Cardiovascular examination

Examine the patient lying down at a 45 degree angle. Exposure of the chest(take off the shirt if possible)

Begin Examination by inspection of the general condition of the patient

“The patient is lying comfortably at a 45 degree angle. He appear ?alert, ?concious, ?not in any immediate pain or in any respiratory distress(describe what you see, don’t memorise script). Count the respiratory rate.###IMPORTANT

Examine the fingers for signs of clubbing, peripheral cyanosis, splinter hemorrhages, and Osler nodes.Examine the hands and look for Janeway lesion.Check the pulse for rate, rhythm and regularity. Compare the radial radial pulse (indicate subclavian artery stenosis due to aneurysm), and radio-femoral delay(indicate coarctation of aorta).--> Some doctors say radial radial delay is due to coarctation of aorta, but my logic and my findings find no reason to support such claims. No literature said that radial radial delay is due to coartation. If you find one, please let me and others know

Check for collapsing pulse which indicate aortic regurgitation,arteriovenous fistula, Patent ductus arteriosus, arteriosclerotic aorta or hyperdynamic circulation due to anaemia, pregnancy, thyrotoxicosis etc.(Remember all the pulse character such as plateu pulse, pulsus bisferiens, pulsus alternans, pulsus paradoxus and what they indicate)

Examine the face for flushing or grayish discoloration (mitral facies) suggestive of mitral stenosis.Examine the eyes and periorbital area looking for corneal arcus and xanthelasma.Check for jaundice and anaemia.Examine the mouth for hydration, central cyanosis and oral hygiene.Next, examine the neck for JVP

Use the right external jugular vein, look for sustained increase on inspiration which indicate constrictive pericarditis or cor pulmonale(Kussmaul’s sign)Hepatojugular refluxà when abdomen is compressed, JVP elevate for less than 4 second in normal person. If elevated more than 4 second, indicate heart failure.Use torch light at an angle, look at the shadow produced.(Datin Norella style)If cannot detect, it is not elevated and hence normal.** Difference between JVP and Carotid pulse should be fingertips by now J

Now examine the precordium. Look for scars from previous CABG or other thoracic surgery. Look for any visible pulsations.Next, palpate the apex beat. Feel for the character(e.g. tapping in mitral stenosis), position and regularity of the apex beat.

Once apex beat is felt, proceed to palpation of the tricuspid area. Feel for thrills and heaves( Once felt will never forget, dun worryJ). Proceed to pulmonary and aortic area feeling for the same thing.

Percussion is not significant in CVS examination except for estimation of the heart border, which is rarely done.

Auscultation for heart sounds.Begin at the apex using the bell of the stethoscope. Listen for low frequency murmur. If murmur is soft, ask the patient to lean to the left and listen for accentuation of the murmur.Still using the bell, listen at the mitral area, listen for pansystolic murmurs which radiate to the axilla.( Mitral regurgutation)Listen at the pulmonary and aortic area. Any murmur end diastolic murmur indicative of aortic or pulmonary regurgitation should be heard. Accentuated by sitting the patient up, deep breath and hold in mid expiration while listening to the murmur.If a ejecion systolic murmur is heard, listen to the carotid artery for carotid bruit.

** in atrial fibrillation, pulse deficit can be elicited by counting the number of auscultated apex beat and radial pulse in a period

of time. Any difference between apex beat and radial pulse of more than 10 indicate deficient pulseà atrial fibrillation.

Lastly, examine the leg for pedal edema. Examine the ankles and Achilles tendon for tendon xanthomata.

R FORGET the RESPIRATORY RATE. --> common killer in short cases

2)Do the asterixis properly. Do not look like you have never done it before.

3) Hypertrophic pulmonary osteoarthropathy is peculiar to chronic pulmonary disease. So, in the exam, say HPO instead of clubbing, which is not specific, as it may be caused by some gastro and cardiac problems.

4)BCG scar --> impress some lecturers with this inspection, annoy others with it.

5) face, don't forget Horner's,nasal polyp, nasal septal deviation,central cyanosis, pharyngitis etc.

6) Neck--> Trachea(be gentle) and lymph nodes(do it fast, don't waste time here)

7) Trunk--> examine front and back except when told otherwise. Chest expansion, do properly. Ur thumbs should go away from each other when the patient INSPIRATE. Make sure ur thumbs are opposed when the patient expirate. To do this, cekik the patient chest during expiration. Ask any previous medicine posting ppl to demonstrate this.Vocal fremitus is described as equal bilaterally, reduced on what site. DOnt say vocal fremitus is normal.Percuss at least 8 spots on the chest including the base, which is in the MID axillary line.Auscultate all ZONES, not lobe. There are 3 zones of the lung, while there is 3 and 2 lobes. Always describe breath sound as being vesicular(normal), bronchial(lobar pneumonia) etc. Do not

say breath sound is normal. If crepitation is present, describe it. Pan inspiratory or mid inspiratory, coarse of fine and at which zone. E.g. bibasal mid inspiratory fine crepitation.

dont forget pedal edema :)

Neuro must knowsCerebral circulation, the circle of willis and its tributaries, basilar artery and areas supplied by it,and dont forget the venous drainageThe Motor and Sensory HomunculusGeneral outline of motor and sensory function of the cortex(no need detail)

PathologyCerebrovascular accident(including Transient ischaemic attack)-->manifestation and localising signs up to managementHow to differentiate ischaemic and hemorrhagic stroke, and their managementsMeningitis-->how to differentiate viral and bacterial etiology from CSF specimen, common etiologic agent,treatment, complicationBrain absess--> what is ring enhanced lesion on CT, what is the causePeripheral neuropathy--> at least noe some other causes besides diabetes mellitusFacial nerve palsy--> Common cause like Bell's, ramsay hunt, Parotid carcinoma etcTic DouloreouxHorner'sTypes of nystagmus, some causes of the different types of nystagmusCerebellar signsand of course, drugs and their side effects

In short, you must be able to localise the symptoms from the clinical manifestation, which is why neuroanatomy is important

Some miscellaneous neuro cases in previous short case is multiple sclerosis,myasthenia gravis and Guillane Barre syndrome...lets hope it wont happen again haha

for this few "atypical" disease, i think we only need to know the clinical

manifestation and diagnostic feature, and of course, the level of nerve involved. for example, GB syndrome is characterised by areflexia, MG by progressive ptosis and weakness, MS by the lesion being disseminated in time and space etc

But if got time do read more on these...its quite interesting..

As for stroke, everything must be fingertip. Sure come out one...so common..Go catch one stroke patient in ward and examine him or her....practice more.

Gastrointestinal and Abdominal Examination

I'm not going into detail step because i'm sure everyone can do

GIT examination. What i'll do is highlight the signs which may be

present but frequently overlooked

Hands- Koilonychia, leuconychia, Plummer's nail(partial

detachment of the nail from nail bed

Dupuytren's-alcoholism, excess use of the hand as in

carpenter,NOT a sign of chronic liver

disease

Asterixis-->always forgotten

scratch marks-obstructive jaundice causing pruritus

jaundice, anaemia

mouth-leucoplakia, erythroplakia,stomatitis, glossitis,

Pigmentation as in peautz jegher polyposis,

neck-virchow nodes and troisier's sign

chest-differentiate between venous stars,spider naevi and

campbell de morgan's spots

abdomen inspection- cullen's and grey turner(discoloration)

abdomen palpation-sister mary joseph nodule, differentiate from

fat hypertrophy in chronic insulin injection

Auscultation-renal bruit, differentiate from portal hypertension

bruit by compression(portal vein bruit disappear on compression)

Signs that can be elicited for fun, but not compulsory:

Murphy's sign-> who dunno dis can go hang themself

Boas sign-> who dunno dis can also go hang themself

Rovsing sign-->erm...here we go again.who dunno dis can go hang

themself

Psoas sign--> in acute appendicitis, attempt to extend a flexed

knee will result in right iliac fossa pain

Cartnet sign--> if the pain is visceral, palpation of the abdomen

after the patient sitted 45 degree with arm cross over the chest

will not cause pain, because the pain is inside, not the abdominal

wall.

The sign of hippocrates--> if gastric outlet obstruction, after

warning the patient what is about to happen, the patient is rocked

from side to side with the stethoscope diaphragm on the stomach.

If there is GOO, succusion splash is heard.

Internal Medicine-Examination of a Diabetic foot

Begin with inspection of the soles of the foot for presence of ulcers, look at

nail for signs of brittlity, between the toes for fungal infections. Proceed to the

dorsal surface of the foot, noting whether or not the foot is pale.

Proceed to the calf note for diabetic dermopathy e.g. necrobiosis lipoidica

diabeticorum, hyperpigmentation, signs of cellulitis, loss of hair and shiny

skin. At the knee, look for deformities of the knee joint such as charcot joints.

Up at the thigh, look for signs of quadriceps femoris muscle wasting which is

a result of diabetic amyotrophy. Also look for insulin injection sites.

Palpate the foot for temperature noting the part that feels cold. Feel the

pulses. If dorsalis pedis absent, proceed with capillary refilling time. Palpate

the knees for charcot joints. Palpate for lipodystrophy in the injection sites.

Always ask patient for tenderness b4 palpating.

Next, examine the sensory perception. Using an orange stick, prick the

plantar surface at 4 points. Go upward until patient can feel. NEVER prick an

ulcer. No need to test soft sensation. When u r presenting, present in "

Sensation is lost up to mid calf". No need for dermatomes because diabetic

neuropathy affect any vulnerable nerve endings. Sometimes, in a same

dermatome, there will be 1 part which can sense and 1 part which cannot.

Do proprioception and say that u would like to test vibration if a tuning fork is

present.

Test for the strength of the quadriceps femoris and proximal muscles.

