Wednesday, June 10, 2009

Infective endocarditis

              Patient usually come recurrent history of fever, tired, night sweat, athralgia, weight loss. May or may not have history of  rheumatic history. Sign: splinter heamorrhage, janeway lesion, osler node, roth spot (heamorrhage, pale at the centre), splenomegally.

duke's criteria: ( 2 majors, 1 mojar and 3 minors or 5 minors)

Major Criteria:

a) positive blood culture (3/4 consequtive blood culture, typical organism

b) positive echo finding (new murmur, vegetation

Minor Criteria:

1) risk factor: IVDU, prosthetic valve, rhematic fever.

2) fever 38'C

3) evidence of vasculitis lesion: (splinter heamorage, optic??,JL)

4) blood culture that not meet criteria

5) echo finding that not meet criteria 

Investigation:

FBC, renal function, blood culture, ESR, urine (microscopic heamaturia), echo, ECG, TB workup (if suspected), 

complication:

a) emboli

b) CF, heart block.

management:

abx (4-6w)

strep : penicillin G and iv gentamicin. staphy (cloxacillin or vancomycin), culture negative of native valve: (penicillin G and Iv gentamiccin)

Monday, June 8, 2009

ENLARGE KIDNEY

Differentials:

  • hydronephrosis
  • acute pylonephrosis
  • polycystic kidney disease
  • renal cell carcinoma
  • renal abcess (usually unilateral)

Describtion:

There is a mass on left/right lumbar region. 

it is firm and non tender

it is ovule in shape, well-define margine and smooth surface. measure is...

can get above and below it. belotable.non pursatile.

it descends inferiorly during inspiration.

resonance on purcussion and no bruit.

Chronic liver disease

Cause of chronic liver disease:(AAudiO)

  • Infective: hepatitis
  • drug: methydopa and methotraxate
  • autoimmune - autoimmune hepatitis
  • alchohol
  • other: primary biliary cirhosis, wilson's disease.

complication: HEPATIK

  • hepatic encephalopathy
  • Portal hypertension + varices 
  • Ascites
  • Tumour (hepatoma)
  • Infection (spontanous bacterial peritonitis)
  • Kidney (hepatorenal syndrome)

Examination: 

general inspection:

  • confuse, drowsienss(hepatic encephalopathy), hyperpigmentation (heamotocromatosis)

hand :

  • leukonychia, duputyren's contracture, flapping tremor, palmar erythema, fingger clubbing (5)

forearm: 

  • scratch mark, tatoo, bruising, injection mark. (IVDU)

face

  • scleral icterus, xanthelasma, parotid swelling

neck

  • lymphadenopathy

chest 

  • spider neavi, gyneacomastia, loss of axilary hair, 

abdomen

  • caput medusa, dilated vein,  hepatomegally, ascites, loss of pubic hair, splenomegally

leg

  • oedema

end examination:

other: testicular atrophy

ask history about alcohol, drug abuse.

Investigation: (aaudio)

  • liver function test : gamma GT, liver damage, bilirubin 
  • Full blood count : anemia(bleeding, folate def, alcohol), thrombocytopenia and leukopenoa (TL - hypersplensim)
  • coagulation profile - lbleeding tendency
  • hepatitis serology
  • antimicrobial antibody (PCB)
  • sm antibody, antinuclear antibody, anti-microsomal antibody - autoimmune hepatitis
  • ascites fluid analysis
  • ultrasound
  • liver biopsy

  

Splenomegally

Describtion.

There is mass on left upper quandrat or left hypocondrium.

It is firm and non tender.

It ovule in shape, well define edge and smooth surface. there is a notch felt on the medial border of the mass. The size is 10 cm.

The mass decends inferiomedially with respiration.

i cannot get above it but can get below it. Not bellotable, non pursatile.

dull on percussion,trob space is dull and no bruit.

so my inference is spellenomegally.

Causes of splenomegally: (CHINA)

  • Congestion- portal hypertension, congestive heart failure
  • Hemolytic anaemia - thalessemia and hereditary spherocytosis
  • Infection :- bacteria (thypoid, typhus, infective endocarditis), Viral (CMV, Infective mononucleosis), paracitic (malaria), fungal
  • Neoplasia (myelo/lymphoproliferative disorder)
  • Autoimmune - Connective tissue disease.

