KraYS Med Tips

Bifacial weakness (flow chart+table)

2011-11-23T15:46:00.000+08:00

Rhaumatoid Arthritis

2011-11-23T15:45:00.002+08:00

- Chronic systemic inflammatory disorder involving the joints

- Peripheral symmetrical non-suppurative arthritis

- Unknown cause (autoimmune)

- Onset : 30-50 years old

- F:M = 3:1

- Mnemonic for diagnosing RA: RF RISES

Ø Rheumatoid factor

Ø Finger / hand joints involved (>6weeks)

Ø Rheumatoid nodules

Ø Involvement of 3 or more joint areas

Ø Stiffness (morning) > 1 hour > 6 weeks

Ø Erosions on X-ray

Ø Symmetrical arthritis > 6weeks

Revised Criteria for the Classification of RA

1. Guidelines for classification

a. 4 of 7 criteria are required to classify a patient as having rheumatoid arthritis (RA).

b. Patients with two or more clinical diagnoses are not excluded.

2. Criteria^av

a. Morning stiffness: Stiffness in and around the joints lasting 1 h before maximal improvement.

b. Arthritis of 3 or more joint areas: At least 3 joint areas, observed by a physician simultaneously, have soft tissue swelling or joint effusions, not just bony overgrowth. The 14 possible joint areas involved are right or left proximal interphalangeal, metacarpophalangeal, wrist, elbow, knee, ankle, and metatarsophalangeal joints.

c. Arthritis of hand joints: Arthritis of wrist, metacarpophalangeal joint, or proximal interphalangeal joint.

d. Symmetric arthritis: Simultaneous involvement of the same joint areas on both sides of the body.

e. Rheumatoid nodules: Subcutaneous nodules over bony prominences, extensor surfaces, or juxtaarticular regions observed by a physician.

f. Serum rheumatoid factor: Demonstration of abnormal amounts of serum rheumatoid factor by any method for which the result has been positive in less than 5% of normal control subjects.

g. Radiographic(X-ray) changes: Typical changes of RA on posteroanterior hand and wrist radiographs that must include erosions or unequivocal bony decalcification localized in or most marked adjacent to the involved joints.

- ^avCriteria a–d must be present for at least 6 weeks. Criteria b–e must be observed by a physician.

Parkinsonism

2011-11-23T15:45:00.001+08:00

- A clinical syndrome characterized by (cardinal signs)

o Tremors (rest tremors)

o Rigidity (cogwheel)

o Bradykinesia (slowness in execution of motion / slow movement)

- Types of parkinsonism

o Primary parkinsonism = Parkinson’s disease (PD)

o Secondary parkinsonism – neuroleptics/antipsychotics (especially typical antipsychotics e.g. haloperidol), Wilson’s disease, stroke.

o Parkinsonism plus syndrome (PPS) – Progressive Supranuclear Palsy (PSP), Multiple System Atrophy (MSA).

[NB: since secondary parkinsonism is treatable thus it is important to recognized and accurately diagnose this.]

- Clinical diagnosis of PD:

o Asymmetrical signs of parkinsonism

o No clinical evidence of PPS & secondary parkinsonism

o Marked response to dopaminergic drugs

o Postural instability is the 4th cardinal sign, but it emerges late in the disease, usually after 8 years or more.

Proposed stages of Parkinson's disease (PD) based on extrapolations from pathologic, clinical and brain imaging studies. Broken black lines indicate that, by itself, Lewy (-synuclein) protofibril or fiber pathology is not sufficient to make the pathologic diagnosis of PD. Broken blue lines represent non-motor signs that usually precede clinical recognition of PD, including impaired olfaction, sleep and mood disturbances, and constipation. Broken yellow lines indicate that fluctuations may be less apparent in the late stages of PD. (Taken from Harrison's online)