Next, elicit the reflexes in particular the ankle jerk. Ankle jerk will be absent in

advanced diabetes.

Complete the examination by examining the upper limb, including nail

candidiasis. Say that u would check for postural hypotension which is due to

autonomic neuropathy in diabetes.

By now, I hope that everyone should be able to recognize a Cushingnoid

patient even before you examine a patient. Therefore, it is more of a

showmanship for a short case of a patient with Cushing's syndrome/disease.

As Cushing's has clear cut characteristics, it is nice if a medical student is

able to ellicit the causes and the complications of Cushing's along the

examination. There ius no need for a thorough examination of a particular

body system as you'll be needing to go through almost the whole body.

Below is a rough guide which welcomes comments and criticism to improve

it.

1. Hands - Inspect the hands for any deformities, vasculitic lesion or

pulp atrophy which may be suggestive of autoimmune origin such as

rheumatoid arthritis and SLE. Therefore, you should also run your

fingers briefly along the small joints of the hands to palpate for the

joins for signs of any swelling or tenderness. Have a light pinch at

the skin of the dorsum part of the hand, yours and the patient's to

compare the skin thickness (usually paper thin in Cushing's).

Remember, exogenous steroids administration may cause skin

thinning.

o the skin thickness in normal person is 1.8mm

2. Forearms - Inspect for any bruises which may be suggestive of side

effects of steroids or complication of Cushing's syndrome.

3. Facial - Look out for any plethoric features, malar rash or acnes.

These are suggestive of Cushing's as well. Discoid rash is almost a

pathogmonic feature especially if it is also found at the back of the

ears.

o Do not forget temporalis deposition of fat giving the characteristic

moon facies

4. Hair - Stroke the patient's hair (Inform the patient before doing this!!)

to examine for alopecia (more hair may fall off or patches of

baldness can be seen).

5. Eyes - Examine the eyes for any signs of cataract. This may not

require fundoscopy as sometimes it can be severe enough that it can

be seen by the naked eyes. You may use two pentorches (one below

the face pointing upwards and the other having a quick flash at the

eye). This can be due to side effect of Cushing's or a diabetic patient.

Remeber, Cushingnoid can be diabetic as well.

6. Oral - Examine the oral cavity at the mucous membrane for any

ulcers. This can be a sign of SLE. Superimposed thrush can be

present too, which may be a diabetic sign.

7. Upper torso - inspect and feel the supraclavicular fossa and

interscapular area for fat pads. These are the signs of a Cushing's:

Buffalo hump and supraclavicular fat. Also, try to elicit tenderness

along the vertebra spine by gently pressing from the cervical spine

downwards to sacral spine. Ask the patient if there's any pain felt, as

this can be a sign of osteoporosis as a result of exogenous steroids.

o Spine tenderness have a tendency to affect weight bearing spines i.e

lumbar. Alternately, you can palpate downwards from thoracolumbar

junction as this may save you some time instead of palpating from

cervical spine.

8. Abdomen - Inspect for purple striae on the abdomen as a sign of

Cushing's. Remember that adequate exposure is the key in finding

the purples striaes. Medical students tend to miss the sign as they

had not lower the pants enough to expose the lower part of the

abdomen. Try to palpate for any adrenal masses. (Adrenal

adenoma)

o Striaes can also be found in inner thigh and axilla.

o In the abdomen, you may also want to elicit hepatomegaly due to fat

deposition in the liver or due to increased in workload of the liver to

metabolise the excessive steroids.

9. Legs - You may look for bruises and skin thinning here as well.

However, if there is positive findings on the forearm, most likely there

will be findings on the legs. It is nice to show to the examiner that

you are observant, but some examiners may not mind if you missed

this. (Correct me if I'm wrong)

o in the legs, pedal edema can be a sign of mineralocorticoid excess,

so be aware!

10. Proximal myopathy - In a patient with Cushing's, there tend to have

proximal myopathy. Test both upper limb's muscle for shoulder

abduction and adduction (you may use the chicken wing manouever)

as well as the flexion and extension of the arm.

11. Tell the examiner that you would like to end the examination by:

o getting the patient to squat to confirm for proximal myopathy.

o measure the patient's blood pressure

o (optional) - test the urine for glucose

o (optional) - check the visual fields ( possible pituitary tumor,

adenoma,etc)

o (optional) - examine the fundus for optic atrophy, papiloedema, signs

of hypertensive or diabetic retinopathy

So, if there's any mistakes here, do correct me. I'm more than willing to share

the differences as well.

Here's a brief rundown of the causes of Cushing's syndrome:

exogenous steroids

pituitary adenoma

adrenal adenoma

adrenal carcinoma

ectopic ACTH (small cell carcinoma of the lungs)

Some extra stuff for you to ponder:

1. Classification (Types) of Cushing's syndrome

2. Investigations for Cushing's syndrome

3. Management for the Cushing's according to the causes.

Since the kidney is one of the main homeostatic organs,the most important thing in Nephrology is Anatomy and Physiology. From the glomerulus to the collecting duct, make sure you know which part is responsible for certain ion absorbtion and maintainance of acid-base balance.

Gross anatomy : Cortex,medulla, renal pelvis, renal papilla etc

Part of the nephron which is responsible to release renin and maintainance of blood pressure.

Control of calcium and other ion concentration.

Erythropoetin secretion regulation

Creatine and urea level: What does it signify?

Proteinuria: Nephrotic and Nephritic syndrome and its causes

Spot Urine Protein: Creatinine index : MUST know. What does it show?

UTI-> As important as URTI in Respiration(means very important la). Common organisms, Urease producing ones, and why is it so important to know whether the causative agent produce urease or not

Urine dipstick interpretation: Wat changes can be expected in UTI and nephrotic syndrome

Hypertension in the young

Renal Failure : Acute and Chronic: Pathophysiology

Nephrology needs understanding of the Physiology to be able to make sense of what is happening to the patient. Thus, don't memorise blindly, please understand the physiology and relate it to the disease.

1. Definition of the rashes: (its all in 1 page of Talley's if you care to

look)

o Macule

o Papule

o Nodule

o Pustule

o Vesicle

o Bullae

o Keratosis

o Lichenification

o Purpura

o Petechiae

o Echymoses

2. How to differentiate them?

3. What disorder can give rise to them?

4. The common place they appear in different disease :

e.g. HSV 2 viral infection, HPV infection, Molluscum contagiosum

5. The "hi-tech" rashes :

condylomata acunimata, condylomata lata, snail track rash, gumma,

pyoderma gangrenosum: Where are they usually found and in what

condition

6. Common bacteria and viral pathogen :

the "cardinal sign" Staph aureus, Strep pyogenes, poxviridae,

HSV,HPV and STDs Syphillis

7. Steven-Johnsons Syndrome (SJS) - Definition, what agent can

induce S-J syndrome, the severe form TEN(stands for what, find

out).

8. What other conditions lead to target lesions?The most important thing in Dermatology is definition.Remember the definitions well.

Internal Medicine

Quite worried that some of my colleagues going for exam can't tell me much

about diabetes mellitus. So what is written here is the basic must-knows.

1. Classification of diabetes--> Contrary to popular belief, there are

actually 9 types of diabetes. We frequently say there's only 2(or at

most 3) because that's the most "popular" diabetes. Find out(from

Papa Robins). Find the difference between type 1 and type 2.

2. Pathophysiology of diabetes (Why some is more common in

obesed people and some people with diabetes are lean, What

happened in diabetes that can lead to diabetic Ketoacidosis)

3. DKA and Non ketotic hyperglycaemic attack--> what are the

difference? DKA can occur in which type(s) of diabetes? What to do

with people who have DKA?

4. Types of OHA : Classification, rough idea on the mode of action.

Which one is contraindicated in renal, hepatic and heart

failure(MUST KNOW, or you will kill the patient)? What are the

advantages of certain agents and the side effects(besides

hypoglycaemia, of course)

5. Insulin : Types(long acting, intermediate and short as well as rapid

acting), what combination regimes are used, why certain insulin

cannot be mixed and must be given by different syringe, where is the

site of administration of insulin. And, is it given subcutaneous or

IMly?

6. Hypoglycaemic attacks : How to differentiate with DKA? What if

patient is on Beta Blockers?

7. Complications of Diabetes: From top to toe, must know~

Especially the diabetic foot ulcers. Why it happen and how to avoid

it?

8. What advice would you give a patient newly diagnosed with

diabetes? Is it curable?

9. Foot care in diabetes: Rough idea

10. (my favourite question) How many types of diabetic neuropathy?

Why does it manifest in different way in different person?**no need

answer also nevermind:)**OSCE : Examination of the lower limbs of patient with diabetes: What to look for.

PPD question : What about some traditional preparations (Misai kucing, Hempedu Bumi etc), does it help? Patient insist on taking it, what would you do?

Good luck~ All the best :)

lease make sure you know how to examine the hands for

rheumatological problems.

Questions

What is the difference between arthralgia,arthritis and

arthropathy?

Causes of arthralgia

Rheumatoid Arthritis

Explain the pathogenesis of Rheumatoid arthritis(RA)

Who is more prone to develope RA?Why?

How is RA different from other types of arthritis e.g.

osteoarthritis?

Explain something on Still's disease(Juvenile RA)

Differential diagnosis for symmetrical arthritis? What

investigations would you do to confirm?

What are the criterias used to diagnose RA?

How do you define morning stiffness?

What complications can arise from RA?

How to manage RA?

Gouty Arthritis

What is the cause? Briefly describe the pathogenesis.

What are the risk factors?

Why is it that the most common site for crystal deposition is the

1st metatarsophalangeal joint?

Describe the pattern of joint involvement.

How can you classify the attacks?