Causes of splenomegally

  • cirhhosis with portal hypertenion
  • infection: infective mononucleosis, acute viral hepatitis
  • hematological disorder : lymp/myeloproliferative disease
  • connective tissue disease :SLE

Hepatomegally

Normal liver span: women 6-10cm man 8-12cm.

Describtion:

there is a mass on the RIGHT UPPER Quadrant:

- shape, size, edge, surface, consistency

- tender, pursatile, move up and down with respiration.

- ausculatation: bruit

eg: there is a mass on right upper quadrant which move with inspiration.

It is has irregular shape, smooth surface, well define age and firm consistency, liver span is 15 cm.

Cant get above it but can get below it.

it tender on palpation, non pursatile, dull on purcusssion and no bruit. 

so my differential diagnosis will be acute hepatitis, acute biliary obstruction, acute cholangitis and acute congestion of liver secondary to cardiac failure.

we should also consider other c auses of hepatomegally: (DIA MIC)

  • Drug/toxic: alcohol
  • Infection: hepatitis, abcess (amebic, pyogenic),thypoid
  • Autoimmune : lupus hepatitis.
  • metabolic: Wilson's disease
  • Infiltative: benign (fatty liver), malignancy (lymp/myeloproliferative), hepatoma, metastasis.
  • Congestion: Congestive heart failure

Tender liver:

  • acute hepatitis
  • acute cholangitis
  • liver abcess
  • acute bilirary obstruction
  • acute congestion of liver due to congestive heart failure

Irregular and firm liver

  • hepatoma, cirrosis, metastases and cystic liver.

Tuberculosis quiz

what is the side effects, interection and contraindication of the TB medication. remember  (IRP SE)

1. Isoniazide

  • SE:
  • I:
  • CI

2.  Rifampicin

  • SE:
  • I:
  • CI:

3. Pyrazinamide

  • SE:
  • I:
  • CI:

4. Streptomycin

  • SE:
  • I:
  • CI:

5. Ethambutol

  • SE:
  • I:
  • CI:

(complete within 5 min)

pneumonia quiz

1. How do u classify pnemonia?

2. What pathogens responsible?

3. CURB-65?and it interpretation?

4. What antibiotic that u gonna use?

Bronchiectasis

Chronic suppurative inflammation of bronchi that result in permanent dilatation of the airway disease.

causes:

  • postinfection : TB, pertussi, aspergillosis
  • endobronchial  obstruction - bronchial adenoma and carcinoma.
  • congenital - kartagener syndrome (chronic sinusitis, situs inversus, bronchectasis, hypogammaglobulinemia)

cx: 

  • purulent sputum, cough, hemoptysis.
  • clubbing and coarse crepitation.

complication : cerebral abcess, amylodisis, pneumonia.

investigation:

  • sputum AFB and culture
  • sputum culture (s. aureus, s.pneumonia, H. influenza, p aeruginasa)
  • CXR - trime line, ring like shadow, focal opacity.
  • aspergillus preceptin test
  • CT chest - gold standad in veiwing bronchial dilation. 

Mx:

  • chest physio
  • abx
  • surgery - resec segment

Sunday, June 7, 2009

Pleural effusion

Pleural Effusion is fluid in pleural cavity. Must know the causes is: It is divided into exudate and transudate.

Exudate :

  • Malignancy  (lymphoma, Mg metastasis, bronchogenic carcinoma, mesothelioma) 
  • infection (TB, pneumonia)
  • connective tissue disease (SLE, RA)
  • hypothyrodism

Transudate

  • heart failure, pericarditis, fluid overload ( due to increase venous pressure)
  • nephotic syndrome, chonic liver disease and malabsorption ( hypoproteinemia)

Light criteria (1/3) - indicates exudate.

  1. Pleural protein : serum protein > 0.5
  2. Pleural LDH : serum LDH >0.6
  3. pleural fluid LDH >2/3 of upper limit of serum LDH.

On examination :

general inspection: sign of maligancy, hypothyrodism, connective tissue disease (SLE, RA), oedema, any neck swelling. 