- Treatment of PD:

o Early stage : dopaminergic drugs (i.e. dopamine agonist e.g. Mirapex / pramipexol & Requip / ropinirole)

o Late stage : brain surgery (Deep Brain Stimulation / DBS, pallidotomy & thalamotomy)

- Differences between PD & PPS

	Parkinson’s disease (PD)	Parkinsonism plus syndrome (PPS)
1	Response to dopaminergic drugs & brain surgery are good.	Poor response
2	Better long term prognosis (less aggressive course)	Poorer long term prognosis (more aggressive course)

Unilateral Facial Weakness (flow chart)

2011-11-23T15:44:00.000+08:00

Case based learning (COPD)

2011-11-23T15:42:00.000+08:00

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Speech disorder

2011-11-23T15:40:00.000+08:00

Dysphasia / aphasia

Ø Impairment of the production and/or the comprehension of spoken or written words.

Ø Content of speech is abnormal. (language dysfunction)

Ø Assessment: mnemonic - CNS-RW

1. Comprehension

· 3 step instructions:

i. close your eyes/闭上您的眼睛(chinese simplified)/ अपनी आँखें बंद करो (Hindi)/ tutp mata (Malay)

ii. lift up your left hand /提起您的左手(chinese simplified)/ अपने बाएँ हाथ उठा (Hindi) / angkat tangan kiri (Malay)

iii. touch your left ear /接触您的左耳朵(chinese simplified)/ अपनी बाईं कान स्पर्श (Hindi)/ sentuh telinga kiri (Malay)

2. Naming objects

· Pen, key, book, card

3. Spontaneous speech

· Ask about his day, family, visitors, occupation

4. Repetition of sentence

· I want to go to the toilet /我想要去洗手间 (chinese simplified)/ मैं शौचालय जाना चाहती हूँ (Hindi)/saya nak pergi ke tandas (Malay)

5. Writing

· Write a given sentence e.g. regarding residence – I live in an apartment at Damansara Utama./ 我在公寓居住在damansara utama(chinese simplified)/ मैं एक अपार्टमेंट में damansara utama में रहते हैं (Hindi)/Saya tinggal di Damansara Utara dalam sebuah rumah bertingkat.(Malay)

· Write out a given instruction – “lift up your left hand” /提起您的左手(chinese simplified)/ अपने बाएँ हाथ उठा (Hindi) / angkat tangan kiri (Malay)

Ø Types of dysphasia :

Clinical features	Expressive (Broca’s) dysphasia	Receptive (Wernicke’s) dysphasia	Conductive dysphasia	Nominal dysphasia
Comprehension	Normal	Impaired	Normal	Normal
Naming objects	Impaired	Impaired	Impaired	Impaired
Speech	Telegraphic (staccato speech)	Paraphasia Neologism	Paraphasia Neologism	Lack nouns
Repetition	Impaired	Impaired	Impaired	Normal
Writing	Impaired	Impaired	Impaired	Pauses (lack nouns)
Spontaneous	Non-fluent (mute if severe)	Fluent	Fluent	Pauses
Site of lesion	Left inferior frontal gyrus	Left superior temporal gyrus	Left arcuate fasciculus	Left temporal lobe

Dysarthria

Ø Imperfection in articulation of speech.

Ø Content is normal.

Ø Subtypes:

o ”Hot potato” speech = Pseudobulbar dysarthria

o Nasal speech = Bulbar dysarthria

o Scanning / staccato speech(syllable by syllable) = Cerebellar dysarthria

o Monotonous, soft speech = Parkinsonian dysarthria

Dysphonia

Ø Impairment in production of voice (soft / hoarse voice)

Ø Content of speech is normal.

Ø E.g. vocal cord palsy

Speech disorder (flow chart)

2011-11-23T15:39:00.000+08:00

Knowing the language of a disease

2011-11-23T15:38:00.001+08:00

Palpation of the radial pulse is often one of the first things that doctors do when examining a patient. The pulse is examined for its rate, rhythm and character. The peripheral pulses are also examined to see if they are equally and symmetrically felt. Each of these aspects of the pulse can offer diagnostic clues to the doctor who understands the language of diseases.