Define pseudogout. How do you differentiate it from gouty

arthritis.

How would diagnosis be confirmed?

What is a tophy? Does it happen in every gout case? If not, when

does it happen?

What are the complications of prolonged hyperuricaemia?

How would you treat an acute attack of gouty arthritis?

What advice would you give the patient to reduce attack rates.

Systemic Lupus Erythematosus

What is it?

What are the causes?

If there are joints involvement, what would be the pattern?

What criteria is used currently to diagnose SLE?Explain

What blood test should be done to confirm SLE?

Are there any correlation between complement level and disease

activity? Explain.

Explain the complications of lupus.

Prognosis. Patient usually die of?

Management & advice to the patient

Systemic Sclerosis a.k.a Scleroderma

Epidemiology

A bit of pathogenesis

Types of scleroderma, how to differentiate them in PE.

What is CREST syndrome?

How do you differentiate a rheumatoid nodule, a calcinosis and a

gouty arthritis clinically?

Which complication of scleroderma is the most common?

What are the autoantibodies looked for to confirm scleroderma?

Can they be used to differentiate between the types? How?

Prognosis? What is the most common cause of death?

Management.

Psoriasis

What is it?Briefly describe the pathogenesis.

Explain the possible pattern of skin lesions. Which one is most

common?

Explain the types of joint involvements of psoriasis.

How to differentiate RA and psoriatic arthropathy?

Management

Seronegative spondylytis(SS)

Explain what is meant by this term.

Give examples of SS and explain.

Posted by Jeffreyat 7:42 PM

7 comments:

cheeweishen said...

Psoriasis:

It is a genetically- determined inflammatory and

proliferative disorder of skin charac by increased

epidermal turnover resulting in thickening of epidermis

with thick keratin deposition.

Possible patterns of skin lesions:

1. Pustular psoriasis

2. Guttate psoriasis

3. Flexural psoriasis

4. Erythrodermic psoriasis

5. Plaque psoriases- most common

Types of joint involvement:

1. Asymmetrical DIP arthropathy

2. RA like hands

3. Asymmetrical large joint mono or oligoarthropathy

4. Spondyloarthropathy and sacroilitis

5. Arthritis mutilans

For psoriatic arthropathy- there would be presence of

nail pitting, onycholysis with or without plaques on the

skin esp on the extensor surface and the arthropathy

mainly involves DIP while in case of RA, DIP joint as a

rule is not involved.

Treatment :

1) Topical: emollients, coal tar ointments, dithranol,

calipotriol

2) Systemic: steroids, MTX( in severe refractory disease)

Seronegative spondylitis:

1) rheumatoid factor seronegative 

2) usually larger joints are involved such as knees,

ankles and sacro-iliac joints

3) if peripheral joints are involved, they are usually

asymmetrical

4) characteristic articular features include enthesitis

( inflammation at sites of tendon insertion),dactylitis and

sacroilitis.

5) strong association with HLA-B27

Examples are: 

1. Ankylosing Spondylitis

2. Reactive arthritis

3. Psoriatic arthritis

4. Enteropathis arthritis

April 28, 2009 at 5:47 AM  

cheeweishen said...

Systemic Sclerosis:

More common in female 4 to 1 ratio.

Disease patterns:

1. Limited scleroderma

Scleroderma limited to face, neck and limbs distal to

elbow and knee

Usually begins with Raynaud phenomenon

CREST( Calcinosis, Raynaud’s, Esophageal dysmotility,

sclerodactylyl, Telangiectasia)

Anticentromere Ab

Renal crisis rare while pulmonary hypertension more

common.

Better prognosis.

2. Diffuse scleroderma

Scleroderma involving trunk and proximal limbs as well

as face and distal limbs

Usually begins with dactylitis and arthritis

AntiScl 70 Ab

Renal crisis more common than pulmonary hypertension 

Most common cause of death: renal failure

Management:

a) Supportive: NSAIDs, PPI, vasodilators

b) Specific: D-penicillamine

April 28, 2009 at 5:56 AM  

Jeffrey said...

Difference RA-Psoriasis

clinically your answer is correct. Confirm by doing blood

test where Psoriasis will often show normal ESR and no

rheumatoid factor.

Local treatment by intra articular injection of steroids

can also be employed in joint disease.

As for SS, one more example is infective,e.g. salmonella

arthritis.

In scleroderma, pulmonary fibrosis is second only to

dysphagia as a complication. SOme authorities said

dysphagia is not a complication, its a manifestation of

the disease. However the new term used "limited

cutaneous scleroderma" refers to skin manifestation,

therefore any internal disease is considered

complication. This makes Dysphagia as the most

common complication of scleroderma.

In diffuse scleroderma, besides anti

topoisomerase(Scl70), anti RNA polymerase I and III is

also frequently used and is highly specific.

I'm not sure bout this, but in Malaysia the most common

cause of death in scleroderma patient is cor pulmonale

due to pulmonary hypertension as a result of fibrosis.

Maybe what you read is different, being in a different

country.

Good one....most of your answers are the same as mine,

perhaps we're using the same book? hahaha..

btw you can add me to your facebook account at

jeffsylee@yahoo.com if you please...

Have a nice day:)

April 28, 2009 at 6:50 AM  

cheeweishen said...

thx... reali lucky to bump into u as i learn so many

things. lol

for the differentiation i think gouty arthritis would

presents with all signs of inflammation with or without

tophi overlying but for rheumatoid nodule it is local

swelling mainly over area of pressure e.g olecranon. for

sclerodactylyl the overlying skin would be smooth, shiny,

tight..

to be honest, i hav no ideas...lol

is it possible to explain why gout is common in MTP

joint( podagra)?

April 28, 2009 at 8:41 PM  

Jeffrey said...

Rheumatoid nodules are firm and most of the time its

non tender compared to Gouty tophy...the common sites

as you said is the olecranon, etc while tophy often

appear at the places where temperature is lower,e.g.

MTP joints and even earlobes

As for calcinosis, it is hard and non tender, as compared

to RN and tophy.

To recap

RN-firm,non tender

Calcinosis-hard,non tender with shiny tight skin etc

Tophy-hard,tender to touch

Why is the podagra most affected? It is not proven yet

but 1 hypothesis states that uric acid calcify better at

area with lower temperature and higher pressure. This

makes the podagra and the joints of the lower limbs

ideal for calcification. Haha i forget the chemical

equation, because I saw it in 1st year where i know

nothing about gout~ I think its in the new england

journal of medicine,but i forget what volume..

April 28, 2009 at 9:31 PM  

cheeweishen said...

thx once again... i think u can be a lecturer as well in the

future

Gouty arthritis- crystal arthritis characterized by

deposition of MSUM in the joints due to overproduction

of uric acid or under-excretion.

Risk factors: regarding to the pathogenesis

e.g if overproduction- maybe genetic e.g lesch nyhan

syndrome or env- lifestyle.

if underexcretion- maybe due to drugs such as thiazide,

low dose ASA; insulin resistance and aging

Pattern of joint involvement: small e.g finger and toes

joints and large joints e.g knee, ankle, elbow and wrist

usually mono-to pauciarticular involvement.

Regarding the attack, there r mainly 3 periods with

acute, intercritical and chronic tophaceous arthropathy.

Pseudogout- crystal arthritis characterized by deposition

of calcium pyrophosphate dehydrate.

Differences from the gout:

The pattern of joint involvement is different from gout,

tending to affect the wrists, knees, shoulders and

elbows 

Attacks are generally more prolonged (2–3 weeks). 

Pseudogout tends to affect more elderly patients,

usually on a background of nodal osteoarthritis. 

To confirm the diagnosis- joint aspiration to see

negatively birefringent crystal.

Tophi- chalky deposits of monosodium urate

In my opinion, I dun think it happens in gout case and I

think it happens with prolonged hyperuricemia.

Complication of prolonged hyperuricemia-uropathy??

For the acute attack- mainly analgesics like NSAIDs or if

CI or not effective- colchicines or again intolerant or CI-

intra-articular injection of steroids.

To reduce the attack rates- advice mainly non-

pharmacological e.g weight reduction, diet control esp

red meat, beans, alcohol, seafood or pharmacological if

indicated.

Seems like nobody wanted to revise on Gastroenterology, so lets play my favourite topic : Infectious Disease~

1) Classification of Fever

2) Causes of Fever

Respiratory tract infections

What is the most common etiologic agent?

What are the difference between influenza and common cold? Are there any difference in terms of treatment?

How often are influenza vaccines given?Any reasons?

What is pneumonia?Classifications based on anatomy?Common etiology? What are the signs and symptoms? How to manage?Causes of coughCauses of bronchiectasisWhat are the symptoms of bronchiectasis? Complications?Explain what is meant by empyema.

Neurological InfectionsDefine meningitis,meningism, encephalitis and encephalopathy.Route of infection of meningitis

Common etiology?SYmptoms of meningitisHow to differentiate viral and bacterial meningitis?What signs indicatate meningism? How to do it?Treatment for bacterial meningitis? How would you select the antibiotics?What is post infectious encephalopathy/polyradiculopathy? What etiology?What are 2 infectious causes of 7th nerve palsy? WHat syndrome do they cause? How to manage?

Neurology 1- Review of the Common diseases

Meningitis

Explain the layers of the meninges

Common etiology, and mode of infection.

What is meant by the term Meningism?

What signs can be elicited in a patient with meningitis? Is the sign

positive for any other conditions? How sensitive of specific is it for

meningitis?

How do you differentiate a viral,bacterial and fungal cause of

meningitis?

How do you do a lumbar puncture? What is the contraindications

and how to make sure there are no contraindications?

What are the complications of meningitis?

Principles of management.

