diet
In severe, we regulate diet and do insulin therapy.
In DM2:mild form-diet
Moderate:Diet+oral hypoglycemic drugs
Severe:Diet+oral hypoglycemic drugs+Insulin
Note that in Severe case of DM2, patient is regressing into type 1 clinical features.

Complications:
Acutes: Ketoacidotic coma, Hyperglycemic coma, Hypoglycemic coma and Lactacidemic coma.

Chronics: Angiopathies, Retinopathy,Cardiomyopaties, Ischemic Heart Disease, Diabetic Foot, Encephalopathy,Respiratory Diseases, Nephropathy etc.

Prevention:

Healthy Diet

• Eat a variety of foods from all the food groups


• Choose foods high in fiber and low in cholesterol and fat (especially saturated fat)


• Eat plenty of fruits and vegetables (at least half your plate should be made up of these foods)


• Choose lean meats


• Choose whole grains over processed foods


• Consume foods in as close to their natural state as possible


• Eat in moderation and exercise portion control

Stay Active

• Lowers blood sugar: 1 minute of exercise can lower your blood glucose level by 1 to 1.5 points


• Lowers blood pressure and cholesterol


• Helps improve weight management


• Lowers your risk for heart disease and stroke


• Helps insulin work more efficiently


• Strengthens your heart, muscles and bones


• Decreases body fat and increases muscle mass


• Improves blood circulation


• Reduces stress and improves self esteem


• May help curb appetite


• Keeps body and joints flexible

Let us note that the reason this is being discussed is not to bring fears into our heart but to enlighten us about the disease and see reasons why we should have healthy lifestyles(reduce that pot belly of yours) and when diagnosed of it, follow your treatments.
                                                                                                                               Adenuga O.A

Questions

Question: 5% Dextrose in Normal Saline is: 

A.Hypotonic 
B.Isotonic
C.Hypertonic
D.A blood Substitute