Strengthening the Reporting of OBservational studies in Epidemiology

STROBE is weird abbreviation for STrengthening the Reporting of Observational studies in Epidemiology. 

What is This?

It is 22 items check list, that should be present in a article reporting on three main study design of observational analytical epidemiology

1. Cohort 

1. Case control 

1. Cross-Sectional 

It is kind of guidance for Dummies to know how to report the observational studies.  

It is developed 

• To assist the authors when reporting the observational analytical studies 

• To  support the journal editors and reviewers for considering the publication of article 

• To help readers when critically evaluating the article. 

It has 22 items, just like a checklist to produce a good report . 

• Title 1 is related to title and abstract of report/article.

• Titles 2-3 are related to Introduction.

• Titles 4-12 are related to Methods.

• Titles 13--17 are related to results.

• Titles 18-21 are regarding discussion.

• Title 22 is related to other information like funding etc 

Here is STROBE checklist... Click on Download to Download .
Source: www.strobe-statement.org and WHO. 

Non- medical studnets and self medication .. .... Strange

Yesss .... Self-medication.. I don't think so that u are quite familiar with the term self-medication.
Here let me explain for you .
Self Medication: According to WHO, Self-medication is the selection and use of medicines by individuals to treat self-recognised illnesses or symptoms. Its the part of Self care..

Of course, Every body is conscious about his / her health. and if some thing "WRONG" happens to his/ her health, That person is going to take some serious actions against that "WRONG" thing.
For example, If some one's eyes are red, itchy and burning, he is going to take self care, he'll simply just take out his eyes ????????

     absolutely not..... He is going to visit doctor ASAP.

            Same is with the Self-medication. It is as wrong as taking your eyes out with fork. If you feel some thing "WRONG"  just visit the physician or pharmacist. Over-smartness is dangerous for your health.
Now, back to topic
There was recent study on the non-medical students of Karachi, Pakistan, where scientists tried to figure out the self medication of Abx ( just being fancy. abbreviation of antibiotics ).
Main researcher was Syed Jawad Shah.. Hi S.J Shah.. I hope you fine :P Nice work dude. (co authors .. sorry for not getting credit :D )
Was published on open peer review journal BMC ..

key Findings:

1. 205 respondents (47.6%) out of 431 reported using antibiotics not prescribed by a doctor in the last six
months.
2. The most common antibiotic used for self-medication purposes was amoxicillin which was used by 81(41.4%) study participants. Amoxicillin was followed by Metronidazole (30.5%), Ciprofloxacin (12.7%) and Cotrimoxazole (9.5%). Erythromycin and Ampicillin/cloxacillin were used by 6.7% and 6.2% of the sample population respectively and other antibiotics were amongst the less frequently used antibiotics.
3. only 21.8% of the students (93 out of 427) reported experiencing adverse effects after antibiotic usage. Of the 71 students who specified which adverse effects they had experienced, 19 reported presence of abdominal complaints after antibiotic usage (26.7%), 13 reported an allergic reaction (18.3%), 9 reported sleep disturbance (12.7%), and 8 reported weakness (11.3%).
4.63% non-medical student didn't heard of antibiotic resistance. Some thing predictable.

It was alaaa research.
Source : http://www.biomedcentral.com/2050-6511/15/74/abstract
And Pdf Source .. Just click on Click this :P

Pharmacy crushes :/

Hi i am sohail .. Student of final year P Harm-d lol .
during these 5 years i liked numerous girls tall, small , beautiful awful balck white brown asian... but couldn't talk to any of them ... YEEAAAAAH I KNOW I AM LOOSER :p
but thats how it works in pharmacist life :/ am i right or am i the only looser pharmacist :P ?
So here s my first story when i was in first year .... make that cloud over your head and make it seem like u are remembering some thing :P
I was in the lab and one of my crushes came near and asked "BHAAAAI where is beaker ... "
lol BHAAAAAAI what the hack is BHAAAAAAI  with 5 A in it :( (bhai means brother )
i went out of the lab with broken heart :( how can a girl that u like can call u BHAAAAAI with 5 A in it :/
yeah that was the one of the inspiring event for me ... that day i decided to work hard and invent or make the medicine, indicate the medicine only for boys . so boys can use it..... wait a minute what are uses :/ here are uses of that medicine
1. boys can develop guts to express themselves or their feelings to their crushes before the BHAAAAAI time comes
2. boys can a get a girl the like
3. boys can deliver their thoughts without saying any thing to their crushes
yeah i know its not funny :P its more imaginary and in my imagination it is funny lol that is how pharmacist joke :P
... and the medicine will be called "CRUSHOLOL" awkward moment .. why pharmacist joke ends in LOL or OL thats another joke man .. pharmacist talk in LOL language :P
atenolol , ketolol sotalol and leave me lol :P
its not funny for common people :) thts pharmacist joke
we have a teacher his jokes are so silly .. he said jaundase is an enzyme that causes jaundice :/ ITS funnnnnnny people laugh HAHAHAAHA ...
BTW i love pharmD :) thats how pharmacist end :) seee u

Logic of Wound healing Using sugar

Every one is familiar with the effect of sugar on wound healing. And I also want other people to enjoy learning this.
sugar effects in wound healing:

1.       Sugar drains moisture in therefore draining it out of bacteria in surrounding tissue leading to bacterial dehydration ultimately as bactericide.