Cerebrovascular accident

Stroke, stroke in evolution, Transient ischaemic attack and minor

stroke.....Define

How many types of stroke? How to differentiate?

What are the typical presentations of stroke?

Will the Babinski reflex be positive in the right foot of a patient

with a stroke of the right side of the brain?

What is the most common site affected if a branch of the middle

cerebral artery is involved? What would be the signs? What

happens if the trunk of the MCA is thrombosed?

A 61 year old man who is a known case of hypercholesterolaemia

presents to the A&E department with vomiting, dizziness and

numbness on the left side of the face for the past 1 day. On

examination,left sided partial ptosis and myosis,diminished gag

reflex, dysdiadakokinesia. and past pointing. Based on this

information, what do you think the problem is? What other signs

would you look for?

How would you manage an emergency case of stroke?

Thats all for now~more complex neurological problem coming

soon:D

Posted by Jeffreyat 10:47 PM

2 comments:

cheeweishen said...

Stroke:

TIA/ minor stroke- clinical syndrome charac by acute

disruption of blood flow to an area of the brain and

corresponding onset of neurologic deficits related to the

concerned area of the brain lasting less than 24 hours. 

Types of stroke-

1. Ischemic( embolic, thrombotic or cerebral

hypoperfusion)-80% of cases

2. Hemorrhagic ( intracerebral or subarachnoid

hemorrhage)

In case of embolic and hemorrhagic stroke, stroke dev

suddenly and in the latter case, it continues to worsen

with time.

In case of thrombotic stroke, it develops more gradually.

Typical presentation- focal neurological deficit related to

the artery involved e.g anterior , middle cerebral artery

syndrome and brainstem syndrome( posterior

circulation)

I dun think the babinski reflex would be positive in the

right foot if the lesion is in the right side as it is due to

cortical lesion such as internal capsule stroke that is due

to damage to the corticospinal tract which descend from

precentral gyrus thru internal capsule, midbrain

cerebral peduncle and pons and decussate at medullary

pyramids to supply contralateral limbs.

In case of a branch of middle cerebral artery

involvement, face and arms are most commonly affected

with contralateral hemiparesis( superior division),

contralateral homonymous hemianopia and Wernicke

aphasia( inferior division) while main trunk involvement

usually results in contralateral hemiplegia, eye deviation

toward the side of the MCA infarct, contralateral

hemianopia, and contralateral hemianesthesia.

As for the 61 yo man who presents with left sided partial

ptosis and miosis( Horner syndrome), vomiting,

dizziness( vestibular nuclei) , diminished gag reflex( IX),

dysdiadakokinesia. and past pointing( cerebellar sign), it

suggests lateral medullary syndrome due to involvement

of left posterior inferior cerebellar artery involvement.

So I would look for left-sided loss of facial pain and

temperature sensation with contralateral loss of pain

and temperature sensation.

For emergency case of stroke, I would say ABC+

depends on the type of stroke u suspect lo…

For ischemic- thrombolytics? ASA together with blood

pressure and glucose management as well.

For hemorrhagic- BP control with prevention of

vasospasm- nimodipine together with surgery.

Meningitis

Meninges- dura, arachnoid and pia mater

Etiology- irritation of meninges with microbial infection

or subarachnoid hemorrhage, drugs….

Meningism- triad of nuchal rigidity, photophobia and

headache which reflects the irritation of meninges.

Signs- nuchal rigidity, Kernig and Brudzinski sign. Which

my present in case of meningitis and SAH.

To differentiate the cause of meningitis, hmmm, I think

mainly from the history of patient together with Csf

analysis with lumbar puncture performed which involves

insertion of a needle to the spinal canal for the

extraction of csf. Contraindication for LP- lncreased ICP

which requires fundoscopy and CT.

Complications of meningitis-

1) Raised ICP

2) Hydrocephalus

3) Seizure

Principles of management of meningitis: depends on the

cause

For viral- mainly symptomatic

For bacterial- IV Cephalosporins 3rd or 4th generation

For fungal with antifungal- amphotericin

Actually when is steroids indicated? Dunno. Any ideas?

April 30, 2009 at 11:37 AM  

Jeffrey said...

Definition of TIA is the deficits last less than 24 hours

When the deficit last more than 24hrs, but less than 7

days, its called a minor stroke.

Stroke-in-evolution is when more symptoms appeared

until a full blown disease happen.

Typical presentation of a stroke patient depends on the

arteries involved. In most cases, the affected upper limbs

will be hyperflexed while lower limbs hyperextended.

In the case of lateral medullary syndrome, also look for

loss of convergence reflex and exagerrated jaw jerk. I

got this case for my short case:P

For acute management of ischaemic stroke, thrombolytic

should be given as fast as possible before neurological

deficit become permanent. rTPA e.g. Alteplase is

prefered in M'sia, while for some reason Streptokinase is

contraindicated(i forget why). Therefore for any case of

stroke a CT must be done and treatment given in 3

hours 

Steroids is generally avoided in meningitis except when

the disease cause increased in ICP which may cause

more serious damage. It is given then tapered off as soon

as possible.

Revision on Gastroenterology

Enough of politic rubbish which is able to make my blood pressure

shoot up. Now lets revise on gastroenterology

Common symptoms

abdominal pain or discomfort

Bloating

Nausea and Vomiting

Diarrhea

There are hundreds cause of abdominal pain from abdominal

trauma to carcinoma of the innards. It is easier to group together

the site of the pain to point to the problematic organ. Therefore,

there are upper,mid and lower abdomninal pain. Upper abdominal

pain mostly is due to problem in the stomach, liver, bile

duct,duodenum or pancreas. Mid abdominal pain often due to

small intestine and lower abdominal pain is due to large intestines

or the reproductive organs.

Question

How to differentiate between a visceral pain and a musculoskeletal

pain(abdominal wall pain) in the abdomen clinically(From physical

examination)? Not from Hx, not radiologically and not from

any investigation.

I will provide the answers only if anyone care to know or try

answering... :)

Lau hia, zhen hsiung, i tell u all before, faster answer hahaha :D

Bloating of the abdomen can be due to massive ascites and

overproduction of gas by the intestinal flora.

Easy question : How to differentiate by physical examination?

What makes overproduction of gas happen? Food (lactose

intolerant individual) and overgrowth of intestinal flora due to

stasis of the intestine can cause it.

Question

Sometimes patient complain of feeling bloated in the abdomen

when there are no overproduction of gas or ascites. what do you

think makes them feel that way? Hint : hypersensitive?

Nausea and vomiting- again there are so many causes. so just

classify them into GI and non GI cause. GI causes :

Infection,obstruction, inflammation Non GI cause : Neurological

e.g. motion sickness, increased ICP, Drug induced e.g.

alcohol,opiates,digoxin, hepatobiliary disease, UTI, pregnancy.

So when asking bout vomiting ask for the timing, the volume, the

content of the vomitus.

Question

Name 2 infectious agent that cause vomiting but no diarrhea

Diarrhea.......bermacam diarrhea.

Secretory diarrhea- too much excretion of fluid into bowel. Caused

by infection, neoplasm,endocrine cause e.g. carcinoid and Z-E

syndrome)

Osmotic diarrhea-the more you eat, the more the diarhea is. If you

fast it disappear.

Question: What's the most common cause?

Exudative diarrhea occur if there is inflammation of large bowel.

Small amount but frequent and may be bloody or mucoid. Common

cause is infection(Shigellosis and amoebiasis), IBD and

Malignancy

other special types such as fatty stool (Steatorrhea...correct

spelling rite?) may be cause by bile deficiency due to obstrution or

terminal ileum damage or drugs.

Question : Why is there diarrhea alternating with constipation in

patient with colon cancer?

What is peptic ulcer disease? What cause it? Presenting

symptoms?

What is the triple therapy for peptic ulcer disease caused by the

bacteria?

How do you manage hepatitis B and hepatitis C patients?

What are the complications of hepatitis?

Differences between Crohn's and UC?

Complications of IBD

What is functional dyspepsia and how to manage?

sounds fun hor....look it out la if free nothing to do..

Posted by Jeffreyat 5:58 AM

8 comments:

cheeweishen said...

since there r lots of questions, i would like to try out the

2 infectious agents which cause only vomiting without

diarrhea- are they B. cereus and Staph. aureus?

April 23, 2009 at 3:44 AM  

Jeffrey said...

you are right! There are 2 different pathology of

Bacillus.cereus enteritis giving 2 form of disease:

Diarrheal and Emetic forms. Both have different

pathogenesis~

Good one... may I know who are you?

April 23, 2009 at 6:54 PM  

cheeweishen said...

of course. i m a medical student too. lol.

if possible, i wana try out another question. to

differentiate musculoskeletal from visceral pain, in my

opinion, in the former, superficial tenderness would be

ellicited. 

hope i got it correct.

again, thx for sharing....

April 24, 2009 at 9:52 AM  

Jeffrey said...

superficial tenderness is elicited by light palpation of the

abdomen. However, it is difficult to differentiate deep

and superficial pain because if superficial tenderness is

elicited, deep palpation will result in pain also.

One sign to look for is the Carnett's sign(is the spelling

correct?). The theory in this sign is that if the pain is

from the abdominal wall, the pain will remain unchanged

or intensify if the abdominal muscle contract.

Starters for Internal Medicine

Endocrinology

Thyroid

What are the signs to look for when examining a patient with a

thyroid problem?

What is the best way to visualise a mass in the neck?

Are there any non pathological cause of hyperthyroidism? If yes,

how do we manage?

What is meant by thyroid storm?

a patient's blood test show that she have subclinical

hypothyroidism. Explain what is meant by this and plan your

management.

a 71 year old lady presented with anorexia, depression, weight

loss and muscle weakness for 2 years duration. There is no history

of heat intolerance or tremor. ECG showed changes consistent

with atrial fibrillation. On examination, the only finding is eyelid

ptosis. Neck examination show a mildly enlarged thyroid gland.

What is your differentials? What investigation would you do?

1. Know how to examine correctly. Not by theory, but you must show

that you have done it one hundred times. If you are not too confident

now, take one of your friends (same gender, of course, then you are

sure of your intention...) and examine each other on each of the

systems (CVS, Resp, CNS). Do it until you feel comfortable and

confident. It is always easy to examine a normal subject, and one

that you can repeat again and again - until you are happy yourself.

So choose a good friend, not one that will always laugh at you!

2. Make a list of the common cases, and know what to expect. The

following are not exhaustive:

o CVS:

Cardiac failure - leg oedema (don't forget sacral), JVP (know how to

assess correctly), ascites may be there too. Check for large pleural

effusion

Valves - BEWARE: mediastinal scar, and also infraclavicular scar

from pacemaker implantation. Check patient's pulse if in Afib

(irregular, irregular). Learn to differentiate systolic and diastolic

murmur. Honestly, you are less likely to be given a diastolic murmur

of mitral stenosis. If there is aortic regurgitation (early diastolic) they

may put the patient in exam. The usual, the most common one is

either pan-systolic murmur of mitral regurgitation, or mid-systolic

murmur of mitral valve prolapse. Occasionally VSD may be brought

in, and the murmur is quite easy and you will suspect this in a young

patient with left sternal pan-systolic murmur. Do not forget other

findings too, like malar flush, central line etc.

'Intermediate cases' - means not a very classic case eg. a patient

with pacemaker and has atrial fibrillation, may be put in due to lack of

cases.

In checking the pulse, complete everything - ie ensure the rhythm

is regular or irregular - many candidates hesitate when prompted -

that displays lack of confidence. This is a simple thing! Just keep

your finger on the pulse for long enough - between 20-30 seconds.

Tips on murmurs - listen long enough at two areas - apex (mitral)

and lower left sternal - most of the murmurs can be found there. At

least 30 seconds, if you are unsure, or if you cannot hear anything

on the first instance. Do not forget to check for radiation, for mitral -

axilla, for aortic - neck.

o Respiratory:

The common one is pleural effusion - be very fluent with the

features then it will come handy. Others like consolidation due to

pneumonia or malignancy (watch for clubbing). Then check

forlymphadenopathy.

Others - if there is pulmonary fibrosis for sure they will put in. (do

you know what are the features of pulmonary fibrosis?). Others are

like empyema, lung abscess, bronchiectasis (usually clubbing

with crepitations on lungs)

o Abdominal:

Hepatomegaly, splenomegaly, hepato-splenomegaly and renal

mass are the common cases.Beware! 'Abdominal' may actually

be haematological, or renal depending on the findings. So be open

minded. Obviously jaundice with hepatomegaly is abdominal (hepatic

eg hepatitis, liver failure/cirrhosis), while hepato-splenomegaly or

splenomegaly without features of chronic liver disease suggest

haematological - in this case be prepared to discuss

myeloproliferative or lymphoma as diagnosis.

If you find renal mass with fistula on the hand, then you should have

clearly in mind what diagnosis you are dealing with. All in all - be

fluent with differential diagnosis of each of:

Hepatomegaly

Splenomegaly

Hepato-splenomegaly

Other abdominal mass/renal (be prepared to discuss possibilities

of diagnosis)

Ascites

Of note, abdominal examination is a one system in which

examiner can assess whether you are gentle or rough with the

patient. One thing, as I made comment last time, when examining

for the liver and spleen, be sure you are pressing you tip of

fingers/hand in during inspiration, watch if patient has any

tenderness as well.

o CNS:

This is quite vast, so you must be prepared. Do not be overwhelmed

with whatever comes, as long as you know the right techniques, you

will pass. Many students simply do not know or cannot perform

correct CNS exam. You must be fluent with Cranial Nerves

exam, Upper limb exam andlower limb exam - do practice this.

Practice how to check for rigidity, how to perform correcttendon

reflexes, Hoffman's sign, Babinski, Cerebellar.

o Sound too overwhelming? I do not think so. You have undergone all

that, and we had dealt with each system on a real patient. All you

need is revise, and be fluent with the techniques.

3. Presenting the findings. This is an area where many fail to

impress, pity, after performing a good clinical examination, your effort

is wasted if you don't know how to present your finding. You also

need to practice this. Practice in front of a friend - or in front of a

mirror! for each case, eg practice presenting finding of a left upper

limb UMNL for instance, or atrial fibrillation with MVP.

When presenting:

o Look at the examiners - both if there are two of them

o Never look down or stare at patient, as if you have forgotten

something

o Present your finding as you have found them - no need to worry.

A clear case is clear, a less clear one is as is, even to the examiner.

If you have examined correctly, most likely your finding is correct -

present them as is, even is one finding seems to contradict the other.

As a yr 3, the examiner usually are willing to compromise, and

correct you, or give second chance, so always listen to the hint...

o Present the negative and positive findings - sometime negative

finding is important, so you mention them, this is to convey to the

examiner that you are looking for it, but have not detected it - as, in a

rare case, may be the sign is there, and you have missed it - you will

get a second chance. But if you did not mention at all, you may be in

trouble.

Examine the respi system1) Rheumatoid arthritis with lobectomy2)Lung Cancer3) Pleural effusion4) Bronchiectasis due to agammaglobinaemia

Examine the cardiovascular system1) Mitral regurgitation pansystolic murmur2) atrial fibrillaion

Examine the Neurological system1) Upper limb CVA2) Lower limb for ___?

Examine the neck for Graves disease

Examine the GI system for hepatosplenomegaly due to beta -thalassaemia

CVS: heart failure ( not sure about this but I met patients telling me they went upstairs for exam before) , murmurs

Respi: Pneumonia, P. effusion.

GIT: Hepatosplenomegaly plus its causes. I got this and the q was like : Examine the abdomen system. Read question carefully!

Neuro: Parkinson's, stroke, you get the drift la.

Endocrine: Cushing's, Diabetic foot, Hyperthyroidism

Others:Rheumatoid, Scleroderma, Thalassaemia,

For my scleroderma case, the q was like " Look at the patient and describe what you see." Oh ya, please recognise Raynaud's!!! It was super cold that time and I think my patient was having one episode of it.

Not too sure about renal system la, but if got polycystic kidney, could come out.

These are some of the short cases that we get.we were divided into ten stations with 2 cases in each stations.1) AR and TR2) hepatomegaly + Jaundice3) CCF 4) Guillain Barre Syndrome5) TB (mantoux test > 20mm induration)6) CVA - upper limb weakness7) AR8) Horner's syndrome9) Lymphoma10) Unilateral Ptosis due to surgical 3rd cranial nerve palsy. The patient is

chinese uncle from ward 1, the pupil is dilated with reduced constriction to light) According to the doc, the diagnosis is PCOM aneurysm.11) Ascites and hepatomegaly12)PSM13) Lower limb numbness14) Mitral stenosis15) TR16) Diabetic neuropathy

Cases that we expected but didn't come out were SLE, RA, Scleroderma, Cushing's etc. Dr rashidi said COAD is more for fifth year-spot diagnosis.

1) This patient is a 45 year old man complaining of recurrent episodes of syncope. Please examine the neck.

2)(A grossly obese patient with plethora lying on the bed) Look at this patient and conduct the relevant investigations.

3) (Patient on wheelchair with tremor) This patient have dementia and tremor. Conduct an examination to confirm the diagnosis.

4)(patient with tapered nose and stretched skin) Please examine the relevant systems.

5)(patient with partial ptosis) Please examine the eye.

Remember, ptosis is defined as drooping of the upper eyelid associated with

the inability to elevate the eyelid completely.

Before inspection, be reminded that it would be easier to examine with the

patient sitting up rather than lying down. ( Any examination on the head are

examined with the patients sitting up anyway) Here's a brief rundown of the

anatomy aspect of the possibl ptosis causes.

Key

Points for Inspection:

Is the ptosis genuine? ( There could be a pseudoptosis sign where the

"ptosis eye" is the normal eye and the seemingly normal eye is abnormal.

Deception can be great when panic strikes in short case exams. Usually it

can be due to facial nerve palsy, so look for other signs)

Is it unilateral or bilateral?

Is the ptosis complete or partial?

Look at the size of the pupil

- small pupils (miosis) in Horner's syndrome (look for other Horner's sign

such as enopthalmos, anhydrosis)

-large pupils (mydriasis) in 3rd nerve palsy which the eye is positioned down

and out and failure of reaction in of pupil to light as well as accommodation.

Be sure to rule out other trivial causes although unlikely:

-small eyes (Japanese, Korean, Chinese, etc)

-congenital ptosis

-mechanical ptosis due to edema, mass effect of tumor and scars

-botulism

For Myasthenia Gravis patient, you can try asking the patient to maintain an

upward gaze for more than 30 seconds (A gradual lowering of gaze is

indicative). Similarly, you can try to elicit the Pick's sign as mentioned by

Dekan, although it is very rare.

Finishing the Examination:

The

actions of the IIIrd, IVth and VIth nerves on the eye movements of the right

eye.

III= Oculomotor, IV=trochlear, VI= abducent

Completion

Say that you would like to take a history from the patient to try to find the

cause of their ptosis. (History is still essential anyway, but if your supervisor

says otherwise, follow him/her)

There are few common causes of ptosis you must be aware of among the

long list of rare ones:

Unilateral:

- 3rd cranial nerve palsy (complete ptosis)

- Horner's syndrome (partial ptosis)

- Syphilis

Bilateral:

-Congenital ptosis

-Myopathies (MG, dystrophia myotonica)

-Syphilis

Take Home Learning Issues:

1. State the causes of Horner's syndrome

2. Explain the management of Horner's syndrome

3. Revise the cranial nerve examination.

Syncope is defined as a transient loss of consciousness and postural tone,

with subsequent spontaneous recovery. This is usually precipitated by a

decrease in the blood flow to the brain.

For simplicity purposes, we shall divide it into 3 categories, namely cardiac

etiologies, neurologicaletiologies, as well as other causes.

1. Cardiac etiology

o Structural heart disease - this can cause an impaired cardiac

output, such as valvular disease (especially aortic stenosis) and

outlet obstruction (HOCM, hypertrophic subaortic stenosis).

o Arrhythmia - extreme abnormalities in the heart rate can alter the

cardiac output as according to the formula Stroke Volume X Heart

Rate. Bradycardia decreases heart rate while tachycardia may

decrease filling time, thus affecting the stroke volume, as well as

causing ineffective contraction. In short, very slow heart

rate(<30>180 bpm)such as ventricular tachycardia, supraventricular

tachycardia, ventricular fibrillation and sick sinus syndrome may

cause syncope as a result of significant reduction of cardiac output.

o Ischemia - that being said, any deficit of blood supply to the heart

would decrease the strength of contraction, affecting the cardiac

output as well. Therefore, in certain cases of acute coronary

syndrome, there are patients who came in presenting with syncope

as well.

2. Neurological etiology

o Neurally mediated disease - common causes includes vasovagal

episode, situational syncope and carotid sinus hypersensitivity. You'll

have to find out more yourself about these diseases.

o Orthostatic hypotension - this usually results from fall in blood

pressure on standing secondary to failure of vasoconstrictor reflexes,

as a result of volume depletion (dehydration), autonomic disorders

(Shy Drager syndrome) or anti-hypertensive medications.

o Cerebrovascular Accident - Stroke and transient ischemic attack

may also lead to syncope.

3. Others

o Hypoglycemia

o Pulmonary embolism

o Anemia

o Aortic disection

o ectopic pregnancyThese are the few major differentials in the causes of syncope. Thus, in history taking, the history of syncope in CVS is equally as important in CNS. Beware and keep in mind that syncope is not just neurological!

Sepsis & SIRS

Posted by medik-ukm on Monday, July 19, 2010

Infection:  Inoculation of pathogen into normally sterile tissue

Systemic inflammatory response is triggered by ischaemc, inflammation,

trauma, infection to protect the host from the damaging effect of insult.

However, the response can be overexaggerated when the damage and insult

is too great.

Systemic inflammatory response syndrome (SIRS) criteria---> 2 or more

of the following:

Temp: <36 or >38

HR: > 90 bpm

RR: > 20/ min

WCC: >12 X 10^9/L or <4X10^9/L

MAP: <65 mmHg (Systolic BP < 90 mmHg/ Diastolic BP < 60mmHg)

Sepsis: SIRS with the presence of infection (documented). 

Severe sepsis : SIRS with organ dysfunction (SOFA criteria)

Septic shock : Sepsis-induced hypotension despite fluid resuscitation

Sepsis Organ Failure Assessment (SOFA) criteria

Goal in treating sepsis :

1. MAP > 65 mmHg (To maintain BP > 90/60 mmHg)

2. ScvO2 > 70%

3. CVP: 8-12mmHg

4. Urine output > 0.5ml/kg/h

Recap MAP calculation:

MAP : (systolic - diastolic)1/3 + diastolic

1. There must be at least one joint with definite clinical synovitis. It

is stated in the criteria but often overlooked, even by young doctors/

Masters students. Hence, you don't simply overuse ultrasound to

diagnose synovitis unless you're unsure of your clinical skills (which I

had doubts of you being able to interpret the ultrasound by then)

2. This is a new case of possible RA. Previously treated RA will stay

as RA, hence you can't use this criteria to undiagnose patients with

RA.

3. Other causes of synovitis has been ruled out(not caused by other

disease, such as infective synovitis, etc.

Essentially, the 4 criterias used are:

Joints Involved, the types (Large/Small) and number: (0-5)

Serology (Low-positive/High-positive/Negative) of rheumatoid factor/ anti-

citrulinated peptide antibody(0-3)

Acute Phase Reactants (Normal/ Abnormal ) ESR/ CRP (0-1)

Duration of Symptoms (More / Less than 6 Weeks) : (0-1)

A score of 6/10 or more identifies patients with rheumatoid arthritis, but a

score of less than 6 does not rule out rheumatoid arthritis. Hence,

reassessment can be done as appropriate as the score may be cumulatively

fulfilled over time. 

*Click on image to enlarge*

*Click on image to enlarge*

Infranuclear opthalmoplegia

Posted by alvisto on Thursday, July 15, 2010

CASE :

Young male teenager presented with 1 week history of progressively

worsening vision of his left eye. He claims that he cannot see well with that

eye. He has fever and headache as well. He has severe facial acne.

Cranial nerve examination noted left sided external and internal

opthalmoplegia,and loss of sensation over the left forehead. Other

neurological examination is normal. What can be your diagnosis?

DISCUSSION :

All the 3rd, 4th and 6th cranial nerves, together with opthalmic branch (V1)

and maxillary branch (V2) run forward in the lateral wall of cavernous sinus.

V2 (maxillary branch of trigeminal nerve) leaves the mid-portion of cavernous

sinus to exit the skull through foramen rotundum.

V3 （mandibular branch) langsung not in the lateral wall of cavernous sinus

at all. Exits the skull through foramen ovale as soon as it leaves the

trigeminal ganglion.

So,

Retrocavernous sinus -> 3 branches of CNV, CNIII, CNIV & CNVI

Posterior portion of cavernous sinus -> CNV1, CNV2, CNIII, CNIV & CNVI

Anterior portion of cavernous sinus -> CNV1, CNIII, CNIV & CNVI

Questions :

1. What is the most likely diagnosis ?

Lesions at the left anterior portion of cavernous sinus, which is most probably

due to left cavernous sinus thrombosis secondary to facial acne.

2. What is internal and external opthalmoplegia ?

Internal -> paralysis affecting only the sphincter muscle of the pupil and the

ciliary muscle

External -> paralysis affecting one or more of the extrinsic eye muscles

Total opthalmoplegia -> Internal + External

3. Differential diagnosis ?

- Pituitary Tumour (Pituitary gland is situated between the left and right

cavernous sinus)

- Intracavernous carotid artery aneurysm

- Cavernous-carotid arteriovenous fistula

- Metastases (eg, nasopharyngeal carcinoma extension)

- Meningioma

- Sphenoidal sinusitis

4. What other condition can present with similar conditions ?

Lesions at superior orbital fissure -> Trauma, Tolosa-Hunt Syndrome

(idiopathic granulomatous disease)

Reason : After cavernous sinus, CN3,4,6 and V1 bersama-sama enter

superior orbital fissure. That's all.

5. Why facial acne cause Cavernous sinus thrombosis ?

Facial acne -> Acne pecah -> Kebetulan acne burst at the place of danger

area of the face -> bacteria enters Facial Vein -> ophthalmic vein connects

facial vein and cavernous sinus, and because these connections are

valveless, retrograde infections can spread from facial vein to cavernous

sinus -> Thrombophlebitis of the cavernous sinus -> haha !

6. Other signs/symptoms of cavernous sinus thrombosis ?

- Swollen eyelids, chemosis and proptosis

- Papilloedema

- Usually involves both eye

7. Name 1 condition very similar to cavernous sinus thrombosis ? State the

difference.

Orbital cellulitis. Jawapan dekat Dhingra pg 191.

Summary : Cavernous sinus thrombosis is more acute, involve both eyes.

8. How to confirm cavernous sinus thrombosis ?

CT scan

9. Other source of cavernous sinus thrombosis ?

Dhingra pg 191.

Please correct me if I am wrong, some of these questions is I sendiri fikir

punya. Thanks.

Source : Red book of neuro examination, Dhingra, Oxford

Morning hyperglycemia in Diabetics

Posted by alvisto on Monday, July 26, 2010

There are 2 conditions which can cause this :

1. Somogyi Effect

2. Dawn Phenomenon

1. Somogyi Effect

Also known as "rebound hyperglycemia"

Usually due to:

o missed night meals despite taking insulin regularly

o a person who takes long-acting insulin without supper

o night/ long-acting insulin dose too high

Relative Insulin Excess-> Early morning (2-3am) hypoglycemia ->

Body's counter-regulatory mechanism activated -> Hormones

(cortisol, glucagon, epinephrine) released to counter insulin effect ->

Morning Hyperglycemia

2. Dawn Phenomenon

Can occur in normal person

Exaggerated response in diabetics

In a normal human physiology, counter-regulatory hormones

(cortisol, glucagon, epinephrine) are released during early morning

hours to sustain blood glucose level without food. These hormones

also antagonize insulin effect, hence there is a relative higher insulin

resistance during the night.

In patients with Type I diabetics esp, insulin production is low, hence

there is an exaggerated Dawn phenomenon --> morning

hyperglycemia

It typically occurs (more often) in Type I diabetic patients during

puberty or pregnancy due to marked production of counter-regulatory

hormones (cortisol, glucagon, epinephrine, growth hormone), thus

also causing exaggerated Dawn phenomenon.

How to differentiate then ?

Check blood sugar levels (Dextrostix) around 2 - 3 a.m. for several nights.

If the blood sugar level is low at 2 a.m. to 3 a.m., suspect Somogyi

effect (Rebound phenomenon).

If the blood sugar level is normal or high at 2 a.m. to 3 a.m., it's most

likely Dawn phenomenon.

