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 !
Tuesday, September 27, 2011
Wednesday, September 21, 2011
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
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
Wednesday, September 07, 2011
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,
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,
Tuesday, September 06, 2011
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!
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!
Monday, September 05, 2011
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!
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!
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!
Sunday, September 04, 2011
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
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
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
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