2.       Sugar and honey prevent scarring after injury that they heal ulcers and burns without need for skin grafts, they prevent the build up of stringy kind  of collagen that creates scar tissue. Instead a delicate mesh like collagen structure forms that allow skin to heal.

3.       Granulated sugar is a disaccharide sugar and combines with water.when applies to a wound it commonly dissolves in 4 hours , creating highly concentrated environment on the wound surface.Body fluids are attracted towards wound surface to equalize increased concentrated gradient increasing the volume of exudate( any liquid that filters from circulatory system into lesion or area of inflammation) produced. This appears to wash out wash out the wound and liquify devastated dead tissue .The tissues are removed after every time wound is dressed.

 Now the question is if sugar is too god for wound healing so why diabetic patients take too much time to heal the wound ????

Answer is here

1. Poor circulation: This is due to fatty acid deposits in artries that slow downs blood flow . which in turn limits reach of blood, nutrients necessary for healing.
2. Neuropathy
3. Suppression of immune system :

• wound healing some what depends on immune system (at primary stage). In the hyperglycemic stage (increased glucose / sugar conc. In blood) sugar draws water in blood that suppresses immune system.

• WBCs rely on vitamin c to ingest bacteria and viruses but since sugar and vitamin c has similar structures sugar compete with vitamin c for entering cell this results in suppression of immune system..

I hope it helped you
Regards admin

Drugs and the Liver

Drugs and the liver

The relationship between the liver and drugs is important for three reasons:

• The liver is the principal site for drug metab-olism. Consequently, while liver disease may impair hepatic drug-metabolizing activity, the drugs themselves may reduce or enhance these processes. This consideration applies primarily to lipophilic drugs, which are normally metabolized to hydrophilic compounds for urinary excretion.

•  Liver impairment has other physiological effects, which affect drug handling and disposition, for example:

– increased volume of distribution of hydrophilic drugs in ascites (Ascites is the accumulation of an abnormal volume of fluid in the peritoneal cavity.);

– reduced plasma binding of acidic drugs by low plasma protein levels;

– reduced biliary excretion (cholestasis) causes hyperbilirubinaemia and reduced excretion, e.g. of rifampicinand fusidic acid;

– morphine and overenthusiastic diuretic therapy may precipitate hepatic encephalopathy (It is characterized by changes in mood and behaviour,confusion, disordered sleep rhythm, drowsiness and, eventually, delirium and coma. There is a strong similarity to senile dementia, and it is important to distinguish between them as encephalopathy is potentially correctable.) in patients with cirrhosis

• Drugs may cause liver damage, e.g.paracetamol (acetaminophen) and antidepressants. The bioavailability of drugs may be influenced by patient factors that are unconnected with liver disease: only those connected with the liver will be discussed here.

Liver and drug metabolism:

A full discussion of this complex subject is out of place here, although some specific aspects are outlined below.

Biological (patient) factors influencing drug availability

Pharmacogenetic factors

Two points are relevant here:

•  Slow acetylators are more likely to experience toxic reactions with normal doses of drugs than fast acetylators.

•  Oxidative drug metabolism varies substan-tially (20-fold) between patients, so some patients fail to respond to doses of drugs that cause unacceptable side-effects in others.

Disease state

Although diseases that compromise the blood supply to the liver may be expected to impairdrug metabolism, the data are conflicting, and it is difficult to draw satisfactory conclusions. It isprobable that liver function needs to be consid-erably impaired before significant effects areseen.The effects of liver disease are complexbecause several factors change simultaneously,e.g. metabolism, protein binding, volume of distribution and elimination in the bile. Thegreatest effects are seen when metabolism, especially first-pass metabolism, is high and protein binding is low, because the free plasma concen-tration is then markedly increased. Conversely, the plasma levels of drugs that undergo little first-pass metabolism and are highly protein-bound will be little changed. These effects are listed in Table 1.

Age

The decline in hepatic function with age leads to reduced levels of serum albumin and decreased hepatic metabolism, and these combine with other age-related changes to influence the avail-ability of many drugs. Interacting factors and interindividual variation make it difficult to predict what the effect will be in a particular patient.

Drugs and liver enzyme activity

The metabolism of many drugs may be either increased or decreased by the effects of other drugs on microsomal mixed function oxidase, of which the cytochrome P450 family of enzymes provide the terminal stage.Table 2 lists the more important drugs that are known to induce or inhibit hepatic microsomal enzymes. Generally,enzyme inductionwill reduce the biological availability of drugs and their activity. However, this is clinically significant only with drugs having a narrow therapeutic window and when loss of activity severely compromises the patient, e.g.warfarin, with which loss of activity may result in thrombosis, stroke or death, and the oral contraceptive pill, as enhanced metabolism of oestrogen may cause an unwanted pregnancy.