(which is even more likely if the patient is a type I diabetic at early

onset of puberty/ pregnancy, although Somogyi effect must be ruled

out first)

How to prevent/treat ?

Somogyi effect

Have regular meals and never skip them.

Have a light snack (preferably protein) before bedtime.

Go to bed with a glucose level slightly higher than usual.

Bring your diabetic logbook (with your result of early morning 2am-

3am blood glucose) while consulting your physician, in case your

insulin dose may require adjustments.

Dawn Phenomenon

Exercise  later in the day. It may have more glucose-lowering effect

throughout the night.

Limit bedtime carbohydrates and try more of a protein/fat type of

snack (nuts, peanut butter, cheese, or meat).

Talk with your doctor of a possible medication adjustment (usually

insulin) to control the higher fasting readings (common in DM Type I

at onset of puberty).

Eat breakfast to limit the dawn phenomenon’s effect. By eating, your

body will signal the counterregulatory hormones to turn off. ->

peliknya...

Why bother ?

Good blood glucose control is essential for diabetic patients. The adjustment

of medication (insulin) dose depends on which is the culprit, as one needs to

lower the blood glucose prior to bedtime (Dawn phenomenon) or increase

the blood glucose level prior to bedtime (Somogyi effect). 

Therefore, if the patient is having persistent morning hyperglycemia despite

increased insulin dose, suspect Chronic Somogyi.

Diabetic Neuropathy

Ok...i know exam is over,results are out. But i would like to share

these article as a revision for one of the most important disease in

Medicine, diabetes.

Diabetes can affect all 3 division of the nervous system:

sensory,motor and autonomic nervous system. The most common

early presentation of diabetic neuropathy will be numbness of the

extremities commonly described as "gloves and socks" numbness.

It is a form of peripheral neuropathy and because of that, it affects

all dermatomes. Therefore, during examination of diabetic foot to

look for numbness one need not test according to dermatomes.

Sensation is loss for both pain and light touch and for some

reason, temperature sensation is not affected. Loss of

proprioception is also an early sign, however, patient often does

not notice this because the dominating or main problem to the

patient is often sensory loss. The patient may also complaint of

gait instability. Therefore, this sign must be elicited by the

examining doctor.

In the motor division, neuropathy can take 3 forms : Acute painful

neuropathy, diabetic amyotrophy and mononeuropathy. Acute

painful neuropathy cause burning pain in lower limbs, typically at

night. In severe cases even light touch can become intolerable. It

can be precipitated by drugs such as itraconazole, commonly used

to treat fungal infection in diabetic patients. Diabetic amyotrophy

cause painful,marked wasting of the quadriceps femoris muscle. In

extreme cases it cause absent knee jerk reflex. Diabetic

mononeuropathy refer to involvement of only 1 nerve. The most

common mononeuropathy is the carpal tunnel syndrome. Diabetes

can also affect the cranial nerves, especially cranial nerve VII and

III, causing diploplia. If more than 1 nerve is affected, the

condition is called mononeuritis multiplex.

Autonomic neuropathy manifest in form of postural

hypotension,atonic bladder with urinary retention, diarrhea etc.In

long standing uncontrolled diabetes, gastroparesis can happen

leading to uncontrollable nausea and vomiting mimicking

intestinal obstruction. Diabetic patient often complain of syncope,

lethargy, dizziness. Note that sometimes, these signs can be a side

effect of the oral hypoglycaemic agent, e.g. diarrhea may be

caused by Metformin

,"why is there lucid interval in epidural hematoma?

The answer lies in the anatomy and the blood vessels involve.

My explaination:Epidural hematoma occurs when blood accumulate in the interface between the dura matter and the skull.It usually involve the middle meningeal artery which is located in the interface.When this artery rupture due to trauma or what not, blood will start oozing out. Being arterial, the blood pressure of course will be higher than those of venous originImmediately after trauma, patient(or should i say victim) is unconcious due to the impact of the trauma. He then regain conciousness and complain of nothing.In his head, the middle meningeal artery have ruptured. However, since the blood coming from it is accumulating between the dura matter and the skull, which are rigid structures, the hematoma takes time to form.The period between when the patient regain conciousness and when hematoma become big enough to cause symptoms is called the Lucid interval.

Patient may present with many abnormalities prior to 2nd loss of conciousness due to the hematoma, such as oculomotor nerve palsy. It depends on where the hematoma form.

Compare with subdural hematoma which is due to rupture of the bridging veins. Try to explain why no lucid interval in subdural hematoma.

Summary: Lucid interval happen in epidural hemorrhage because although blood is from a high pressure vessel(an artery), it accumulates in a tight space, thus takes time to accumulate enough to cause symptoms.

CardiologyPresentation of cardiac pathologyAngina-typesAngina-MI differenceSTEMI and NSTEMI and how to differentiate themComplications of MIPrinciple of management of MI and AnginaCCF-at least know the 3 most common cause i.e. MI,dilated cardiomyopathy and systemic hypertension, others such as congenital heart disease, valvular heart disease and cor pulmonale is additionalTypes of CCFEffect of CCF on CXR and ECGComplications of CCFHeart block-ECG changes(may be asked in long case)

Atrial Fibrillation-causes, effect and management. For causes, i use the mnemonic I SMART CHAP, there are other mnemonics such as CVS HaRUS CePat etc...use whichever 1 convenient

I=inflammatory condition such as pericarditis and pleuritis

S=sick sinus syndrome, in old people where there is idiopathic fibrosis of the sinoatrial nodeM=Medications such as verapamil, levothyrosineA=atherosclerosis of the vessels leading to ischaemiaR=Rheumatic heart diseaseT=thyrotoxicosis

C=congenital heart diseaseH=systemic hypertensionA=alcoholP=pulmonary causes e.g. pulmonary embolism and pneumonia

Infective endocarditis- Memorise the Duke criteria inside out,aetiologic agent and appropriate antibiotics is extremely important.many neglect this

Rheumatic heart disease-The bacteria involve, involve what valve, what is the extracardiac features(Duckett Jones criteria)Dont forget the drugs used to treat cardiac disorders.

Consent for Dilatation & curettage

Posted by medik-ukm on Friday, February 25, 2011

1. Introduction

2. Confirm the diagnosis

3. Tell the patient indication for the procedure – to remove retained POC

4. Explain the procedure

- this is aseptic procedure

- duration 15-30 minutes

- NBM at least 6 hours before procedure (ask last meal)

- give patient IV drip

- anaesthetist will review patient before operation to choose mode of GA/ regional

- done in operation theatre

- in lithotomy position

- clean and drape

- bladder catheterization

- vaginal examination to see os open/ close

- bimanual examination to know uterus size and position of cervix

- insert Sim’s speculum to visualize the cervix

-Use vulsellum to grab anterior lip of cervix

- insert uterine sound to measure length of uterocervical canal

- if os is closed, dilate with Hegar dilator – use from 3mm – 8mm

- ovum forceps is inserted to remove POC

- use blunt curate to remove POC

-Ask anaesthetist to give IV pitocin 40 unit to make sure uterus is contracted and

hard so not easily perforated

- use sharp curate until gritty sensation is felt

- hemostasis secured

-remove vulsellum

-send POC for HPE

- count for estimated blood loss

5. Explain complication to the patient

Short term

- uterus perforate

-Bleeding

-infection

Long term

-adhesion,difficult to conceived

-Asherman syndrome

-placenta previa,placenta accrete

6. Ask patient is she has any enquiries

Manual removal of placenta (MRP)

Posted by medik-ukm on Friday, February 25, 2011

 Failure to deliver the placenta within 30 minutes after delivery of the

fetus

 Management :

- monitor vital sign

-observe if there is sign of placental separation

-continue massage uterus

-if still no sign of separation , call MO

-insert large bore IV access (16-18 gauge)

-take blood and send for FBC & GXM

-do catheterization

- attempt control cord traction, if still failed, take verbal consent

for MRP

 Preparation:

1. Give IV antibiotic Flagyl 500mg stat and 400mg TDS + Ampicillin 1

gm stat and 500mg QID for 1 day

2. Ensure adequate analgesia ( GA, epidural ,spinal)

3. If patient already on epidural, procedure can be carried out in LR

 Procedure:

1. Put patient in lithotomy position

2. Clean and drape

3. Scrub and wear MRP gloves

4. Put left hand on abdomen to encourage uterus to contract

5. Re-attempt CCT

6. If failed, the left hand should remain on abdomen

7. Insert right hand into uterine cavity by following direction of

umbilical cord

8. If present of constriction ring at lower uterine segment, slowly

dilate cervical ring until hand able pass to fundus ( forcefully

dilate lead to vasovagal attack)