Here is an example of how an examination of the pulse allowed one doctor to make a diagnosis that startled his students.

Dr X was told that a particular patient had a heart murmur. He was not allowed to auscultate the patient to determine anything more about the murmur. He was only allowed to palpate the patient's pulse. Thirty seconds after examining the patient's pulse, Dr Sandy said: This patient has aortic regurgitation. His students, new to clinical medicine, were all stunned.
They asked him: How did you correctly diagnose a valve abnormality in the heart by simply feeling the pulse?
Elementary, my dear students, Dr X replied. I noted that the pulse was of a collapsing nature. Only a few conditions are associated with a collapsing pulse and a heart murmur. Aortic regurgitation is one of them.

Do you know what cardiac abnormality to diagnose when:

1. The pulse is of small volume and rises slowly to its peak? This kind of pulse is called the anacrotic pulse.

2. The pulse has two distinct peaks during systole? This kind of pulse is called the bisferiens pulse.

3. The pulse disappears during inspiration? This kind of pulse is called the paradoxical pulse.

Brother & Sister Liver

2011-11-23T15:37:00.001+08:00

A review article in the New England Journal of Medicine tells us about the increased cardiovascular risk in people who have non-alcoholic fatty liver disease. Non alcoholic fatty liver disease comprises a spectrum of conditions where fat accumulates in the liver to produce conditions like hepatic steatosis (simple accumulation of fat in the liver), non alcoholic steatohepatitis (or NASH, where the fat accumulation is associated with hepatitis) and cirrhosis liver. NASH is the condition where there is overt inflammation in the liver caused by the fat. It is this inflammation, overt or subclinical, that is believed to be responsible for producing those inflammatory cytokines that damage the liver (leading to cirrhosis) and the endothelium of blood vessels (leading to atherosclerosis and ischemic organ damage). Even before overt cardiovascular disease develops, people with NASH have subclinical evidence of increased atherosclerosis in their vessels as shown by an increased carotid intimal-medial thickness.

The diagnosis of non alcoholic fatty liver disease is often made by an ultrasound examination of the liver. The diagnosis of NASH is made when, in addition, there are elevated liver enzymes. Of course, one needs to exclude other causes (for example, viral causes) of elevated liver enzymes. Speaking of elevated liver enzymes, studies have found that an elevated gamma glutamyl transferase is more significantly correlated with cardiovascular disease than elevated levels of alanine transaminase.

Many people with non alcoholic fatty liver disease have features of the metabolic syndrome (abdominal obesity, hypertension, atherogenic dyslipidemia and abnormalities in plasma glucose). The metabolic syndrome has within it many risk factors for cardiovascular disease and so, it is not surprising that the treatment of non alcoholic fatty liver disease also focuses on treating these risk factors. In particular, treatment with insulin sensitisers (Metformin, Pioglitazone) are recommended for glucose abnormalities associated with non alcoholic fatty liver disease. Life style modification for weight reduction and to reduce abdominal obesity is also to be emphasised. Pioglitazone and Vitamin E may also be useful in reducing the inflammation and fat in this condition even though there is no evidence yet that these can prevent cirrhosis.

1st link
2nd link

HyperNa+ & hyperK+

2011-04-19T08:15:00.003+08:00

Dear Goh,

Hypernatremia:

Definition:
- Serum sodium > 145 mEq/L (> 145 mmol/L)

- Increased thirst and water intake is the first defense against hypernatremia.(An intact thirst mechanism usually prevents hypernatremia. Rarely, excessive sodium intake may cause hypernatremia)

- Urine osmolality helps differentiate renal from nonrenal water loss.

Treatment (Type of fluid for replacement):

1) Hypernatremia with hypovolemia

– