Intensive Talk with Prof Falagas

Summary:
Bacteria develop multiple resistance to antibiotic
By:
1)producing B-lactamase
2)overexpression efflux pump to release extra antibiotic
3)antibiotic modify enzyme
4)ribosomal mutation
Thus appear all superbug such as ESBL, carbapenemase producing klebsiella etc
Pt infected with ESBL +ve had relative risk 1.85 of mortality compared to normal bugs
Treatment of commonest bugs in ICU –Acinetobacter spp.
Recommended to do C+S with MIC
Therapy promptly early
Start therapy right at beginning
Modification therapy as nessasary (de-escalation) early
Tigercycline- a new agt
It evades tetracycline efflux pump and ribosomal protective mechanism
Bacteriostatic
That is limitation no good blood level for therapeutic
Varied response to acinetobacter
Imipenem –launch with 4g/day
Recommend 2g/d as reduce seizure
Not enough as moderate susceptible organism need 1g qid .
Recommended for high MIC acinetobacter to give prolong infusion meropenem 1 g tds as long as 3 hr compared with 30min normally given.
Study proved similar dose with prolong infusion better outcome
Colistin monotherapy
Got 52% isolates for acinetobacter were polymycin only susceptible
The rest need colistin and one other antibiotic (rec add carbapenem)
As highest % of survival
Benault et al. showed Obesity highest rate septic shock
Partly related with leptin def
DM
FOsfamycin-good for Klebsiella spp and pseudomonas spp.
Another talk by gastro
If NDM1 may give fosfamycin + carbapenem.
UGIB
Commonest cause H. pylori followed by NSAID, Antiplatelet
Risk of UGIB-age, multiple co-morbidity and H/O peptic ulcer
If pt got cardiovascular problem, may restart antipltelet after 4-5 days of peptic ulcer

Neurology examination (basic fundamental)

Student, house officer, medical officer hates the most ! neurology system. Coz, no particular song lyrics to sing ! all other system got same chores to sing.-Inspection, palpation, percussion and auscultation.

To me, neurology famous song would be look and proceed + investigator.
The rule no 1- when ask to look at the face, please do look for upper and lower limb grossly also ! This is what i called LOOK thoroughtLY !

Rule no 2-Pretend yourself as a wireman,
rule of thumb - for neuro, first ,level of lesion-brain, cerebellum, brain stem, spinal cord, anterior horn , peripheral nerve or muscle.
After that second question- left or right brain or level of lesion
lAST-cause of the lesion
Then bingo- You are PASSED.

rule no 3- don't panic- apply for all

Rule no 4- common thing come first-apply for ALL physical examination.

Rule no 5- use your rule no2 rule then give the diagnosis with statement like this is a 40 year old (middle-aged) gentleman with left hemiparesis which is due to right cerebral infarct. etc..
Bingo, you are passed then just answer all the question.......to get better marks.


Good luck, the next will be cranial nerve. If you like the blog, pls do CLICK on google ads on top or side to show APPreciation! Your appreciation is my best inspiration!

undergraduate exam tips

Medical Students ask me the tips of passing clinical exam. The answer is stay calm, then perform what you practice everyday. My prof used to tell us if should practice at least 400 times before went for exam .If you failed, then you should also pretend to practice 400-500 times.

Tips no 1 , be systematic. For abdomen, CVS and respiratory. All following the normal song sequence, - Inspection, palpation, percussion and auscultation. For CVS, percussion part can be skipped. Every medical students worried about neuro. Actually neuro also got own sequence. First,inspection, then tone , power and reflex for motor. Then sensory, the last cerebellar system. for upper limb AND lower limb problem. for cranial nerve, just follow the sequence from 2nd to 12th nerve.

tip no 2, don;t panic. If panic, practice 1000 times, also may Failed. TAKE A DEEP breath and made it a norm routine for you.

Tip no 3, know the topics needed to know for undergraduate!
eg for 3 rd year
CVS- valvular disease-mitral regurgitation, aortic regurgitation, aortic stenosis. Mitral stenosis a bit rare. Prosthetic valve normally mechanical.
Respiratory-bronchiectasis,idiopathic pulmonary fibrosis, pleural effusion, pneumonia
abdomen -polycystic kidney disease, hepatomegaly, splenomegaly, hepatosplenomegaly. Pls memorise the causes of hepato, splenomegaly and hepatosplenomegaly.

Tip no4., Do not cause pain for patient! Pt cry or shout. 100 % failed !

Tip no 5, listen to examiner command, do not argue with examiner or else.......


Last, good luck for the candidates. Take exam as a challenge. Failing exam may make you a better Dr. Trust me about that ! all the top Dr failed their exam before.
It not means you should fail to be good ! it just means failing is nothing . It just a system to access the knowledge and coping !

cognition after carotid endarterectomy or stenting

A neurology 77 published a interesting report regarding the topic above.
divided in 2 arms -one for CEA ( carotid endarterectomy) , another CAS (carotid artery stenting)
the NIHSS (NIH stroke scale) assessed at baseline and 1 daY postprocedure. Modifie RANKIN SCALE at baseline, 1 and 6 month. Cognition assessed in the week before procedure and 6 months later.Pt also assessed for mood using Beck depression inventory II.
MRI with DWI performed 1 to 3 days before and 3 days thereafter to assessnew ischemic lesion.]

Result:significant decrease in cogntion sumscore after CAS from baseline to 6 month
NO significant decrease score after CEA.
The mean difference between changes was not statistically significant.
the worst cogntion functioning inpt treated with CAS consistent with higher rate NEW ischemic DWI lesion after CAS

Peripheral neuropathy

Peripheral neuropathy or polyneuropathy-diffuse peripheral lesion, often symmetrical
Onset-
Childhood-CMT
Adult-diabetes
Older adult- paraproteinemia
Acute onset-AIDP, porphyria, toxic, vasculitis,tick paralysis, diphtheria
Chronic-B 12 def, paraproteinemia, diabetes.
Symptom-
Motor-distal weakness predominates.
Sensory-tingling (positive), numbness (negative)
Autonomic-orthostatic lightheadedness, gastroparesis, sweating abnormalities
Diff diagnosis by pattern
Pattern 1 : symmetrical ,prox and distal weakness + sensory loss
CIDP, vasculitis
Pattern 2 : symmetrical distal weakness +sensory loss
DM, drug and toxin, hereditary neuropathies, amyloidosis , paraproteinemia
Pattern 3: Asymmertical distal weakness and numbness
Infectious neurpathy, multifocal trauma, entrapment, vasculitic
Pattern 4: asymmetrical distal or prox weakness without sensory loss
Multifocal motor neuropathy, motor neuron disease, inclusion body myolitis
Pattern 5: asymmetric prox and distal weakness with sensory loss
Malignant infiltration, polyradiculopathy, HNPP
Pattern 6: symmetric small fibre sensory neuropathy without weakness
DM, amyloid, HIV
Pattern 7 marked proprioception loss
HIV, B6 toxicity, sjogren, paraneoplastic
Pattern 8: Neuropathywith cranial nerve involve
HIV,lyme, AIDP, sarcoidosis, malignant infiltration,antiGd1b neuropathy
Acute neuropathies
Guillain barre
Vasculitic neuropathic
Acute intermittent porphyria
Diphteria
Heavy metal
Tick paralysis
Chronic:
Mononeuropathic –trauma entrapment’
Multiple mononeuropathic- vasculitic
Polyarteritis nodosa
Sjogren
Wegener grnulomatosis
HNPP
Multifocal motor neuropathic
Polyneuropathic
DM,
Nutritional eg B12, B6, B1 def ,
Alcoholic
CIDP
Paraneoplstic
Paraproteinemia
Infectious-HIV, CMV, lyme, leprosy
Sarcoid
Metabolic- renal, hepatic or hypothyroid
Heavy metal- arsenic, lead, mercury
Drug- vincristine, flagyl, sisplatin , amiodarone,

History taking

As a physician doing round every day and taking students from time to time.
I found a common weakness for my junior colleague (House officer) and students. Increasing House officer in ward make them taking care of only 6 patients per person but ironically they clark a poor quality of history.

History taking saves lives. proper history can anticipate severity of disease, diagnosis and give proper treatment to patient. MY FELLOW prof. teach me in my first lesson proper history taking which i think i need to share with my fellow juniors.
first, chief complaint!
4 C need to be applied for history taking- condition, cause, confirm and complication

Condition -for example, if pt complaint of chest pain then chest pain is the condition.then you need to ask every thing about chest pain (this condition) from character, onset, severity, associating condition eg sweating, vomiting..... plus precipitating and relieving factor

cause- try to establish the cause for example is it IHD, pneumonia, costocondritis

confirm the complaint- is it real chest pain or just diff in taking breath or worse underlying psychaitric cause! My experience, pt with underlying ischemic heart disease complaint of chest pain admitted for unstable angina when further history taking found wife had extra marital condition and ended up chest pain. ECG all normal. I refer psychiatrict and problem solved!

complication- pt if chest pain due to heart attack , maybe pt will collapse or got ventricular rupture......