There are some drugs whose toxicity may be enhanced by metabolism, because the metabolite causes the damage, e.g.paracetamol (acetaminophen) and isoniazid. Enzyme inhibitionincreases drug activity, if other factors do not change. Again, it is those drugs with a low therapeutic index that are important, e.g.  warfarin, which may provoke severe spontaneous haemorrhage. Phenytoinhas a non-linear dose–response curve, and small increases in plasma levels may give rise to acute toxic reactions, e.g. nausea, vomiting, dizziness, tremor, ataxia and blurred vision, if the steady-state level is near the top of the therapeutic range. With a hypnotic or sedative, enzyme induction only impairs the level of sedation, but enzyme inhibition might result in over-sedation, confusion and serious falls in the elderly. While inhibition occurs rapidly, enzyme induc-tion depends on new synthesis, so the effects take some time to become apparent. Some of the drugs most likely to be affected by changes in liver enzyme activity are also listed in Table 2.

In addition, some drugs inhibit a specific enzyme, leading to higher levels of another drug that is metabolized by the same enzyme, e.g. allopurinol inhibits xanthine oxidase and may cause unacceptable toxicity with azathioprine and mercaptopurine.

Hepatotoxicity

As in other situations, side-effects may be either toxic (type A, predictable) or idiosyncratic(typeB, unpredictable). Table 3. lists some drugs that may produce these effects in the liver, though such adverse reactions are uncommon.

The principal risk factors for hepatic drug injury are given in Table 4, together with the mechanisms involved. Among these effects, paracetamol poisoning is the principal cause of acute hepatic failure in the UK .

Halothane and its congeners are generally very safe general anaesthetics. However, a small pro-portion of patients experience an unexplained fever, with mild signs of liver involvement. Exposure after a patient has been sensitized to halothane or to desflurane, isoflurane and sevoflurane, should be avoided in such patients, as it may cause acute, often fatal, liver failure, usually in obese, elderly females. Reye’s syndrome follows febrile illness in young children, although fortunately only rarely. Affected patients develop signs of liver disease with severe encephalopathy, and there is severe fatty degeneration of the liver. Because there is a high probability that the syndrome can be triggered by aspirin, this is contra-indicated in children under 16 years of age. The mortality rate is about 50%, usually from cerebral oedema.

Reference:  Pathology and Therapeutics for Pharmacists (T H I R D  E D I T I O N)

“Russell J Greene & Norman D Harris”

Regards admin : Hope These helped you ….

Apoptosis Vs Necrosis

Apoptosis	Necrosis
Physiological or pathological	Always pathological
Single cells	Sheets of cells
Energy dependent	Energy independent
Cell shrinkage	Cell swelling
Membrane integrity maintained	Membrane integrity lost
Role for mitochondria and cytochrome C	No role for mitochondria
No leak of lysosomal enzymes	Leak of lysosomal enzymes
Characteristic nuclear changes	Nuclei lost
Apoptotic bodies form	Do not form
DNA cleavage	No DNA cleavage
Activation of specific proteases	No activation
Regulatable process	Not regulated
Evolutionarily conserved	Not conserved
Dead cells ingested by neighbouring cells	Dead cells ingested by neutrophils and macrophages

Avoiding IgA Nephropathy isn’t difficult

What is IgA Nephropathy? In IgA Nephropathy, unknown agents cause the glomeruli to become — and to stay — inflamed. IgA Nephropathy is the world’s most common glomerulonephritis, but its pathogenesis is not known. IgA Nephropathy is considered to be an immune-complex mediated disorder, which means that immune complexes may not be the direct cause of the disease but they help bring about the end result, which is widespread inflammation of the kidneys. How to avoid IgA Nephropathy?

In order to help reduce your chances of getting IgA nephropathy, take the following steps:

1. Manage your blood pressure and cholesterol levels.

2. Exercise regularly.

3. Eat a healthful diet, one that is low in saturated fat and rich in whole grains, fruits, and vegetables.

4. Maintain a healthy weight.

5. Drink alcohol in moderation. Moderate alcohol intake is no more than two drinks per day for men and one drink per day for women.

6. Don’t smoke. If you Tobacco Use Disorder , quit.

7. Consider counseling, stress reduction exercises, and meditation to decrease the stress in your life.

8. Lose weight if necessary. Your doctor can recommend a safe weight loss plan and a reasonable target weight.

9. Take medicine. Your doctor may prescribe medicine to help lower your blood pressure and/or cholesterol levels.

Tell your doctor if you have a family history of IgA Nephropathy or other forms of kidney disease. This way, your doctor can watch for signs of IgA nephropathy.