9. Plane of cleavage is identified

10. Assess degree of adherence and site of attachment of placenta

11. By moving fingers from side to side, this plane of cleavage is

extended until whole placenta free from wall of uterus

12. Placenta is then removed

13. Re-explore cavity to make sure cavity is empty

14. Abandoned procedure if there is placenta accrete

15. Give IM syntometrine / IV pitocin to promote uterine contraction

16. Check placenta for completeness

17. Continuous iv pitocin 30units in 500mls NS at rate 125mls/hr

infusion for 4-6 hours after procedure to maintain uterine

contraction

 Complication

-post partum hemorrhage

-infection

-if placenta accrete --> risk of hysterectomy

Counselling: Couple with Unexplained Infertility

Posted by medik-ukm on Friday, February 25, 2011

1. Explain to the patient wait and see

- spontaneous conception can occur after – 1 year 85%

2 years 90 %

3 years 92-95%

2. Lifestyle modification

- no smoking

- reduced alcohol consumption – female 1-2 units/week

- male 2-3 units/week

3. Avoid stressful condition

- spacing sexual intercourse 2-3days to make sure increase sperm count and

quality of sperm

4. Advice husband

- not taking hot bath or frequent sauna because this can reduced the sperm

count

- do not wear tight underwear -->wear boxer

5. Advice wife on cleanliness and hygiene

- if having vaginal discharge,seek treatment ,need to treat infection first

6. Give folic acid supplement to prevent neural tube defect

7. Give other choice to patient if they don’t want wait and see..

- if still young --> can wait

- if getting older --> clomiphene -->IUI --> IVF

Counselling: Trial of Scar

Posted by medik-ukm on Friday, February 25, 2011

1. Introduce yourself 

2. Confirm the patient's name and problem 

3. Inform the patient that it is good to have her husband together during

the discussion

4. Ask patient whether she knows about her condition, any preference

in her option

5. Inform the patient of the options that she has:

o vaginal delivery --> Trial of Scar 

o LSCS

6. Tell patient that we need to assess the patient condition first whether

the condition is favourable for:

o any short stature -->CPD 

o pelvic cavity size 

o exclude placenta previa 

o exclude other contraindication 

7. Explain that there is risk in every procedure

o risk of scar dehiscence 0.5% (if use oxytocin 0.8%, if use

prostaglandin 2.45%)--> Therefore need to deliver in tertiary

hospital where OT ,NICU and blood bank available

o  we will monitor her closely (baby and vital sign to see sign

of uterine rupture ie tachycardia, hypotension, vaginal

bleeding, sudden loss of contraction, scar tenderness,

continuous abdominal pain in between uterine contraction) 

o can give option to patient for epidural 

o however there is still risk of failed TOS --> need to proceed

to LSCS

8. Explain pro and con TOS

o fast recovery 

o but we don’t know exact time for delivery, need to see

progress of labour

9. Explained another option (LSCS), also explained pro and con

o risk of adhesion lead to difficult surgery 

o risk of injury to bowel and bladder 

o risk of bleeding and blood transfusion 

o the advantage is operation is done in planned environment 

o explain that 2nd LSCS will limit family size 

o if want to do BTL, can do together 

o explained that the next pregnancy should be manage by

LSCS

10. Give opportunity to patient to ask any further questions

11. Ask patient preference whether have decided or not 

12. If can’t answer question from patient, get an appointment to refer

patient to senior colleague or consultant for better picture 

13. Provide patient pamphlet for any further information

Counsel for pap smear

Posted by medik-ukm on Friday, February 25, 2011

1. Introduction

2. Ask patient if she know what we will do

3. Explain indication

-screening tool for cervical Ca

-yearly for two years,if normal then three yearly

- age 20-65 / once sexually active

4. Explain procedure

- duration is about 5-10 minutes

-no analgesia/ LA/ sedation given

- patient will feel uncomfortable during the procedure

-this is sterile procedure, wash hand,do aseptic technique, wear sterile

gloves

- in dorsal position with open leg

- clean the perineum first with sterile water

- do bimanual palpation to know the position of cervix

- insert the Cusco speculum

-visualize if there is any lesion or abnormality if vulva/vagina/cervix

-use Ayre’s spatula to take sample

- rotate the spatula 360⁰

-put the smear on the slide

-make sure the slide have name and RN

- fix the slide with cytofix/ alcohol

-send the slide to lab

-then remove the speculum

-the procedure is finish

5. Explain complication of procedure

-spotting

-if having heavy bleeding come to hospital ASAP

-infection

6. Result

- ready in 1-2 weeks

- if normal, we don’t call. But if abnormal,we will call

- futher management will be done if any abnormalities detected

7. Ask patient if any question

O&G Short case: UV prolapse

Posted by medik-ukm on Thursday, December 23, 2010

Please examine this elderly lady who complained of something coming

out from her vagina.

1. Introduce, establish rapport, ask permission, position the patient

(super duper mark in this)

2. If the question asked to examine the perineum, go straight to the

perineum by asking the patient to lie down in dorsal position and lift

up her cloth while we cover her anterior abdomen with a blanket.

Otherwise, do a general examination, or else you would miss the

causes, differentials and the complications of prolapse (ie, chronic

cough, cachexia to suggest malignancy)

3. Inspect the perineum. Observe for atrophic changes in the labia

majora, and any scars suggestive of trauma. Another sign of atrophic

changes is that the labia minora is no longer concealed as we can

see in non menopausal women. The pubic hair distribution should

also be commented upon. Look hard for any PV discharge or color

changes suggestive of inflammation due to infection or ischemia

(due to kinking of blood supply particularly the vein)

4. Ask the patient if she had any vaginal pessary inside her vagina. Ask

permission to remove it. Observe if there is any protrusion coming

out and comment on that protrusion. If there is none, ask patient to

cough. You should be able to see some urine dribbling down if the

patient had stress or mixed incontinence due to the prolapse. Then,

ask the patient to bear down or any other way which would make the

prolapse to come out (ie standing).

5. Now that the prolapse is out, examine the anterior part of the

prolapse. Comment on the dryness, discoloration, ulcer, pus. Look at

the urethra opening. If there is any swelling posterior to it, it is the

urethrocele. The mass had linear streak it is the bladder rugae lined

by the anterior vagina mucosa. The fold behind it is the border

between the vagina and the bladder...

6. Proceed downward and you can see the cervix opening. Determine if

the cervix is parous or not (ie, parous will have streak while

nulliparous will just had a dot opening) or any peduculated mass,

discharge, abnormal looking. 

7. Try to look at the posterior part but you should be able to see it

clearer later.

8. Palpate the uterus and determine the degree of prolapse. it is

second degree if not all uterus is coming out (ie you cannot get

above it while palpating the uterus upwards) or if you can get above

it means that the whole uterus had prolapsed and hence the third

degree prolapse.

9. Ask patient to be in the simms speculum (like the simms speculum

itself the patient head is flexed and the hip is also flexed to make a C

position). Now using a simms speculum and a sponge holder with

gauze inserted, move the posterior wall of the vagina back and use

the sponge holder to manipulate the front. Comment on the surface

of the prolapsed mucosa (ie, ulcer, skin changes, infection, pus).

Move the speculum downward a bit until you see a prolapse from

posterior vagina. If the prolapse is higher up it is the enterocele and if

it is lower down it is the rectocele. Also, comment on the surface.

10. Do a rectovaginal exam by inserting the index finger into the vagina

(ie like a VE) and the middle finger into the anus. You Should be able

to gauge the thickness of both hence the size of her perineal body.

The thinner the perineal body is, the weaker the supporting muscle it

attaches too.

11. Finish the examination by reintroducing the prolapse back into the

vagina and reapply the pesssary. The pessary should be

compressed and inserted upwards towards the umbilicus before

released inside the vagina (ie the anatomical pelvic passage)

remember to gauge the size of the pessary (by measuring tape)and

clean it with antiseptic prior to reinsertion.

Other systems to examine:

p/s the is controversy over doing a pap smear or not because of the dry

cervix)

1. Respiratory

2. Abdomen

3. Lower limb

4. Connective tissue defect like ehlers danhlos.

Normal Growth for Babies

From a paediatric's point of view, the growth of a child is extremely important.

I mean, what's the point of treating a child who is not growing well?

Conversely, a child who grows well rarely need treatment. Thus, knowing the

normal growth pattern of a child is essential to avoid unnecessary worry or

panic to both ourselves and the parents/

One of the parameters that will tell us whether the child is growing well

recently is the weight. Whenever a paediatric patient have a problem, the first

growth parameter that will be affected is the weight. Thus, it is essential we

know the normal weight variation and gain among paeds patients. How do

we know what weight is appropriate for the child?

The best way is of course by analysing the growth pattern using a growth

chart. Growth chart can show us whether the child is failing to thrive, stunted,

or just wasted with just one glance.

However, most of the time, especially in short case exams we do not have

the luxury of a growth chart. Most of the time, someone will just ask us "Is the

child's weight adequate?", and that can be the end of our exam.

There are some principles that need to be remembered. Firstly, when the

baby was born, he will lose almost 10% of his birthweight during the 1st

week. This is due to water loss, probably from inadequate milk production, or

loss of amniotic fluid swallowed while in the womb. This loss of weight is

absolutely physiological (provided the baby is active and feeding well), thus

there should be no fuss about this. By the end of the second week, the baby

should regain his birth weight.

From the 2nd week to 3 month of age, the baby should gain around 25 to 30

g per day depending on ethnicity and frequency of feeds. Thus, when a 2

month old baby with a birth weight of 3 kg come to us, the expected weight

should range from 4.05kg to 4.3 kg.

From 3 month to 12 month of age, the expected weight of the baby can be

calculated using the formula (X+9)/2, where X is the age of the baby in

month. A shortcut method is that the baby's weight should double its weight

by 6 month, triple its birth weight at 12 month

X=age in years from here onwards

From 1 year to 6 years of age, the weight can be calculated using the

formula (2X)+8.

From 6 years to 12 years, the weight can be calculated using formula [(7X)-

5]/2.

As for height, the child's height from age 2 to 12 years can be calculated

using the formula 6X+77.

Of course, these are all estimations. It raises alarm that there may be

something wrong with the growth of the child. Further investigations and

reference to growth chart is needed to confirm the suspicion.

Head circumference is the last parameter to be affected by any malnutrition

due to the brain sparing effect. However, head circumference measurement

is essential in cases of developmental delay or cerebral palsy. Normal head

growth will be 6cm in the first 3 month, 3cm in the next 3 month and 3 cm in

the next 6 month giving a total of 12 cm in 1 year. After that, the head only

grow around 2 cm per year. Note that in a premature baby, this rule only

applies when his chronological age reach term. (e.g. a premature 34

weeker's head will only start growing as above when he's 6 week old.)