This is the basis for clarking history, if provisional diagnosis already confirmed then need to get risk factor for the cause eg... heart attack - risk factor will be age, sex, diabetis, hypertension, smoking and family history......

If failed to obtain all this, it won't be good history.

One real story happening yesterday, patient presented with tremor but diagnosed by HO as stroke. On examination, pt got cog wheel rigidity worse on one side, mask like facies, bradykinesia. turn out to be Parkinson disease. This happens HO not bother to take proper history and PE!

Support my blog

Recently i had updated my blog but sadly people just read my blog but without showing support.
writing summary blog is quite taxing! you should spend minimum time by clicking the ad sense after finish every article. Who knows! YOU LEARN SOMETHING BY CLICKING IT! iF YOU worried about deviation just right click to open in other page!

Gout

Gout
Gout is a disease characterized by an abnormal metabolism of uric acid, resulting in an excess of uric acid in the tissues and blood.
People with gout either produce too much uric acid (10%), or more commonly or have problem in removing it (90%).

acute and chronic goutyarthritis, kidney stones, and local deposits of uric acid (tophi) in the skin and other tissues.
Gout may occur alone (primary gout) or may be associated with other medical conditions or medications (secondary gout).
Gouty arthritis characterised by sudden onset of a painful, hot, red, swollen joint, particularly in the foot at the big toe. Commonest inflammatory arthritis in men over the age of 40.
Diagnosed by detecting uric acid (monosodium urate) crystals in Joint aspiration which is negative birefringence.
uric acid level should be done but cannot be rule out by normal uric acid!
joint radiograph to see joint destruction.

Genetics (our inherited genes), gender, and nutrition(alcoholism, obesity) play key roles in the development of gout.
20% development of gout if parents got gout

Diets rich in red meats, internal organs, yeast, and oily fish increase the risk for gout.

Attacks of gouty arthritis can be precipitated when there is a sudden change in uric acid levels, which may be caused by
• overindulgence in alcohol and red meats,

• trauma,

• starvation and dehydration,

• IV contrast dyes,

• chemotherapy,

• medications,

o diuretics and some other anti-hypertensive medications,

o aspirin (Bayer, Ecotrin),

o nicotinic acid (B-3-50, B3-500-Gr, Niacin SR, Niacor, Niaspan ER, Slo-Niacin),

o cyclosporin A,

o allopurinol (Zyloprim) and probenecid (Benemid),

o others.

Kidney stones are more frequent in people with gout.
Uric acid crystals can form outside joints.- tophi, can be found in the earlobe, elbow, and Achilles tendon (back of the ankle), or in other tissues.
tophi are not painful but can be a valuable clue for the diagnosis as the crystals that form them can be removed with a small needle for microscopic examination.\

treatment
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
o Examples include indomethacin(Indocin), ibuprofen (Advil), andnaproxen (Aleve). Newer drugs such ascelecoxib (Celebrex) can also be used.Aspirin should not be used
o High doses of anti-inflammatory medications are needed to control the inflammation and can be tapered off within a couple of weeks.



o The primary complications of these medications include upset stomach, bleeding ulcers, and decreased kidney function.

• Colchicine (Colcrys)

o This medication is given in two different ways, either to treat the acute attack of arthritis or to prevent recurring attacks.

o To treat the hot, swollen joint, colchicine is given rapidly (generally, two tablets at once followed by another tablet an hour later).

o To help prevent an attack from coming back, colchicine can be given once or twice a day. While the chronic use of colchicine can reduce the attacks of gout, it does not prevent the accumulation of uric acid that can lead to joint damage even without attacks of hot, swollen joints.

o caution for pt with kidney or liver function.

• Corticosteroids

o Corticosteroids such as prednisone (Meticorten, Sterapred, Sterapred DS) are generally given when your doctor feels this is a safer approach than using NSAIDs.

o When given by mouth, high-dose corticosteroids are used initially and tapered off within a couple of weeks. It is important to take these medications as prescribed to avoid problems.

o Some complications with the short-term use of corticosteroids include altered mood, elevated blood pressure, and problems with control of glucose in patients with diabetes.

o Corticosteroids can also be injected into the swollen joint. Resting the joint temporarily, after it is injected with steroids, can be helpful.


• Probenecid (Benemid)

o This medication helps the body eliminate excess uric acid through the kidneys and into the urine.

drink at least 2 liters of fluid a day while taking this medication (to help prevent uric acid kidney stones from forming).




• Allopurinol

o This medication decreases the formation of uric acid by the body and is a very reliable way to lower the blood uric acid level. Allopurinol is currently the gold standard of maintenance therapy.

o Allopurinol can be still used, but the dose may need to be adjusted for kidney problem pt.

o Common side effects include stomach pain, headache, diarrhea, and rash.





• Febuxostat (Uloric)

o Febuxostat is first new medication developed specifically for the control of gout in over 40 years.

o Febuxostat decreases the formation of uric acid by the body and is a very reliable way to lower the blood uric acid level.

o Febuxostat can be used in patients with mild to moderate kidney impairment.

o Febuxostat should not be taken with 6-mercaptopurine (6-MP), or azathioprine.
It is important to understand that these maintenance medications are used to lower the uric acid well below normal to prevent recurrent gouty arthritis attacks. Generally, doctors want the blood uric acid level to be below 6.0 mg/dL. This level of uric acid is referred to as the "target level" or "goal" of therapy.
IT is not available in Malaysia.

Malaysian candidates only got to uses allopurinol.
for acute attack only can used steroid, colchicine and NSAID!

Support my blog by clicking adsense at side or below. THIS is the inspiration for me to continue on provide summary daily!

Causes of thrombocytopenia

Medical always related with your normal life even for causes for thrombocytopenia.
It is just like economic-supply and demand
In thrombocytopenia- if destruction excess or reduced production

Impaied production-
1) drugs=eg cytotoxic
2) virus infection-dengue, HIV
3) infection-leptospirosis
4)megaloblastic
5)MDS
6)leukemia,Myelofibrosis, aplastic anemia
7)solid tumour
summary-drug, infection , blood dyscrasia-MDS, leukemia and solid tumour infiltration to marrow

excessive dest
Immune mediated
ITP
drug induced-penicillins, Grp IIB-IIIa inhibitors
secondary immune-SLE, CLL, heparin)
post tranfusion purpura
DIVC
TTP

sequestration
splenomegaly
diluional
massive tranfusion

ITP

ITP (Immune thrombocytopenia purpura) is due to immune destruction of platlelet.
Ab coated plt removed following binding to Fc receptors on macrophages
ITP in children – acute, history of recent viral infection-varicella, measles
ITP adult- less acute, seen in women, may be asso with autoimmune disorders such as SLE, thyroid diseases
CLL and solid tumours
Infections with virus- HIV
Clinical- major bleed rare, easy bruising
Inv-FBC, bone marrow-increased megakaryocytes
Treatment-Plt> 30x 109 no urgent trt
First line- steroid 1mg/kg body wt
IV igG is effective if needed rapid rise
Second line-splenectomy
Third line –failed both then danazol, other immunosuppressive such as azathioprine,ciclosporin , mycophenolate mofetil

Guillain Barre syndrome

Guillain Barre syndrome Also called as acute infective demyeliting polyradiculoneuropathy (AIDP)
Got few variant Include AIDP, AMAN (acute motor axonal neuropathy) ,AMSAN(acute motor sensory axonal neuropathy) ,acute ataxia and opthalnmoplagia (Fischer syndrome)
Presentation: acute onset paresthesia in distal upper and lower limb
Afebrile
After recovering from viral attack (such as diarrhea or URTI)
Absence of reflex
May got vent failure (1/3 pts)
Diagnosis:L electrodiagnostic, AIDP-demyelinating picture
CSF-albuminocytologic dissociation (increased protein without pleocytosis)
Management: Vent support if vital capacity < 15ml/kg
IV immunoglobulin or plasmaphresis

Role of IV immunoglobulin in sepsis

Sepsis is the inflammatory response of the body to severe infection, which can be caused by a variety of bacteria. Deaths due to sepsis and septic shock remain high despite giving antibiotics, especially if the lungs, heart and kidney are affected.

Intravenous immunoglobulin preparations contain antibodies that help the body to neutralize bacterial toxins.
There are two types of preparations, polyclonal immunoglobulins contain several antibodies and monoclonal immunoglobulins target a specific antigen.
The cochrane reviews found 24 trials of polyclonal immunoglobulins, with 17 in adults (1958 participants) and seven in newborn infants (338 participants); 18 trials (a total of 13,413 participants) were of monoclonal antibodies.
Both standard and IgM-enriched polyclonal immunoglobulins decreased the number of deaths in adults but not in infants.
In the monoclonal immunoglobulin trials, anti-endotoxin antibodies showed no benefit while the anti-cytokines showed a very small reduction in deaths among adults with sepsis.
h The reduction in deaths observed with polyclonal preparations needs to be confirmed in large studies that use high quality methods.
Most of the trials were small and the totality of the evidence is insufficient to support a robust conclusion of benefit. Adjunctive therapy with monoclonal IVIGs remains experimental.

Management of Glucose during fasting month.

Yesterday marked the starting of Ramadan ( a fasting month) for all Muslim.
Here is the brief account for management of diabetes during fasting month.
First we classify the diabetes patient to low , moderate to high risk.
Briefly low risk patient is the well controlled diabetes without target organ damage.
Very high risk patients are those with poorly controlled diabetes, recurrent hypoglycaemia, previous DKA (ketoacidosis), HHS (hyperosmolar ,hyperglycemia states), dialysis or pregnant lady.

Followed by knowing the potential complication they may face.
1-hypoglycemia
2-hyperglycemia
3-DKA
4-dehydration and thrombosis

Hypoglycaemia is due to reduced food intake.
Then why hyperglycemia ? accoding to the extensive EPIDIAR study which showed a fivefold increase in the incidence of severe hyperglycemia (requiring hospitalization) during Ramadan in patients with type 2 diabetes (from 1 to 5 events/100 people/ month_1) and an approximate threefold increase in the incidence of severe hyperglycemia with or without ketoacidosis in patients with type 1 diabetes (from 5 to 17 events /100 people/month_1) .
Hyperglycemia may have been due to
1.excessive reduction in dosages of medications to prevent hypoglycemia.
2.Patients who reported an increase in food and/or sugar intake had significantly higher rates of severe hyperglycemia

DKA particularly for those diabetic type 1. Particularly increased for those who reduced insulin injection with assumption food intake reduced during the month.

Dehydration and thrombosis
The dehydration may become severe as a result of excessive perspiration in hot and humid climates like Malaysia .It also happens among individuals who perform hard physical activities.
In addition, hyperglycemia produces a osmotic dieresis which further exacerbate the dehydration.
contraction of the intravascular space can further exacerbate the hypercoagulable state that is well demonstrated in diabetes .Increased blood viscosity secondary to dehydration may enhance the risk of thrombosis and stroke. Arab study found increase retinal vein occlusion during fasting month but not stroke and IHD.

General considerations

Individualization.

Frequent monitoring of glycemia

Nutrition.
It most likely to arise from inappropriate diet or as a consequence of over-eating and insufficient sleep. Therefore,the diet during Ramadan for diabetic patients should not differ significantly from a healthy and balanced diet.
ingesting large amounts of foods rich in carbohydrates and fats, especially at the sunset meal, should be avoided.

Exercise.
Normal levels of physical activity may be maintained. However, excessive physical activity may lead to a higher risk of hypoglycemia and should be avoided

Breaking the fast.
All patients should understand that they must always and immediately end their fast if hypoglycemia (3.3 mmol)

The fast should also be broken if blood glucose reaches (3.9 mmol/l)
in the first few hours after the start of the fast,

Type 2 Diabetis
Patients treated with oral agents. The choice of oral agents should be individualized.
In general, agents that act by increasing insulin sensitivity are associated with a significantly lower risk of hypoglycemia than compounds that act by increasing insulin secretion.

Metformin. Patients treated with metformin alone may safely fast because the
possibility of severe hypoglycemia is minimal.
2/3 of the total daily dose with the sunset meal and the other third before the
predawn meal.

Sulfonylureas.
It has been suggested that this group of drugs is unsuitable for use
during fasting because of the inherent risk of hypoglycemia. However, severe or fatal
hypoglycemia is a relatively rare complication of sulfonylurea use.
glyburide or glibenclamide may be associated with a higher risk of hypoglycemia than other
second-generation sulfonylureas, specifically gliclazide, glimepiride, and glipizide

Short-acting insulin secretagogues.
Members of this group (repaglinide and nateglinide) are useful because of their
short duration of action. They could be taken twice daily before the sunset and
predawn meals.

Incretin-based therapy.
Therapies that affect the incretin system include glucagon-like peptide-1 receptor agonists
(GLP-1ras) exenatide and liraglutide and dipeptidylpeptidase-4 inhibitors (DPP-4is) alogliptin, saxagliptin, sitagliptin,and vildagliptin. These classes of agents
are not independently associated with hypoglycemia.
Exenatide in particular can be dosed before meals to minimize appetite and promote weight loss.
With its short half-life of 2 h, it is not associated with a substantial effect on fasting
glucose.
DPP-4is are among the best tolerated drugs for the treatment of diabetes.
They are moderately less effective in A1C lowering than GLP-1ras and do not require titration.

alpha-Glucosidase inhibitors.
Acarbose,miglitol, and voglibose slow the absorption
of carbohydrates when taken with the first bite of a meal. Because they are
not associated with an independent risk of hypoglycemia, particularly in the fasting
state, they may be particularly useful during Ramadan
Insulin
judicious use of intermediate- or long acting insulin preparations plus a shortacting
insulin administered before meals.

Good luck to Dr during fasting month. It poses great challenge to keep Hbaic in target.

advice for short case examination

In clinical exam and pathway towards becoming a real Dr or specialist. Undergraduate need to undergone several clinical exam. The most striking and scarring is short case exam or so called OSCE (objective short case exam)which takes about 10-15min (average 10 minutes). different stages of OSCE demanding different things from candidate eg, a 3 year OSCE candidate and specialist exit exam demanding different things although they may get similar case.

First and foremost, candidate need to be calm. A calm candidate is a way to achieve success. Saying is better than experiencing it. First, candidate need to stay calm . Take a deep breath before entering it (your hall) and before you approach patient after examiner give you the instruction.

second, listen the instruction properly. Make sure you open your own ear. Do not end up examine the wrong system. Get the hints and do whatever nessasary. If ask when straight to abdomen , do not check peripheral. If ask to skip then skip. the examiner try to make sure you finish in time!

Third, approach patient politely. Remember , patient is your best textbook for disease. In exam, patient is your Future! If he or she dislike, in pain or show unpleasant expression, examiner with no hesistation to fail you. Respect them, examine them as if they are your parents, grandparents and siblings. Do not cause pain -if they are pain then prepare to die. Give correct and clear instruction.

four, smooth examination. Do not sit patient then lie back then sit again. The obstucted exam means troubling patient means failure. The obstructed exam means not finish in time.

Fifth is thank the patient after finished then face yourselves completely to the examiner. Do NOT see back patient during preasentation. It showed inconfidence.

Sixth, do not argue with examiner. If you argue then prepare yourself to fail. if they ask to recheck certain findings, normally you are wrong in undergraduate stages.For postgraduate , it depends on nature of examiner.

Finally good luck to those taking examination.

Brief account of Parkinson disease

Here i will write a brief account of Parkinson disease

Parkinson disease is named after Sir James Parkinson.
It is a movement disorder commonly come out in clinical exam.
PD is the second most common neurodegenerative disorder after Alzheimer's disease.
It charcterized by TRAP
T for tremor
R for rigidity (cogwheel)
A for akinesia/bradykinesia
P for postural instability
When these four feature present , it represent Parkinsonism.
glabellar tap is an optional demonstration
postural instability by righting reflex is a dangerous ACT to perform in exam!
Pls describe the monotonous speech, mask like facies, stoop posture, lack of arm swing and festinant gait.

To confirm idiopathic Parkinson disease or Parkinson disease (PD)
student need to rule out Parkinson plus symptom
such as eyes movement
cerebellar sign

Lymphoma Brief account.

Lymphoma is cancer of lymphatic sys charcterized by:
Painless swelling
Non painful lymph node
Fatigue
Wt loss
Fever
Night sweat
Enlarged tonsil


Causes: inserticide, HIV, drug prevent rejection

QR code and my blog

today marked the new era for my website. Now if you got QR reader for iphone or ipad by clicking the qr reader and scanned my QR code. IT will automatic went to my website.
QR reader is available for free in iphone.

enjoy!
from wikipedia
A QR code (abbreviated from Quick Response code) is a specific matrix barcode (or two-dimensional code) that is readable by dedicated QR barcode readers, camera telephones, and to a less common extent, computers with webcams. The code consists of black modules arranged in a square pattern on a white background. The information encoded may be text, URL, or other data.
Common in Japan, where it was created by Toyota subsidiary Denso-Wave in 1994, the QR code is one of the most popular types of two-dimensional barcodes. The QR code was designed to allow its contents to be decoded at high speed.