- sigmata of chronic liver disease.

chest:
inspection : reduce chest expension, surgical scar, radiotheraphy.

palpation : apex beat, trachea deviation ( in massive pleural effusion), 

purcussion: stony dull

auscultation : reduce breath sound, reduce vocal fremitus.

management:
ix:

  • pleural aspiration send for glucose, protein , LDH, tb test. pH, amylase
  • cxr
  • blood 
  • plueral biopsy 

Tx: 

  • drainage
  • pleurodesis with tetracycline, bleomycin
  • intrapleural streptokinase
  • surgery

asthma vs COPD

1. What is asthma and COPD?

Asthma - chronic inflammatory condition that characterised by reversible airway limitation (obstruction),  hyperresponsiveness to wide range of stimuli and inflammation of bronchi cause smooth muscle hyperthrophy, mucus plugging and epithelial damage.

COPD - chonic inflammatroy progressive irrevesible airway limitation. Related to ephysema and chronic bronchitis. 

2. Cx and examination.

SOB, cough,fever (+-)

COAD: smoking hx, hyperinflated lung

asthma: 

  • symptops: SOB, cough, fever (+,-)
  • history of asthma
  • duration 
  • elimination of other DDX
  • precipitating factor (emotion, cold, dusk, exercise, URTI, chemical) and  occupation
  • assess current severity
  • assess severity of asthma ( freq, noctunal, daytime sym, use of B-agonist inhaler, PEFM)
  • QOL
  • Mhx: eczema, asthma, urticaria, allergic rhinitis.
  • family history of asthma
  • social : smoking

4. Differential diagnosis for SOB

  • MI
  • pneumotorax
  • pulmonary embolism
  • respiratory infection
  • anxiety
  • COPD
  • metabolic acidosis

3. Complication 

COPD:  Respiratory failure and cor pulmonale (heart dz secodary to respiratory dz)

4. Investigation

diagnostic:  CXR (to exclude pneumotorax), ECG , FBC

assess severity: Peak flow meter, lung spirometry, ABG

5. Management 

ASTHMA

aim:

Management: 
  
Aims of treatment:

Management: 
  
Aims of treatment:

Abolish symptoms
Restore normal and best possible lung function
Reduce the risk of severe attacks
Enable normal growth to occur in children
Minimize absence from school employment

This involves:
Patient and family education about asthma
Patient and family participation in treatment
Avoidance of identified causes where possible
Use of the lowest effective doses of convenient medication to minimize short-term and long-term side effects

Control of extrinsic factors

  • Avoid causative allergens: house dust mite, pets, moulds
  • Active and passive smoking
  • Avoid Beta blockers in tablet or eye drop form 
  • Avoid NSAIDS
  • Avoid exposed to materials at works

DRUG.

Asthma self-management: Peak flow meters, treatment plans discussed with each patient
 
-An inflammatory disease + Anti-inflammatory 
 controller therapy started even in mild cases
 
-Inhaled oral steroids
 
-Short-acting relievers: Salbutamol, Terbutaline
 
-Long-acting relief/ disease controllers
 *Long-acting β2 agonists: Salmeterol, Formoterol
 *Sodium Cromoglycate
 *Leukotriene Modifiers: Montelukast, Zafirlukast
 
-Other agent with bronchodilator activity
 *Antimuscarinic agents: Ipratratropium, Oxitropium
 *Theophylline preparations
 
-Steroid sparing agents: Methotrexate, Ciclosporin, 
 Gold, IV Ig, Anti-IgE monoclonal antibody  
 omalizumab.


 

Acute Mx:

specific treatment:

COPD

Acute Mx:

specific treatment:

1) Counseling 
 2) Reduce risk factors
 3) Manage stable COPD
 4) Manage exacerbations
 5) Manage complications


6.THERAPUTIC

to be continued 

uhuk, uhuk cough

            Cough is not just pathological but also pscyological. Some use it for sign of communication. By listening to the cough, we can see at least character and can see the severity of cough.

cough question:

  • acute or chronic
  • duration
  • productive sputum?? dry? colour?
  • aggrevated by cold, food, ??
  • releving factor
  • ass factor sob, fever,  night sweat.

Aute

  • respiratory infection
  • bronchial asthma

Cronic 

  • infection : pneumoconiosis
  • COPD
  • emphysema
  • bronchiectasis
  • TB
  • carcinoma of lung
  • bronchial asthma

History taking:




Headache!!!

             Fening? sakit kepala? is it headache? in history taking of headache, use SRCOPDSARA (emphasis in distribution, duration, character and ass factor) ...what diffential diagnosis that you consider?: (think of structure and pathology)

  • migrain, tension headache, compound headache
  • nerve- trigeminal neuralgia
  • artery - giant cell arteritis
  • infection 
  • increase intracranial pressure (eg tumour, haemorrhage) -pappilodema
  • eye and eye glaucoma, sinusitis
  • drug (opiod overdose, analgesic, rebound headache - bifrontal headache)

Tension headache

  • acute onset lasting from hours to days.
  • describe bilateral of band tight headache, non pulsating.
  • precipitate by emosion. On examintion, neck and scalp tenderness.
  • believed is due to irritation of neurovascular  and scalp muscle.

Migraine

  • acute onset lasting from hours to days.(72hr)
  • aura bfr (visual, sensory and aphasia)
  • describe it as unilateral (usually) pulsating.
  • aggrevated by physical activity.
  • precipitated by food, light, premenstrual sysmp, ocp(eg choc, cheese)
  • ass w nausea and vomitting.
  • recurrent.
  • F.hx
  • coz by dilatation of of blood vessel.

Trigeminal Neuralgia

  • acute onset lasting for mins
  • involve 1 or more distribution of trigeminal nerve
  • clue usually not cross midline.
  • decribe it as instense, sharp and stabbing pain.
  • no neurological deficit.

Giant cell arteritis.

  • acure onset of pulsating headache
  • may hav sudden visual disturbance (eg: amaurosis fugax)
  • ass with malaise, fever and tiredness
  • older age
  • on examination.tender in scalp and temporal/occipital area
  • due to inflammatory granulomatous arteritis of large arteries which occurs which occurs in association with polymyalgia rheumatica.
  • ix: increase ECR and CRP, artery biopsy.
  • tx: high dose of corticosteroid

STROKE

  1. Definition of stroke and tia
  2. Classification 
  3. history and examination
  4. Differential
  5. Complication
  6. Investigation
  7. Management (emergency, specific, supportive, rehabilitation, secondary prevention)

1. Definition of stroke and tia. 

Stroke: Sudden onset of focal/global neurological deficit lasting >24hr.

TIA: transiet lasting less than one hour.

2. Classification

Oxfordshire community stroke project classification (OCSP)

  • Total anterior circulation stroke 
  • Partial anterior circulation stroke
  • Posterior circulation stroke 
  • lacunar stroke

Aetiology

1. Haemorrhage

  • Hypertension
  • Bleeding disorder
  • AV malformation
  • Budd-chiary microanuerysm

2. Ischeamic

  • atherosclerosis
  • emboli (eg: cardiac emboli, hypotension)

3. history and examination

- Ask about neurological deficit.

- Ask abour primary diasease.

- Ask about cardivascular RF.

- complication 

- sign depends in the site where it happen ( cortical vs lacunar), ant, post and middle.

Anterior cerebral artery

  • more leg than arm
  • behavior changes

Posterior cerebral artery

  • cortical blindness
  • cerebellar sign
  • hemianopia
  • cranial nerve palsy
  • spinal tract problem
  • horner syndrome

middle cerebral artery

  • facial weakness
  • body and arm
  • receptive dysphasia 
  • hemosensory loss
  • hemineglect

lacunar

  • dense hemiplegia ( pure motor)
  • loss sensory (numbness without weakness)(pure  sensory)

4. Differentials

  • mass lesion: tumour, abcess, haematoma.
  • metabolic derangement : glucose, electrolyte
  • unique : migrane and fit
  • psychogenic

5. Complication.

early

  • immobility (DVT, bed sore, pneumonia)
  • UTI

late

  • dev contracture
  • seizure/epilepsy
  • psychological effects
  • dependency
  • death

6. Investigation 

Blood 

  • FBC,                                              optional : VDRL, autoimmune screen, thrombophilia and 
  • RBS                                                                 lupus anti- coagulant, homocystiene and CRP
  • Renal Profile
  • Coagulation profile
  • Lipid profile

imaging 

  • CT-brain                                          * MRA, echo, carotid duplex US
  • 12 lead ECG
  • CXR

7. Management

  • correct diagnosis
  • resuscitation
  • acute treatment ( recanalise with thrombolytic eg rtPA, angioplasty+stent)
  • neuronal protection (BP, glucose, sepsis, nutritionm hydration)
  • rehabilitation ( physio, speech and occupational tx)
  • secondary prevention : antiplatelet (eg aspirin, clopidogrel), BP, DM, lipids, endarterectomy)
  • consel/support/patient/ education with pt and family member.

Approach to a fall.

              In past few years, i had a few falls and giving away. Recently, during second week in Taiping posting, i had a fall like one litle of tears drama. During that time, i still gain conscousness. i just dont know y i fall??? so let figure it why i had the fall.

Fall

History: (get from patient or family member)

  1. Detail of the event. (before, during, after)
  2. Different btwn fit or fall.
  3. Effect of the fall/fit.
  4. Find out the cause of the fall/fit.
  5. Family history.

PTOSIS

               Ptosis is drooping of the eye lid. We need to know that 3rd CN that innervates the levetor palpebrea muscle. 

Aprroach to ptosis:

  1. Unilateral vs bilateral eyes
  2. Look at the pupils
  3. Eye movement and squint.
  4. Sympathetic innervation

1. Unilateral vs bilateral 

Unilateral (then check pupil-sympathetic innervation 3rd CN)

  • small pupil - Horner's syndrome
  • normal pupil - medical 3rd CN palsy, DM
  • large pupil - Surgical 3rd CN palsy, here 2 conditions is considered:(if isolated - PCOM aneurysm, if combine; 3, 4, 6 th CN palsy - carvenous sinus or superior orbital fissure syndrome

Bilateral 

  • small pupil - horner's syndrome
  • normal pupil - (think of neuromuscular jnt and muscle) - MG, dystrophia myotonica & Kearns- Sayre syndrome. *, DM
  • large pupil - bilateral 3rd nerve palsy and midbrain lesion.

* progressive external opthalmoplegia , characterised by reduce eye movement, retinitis pigmentosa, prolonged PR interval.

3. Eye movement (H movement yeah)

abduction - 6th CN (LR6)

downward - 4th CN (SO4), absent of intortion of eye. (D, I) 

* vertical eye has additional action (intortion and extortion)

the rest is 3rd CN - adduction,  downward and upward.

( need to know origin, distribution and innervation of 3,4,6 th CN) -??

then, need to know the origin : divide by:

  • supranuclear Opthalmoplegia - abnormal conjugate gaze ( horizontal (pons) or vertical(midbrain)) show doll eye sign.
  • nuclear and infranuclear opthalmoplegia - diplopia, doll's eye response absent.

4. Sympathetic innervation

Saturday, June 6, 2009

Bifacial weakness


           What he is doing now? smilling, thinking? Can we guest what he is doing? One day u may encounter with people who experess less facial expression. Even, u make a joke, their face just show bored or (ur joke not funny enough). Alrite, now let think of y? Either they hinding their emotion or they are showing their emotion or is there any illness ? poor this guy...can express his facial expression...

approach to bifacial weakness:

a) what nerve innervate facial experession? (origin, distributiona and muscle innervated)

  • origin : pons  (near 6th cranial nerve) * if 6th cranial nerve palsy without 7th cranial nerve palsy so not likely due to the lesion at nucleus. - ( coz -tumour, stroke demylination)
  • distribution: Cerebellopontine angle - 5th, 6th, 7th and 8th  CN palsy -(coz-  acautic neuroma, meningioma)
  • patrous part of temporal bone ( geniculate ganglion) - greater petrosal nerve - parasympathetic Inn to lacrimal gland - ( can be fracture to petrous bone, otitis media, Ramsay-hunt syndrome) *check any vesicles.
  • parotid - divide into 5 branches: (temporal, zygomatic, buccal, mandibular and cervical ) (coz- parotid tumour, trauma) check: http://emedicine.medscape.com/article/835286-overview

b) uni or bifacial involvement?

Bifical : (pls check eye contact and any tremor)

  1. extrapyramidal (eg: parkinsonism)  - tremor, good eye contact
  2. pyschogenic disorder (eg: depression ) - no tremor, poor eye contact
  3. pyrimidal disorder ( bifacial weakness) - no tremor, good eye contact.

- usually common case  in 3:  Guillain-barre syndome, myasthenia gravis, dystrophia myotonica. 

(pls study the def, aetiology, clinical, ix,treatment)
 

c) UMN or LMN ?

clue:  UMN - lower half  LMN - whole (LL)

UMN (bi or unilateral ) - most common ( stroke)

LMN - 

 unilateral (remember anatomy)

  • parotid tumour/trauma (check swelling, scar)
  • ramsay hunt syndrome
  • Cerebellopantine tumour (check 5,6, 8 th CN and cerebella synd)
  • tumour/ms/stoke (6th CN involvemnet)
  • bell's palsy ( ??) isolated 7th nerve palsy

bifacial weakness

  • myasthenia gravis ( ptosis, fatiguability, squit, reduce eyemovement)
  • dystrophia myotonica ( frontal balding, temporalis wasting, myotonia)
  • guillain Barre syndrome ( weakness of lims , areflexia)
  • facio-scapula-humeral dystrophy ( shoulder , arm weakness)

d) other cranial nerver involvement?

check especially 5, 6, 7, 8 CN involvement

e) other neurological deficit?

contralateral hemiparesis - stroke

cerebellar syndrome 

check taste of ant 2/3 of tongue and hyperacusis.

Tuesday, February 17, 2009

Ibn al nafis ..


Bismillah hirahmanirrahim...let me start this blog with this biobliography of this muslim scholar who inspiring me till this moment... "ibn al-nafis"

Ala al-Din Abu al-Hassan Ali ibn Abi-Hazm al-Qurashi al-Dimashqi (Arabic: علاء الدين أبو الحسن عليّ بن أبي حزم القرشي الدمشقي‎) (1213 CE – 1288 CE / 687 AH), commonly known as Ibn al-Nafis (Arabic: ابن النفيس‎), was an Arab Muslim polymath—a physician, anatomist, physiologist, surgeon, ophthalmologist, Hafiz, Hadith scholar, Shafi`i jurist and lawyer, Sunni theologian, Islamic philosopher, logician, novelist, psychologist, sociologist, scientist, science fiction writer, astronomer, cosmologist, futurist, geologist, grammarian, linguist and historian—who was born in Damascus, Syria, and worked in Cairo, Egypt.


Ibn al-Nafis is most famous for being the first physician to describe the pulmonary circulation,[1] and the capillary[2] and coronary circulations,[3][4] which form the basis of the circulatory system, for which he is considered the father of circulatory physiology[5] and "the greatest physiologist of the Middle Ages."[6] He was also an early proponent of experimental medicine, postmortem autopsy, and human dissection,[7][8] first described the concept of metabolism,[9] and developed his own new Nafisian[10] systems of anatomy, physiology, psychology and pulsology to replace the Avicennian and Galenic doctrines, while discrediting many of their erroneous theories on the four humours, pulsation,[11] bones, muscles, intestines, sensory organs, bilious canals, esophagus, stomach, and the anatomy of almost every other part of the human body.[12] Ibn al-Nafis also drew diagrams to illustrate different body parts in his new physiological system.[13]

Besides his medical contributions, he wrote works on the Islamic religious disciplines, notably A Short Account of the Methodology of Hadith, which introduces a more rational and logical classification for the science of hadith.[14] He also wrote works on fictional Arabic literature, notably the Arabic theological novel Theologus Autodidactus, a novel which features a feral child, desert island, early science fiction elements, and a coming of age plot, through which he expressed many of his religious, philosophical and scientific themes on a wide variety of subjects.[9] Both of these works were mainly an attempt by Ibn al-Nafis at reconciling reason with revelation, both by highlighting the rationality of Islamic beliefs and by promoting the use of reason in the science of hadith.[15]

reference: wikipedia

"learning shall not be easy for those who are genius ...but it shall be easy and helpful to those who r seeking for it with respect, humble and patience."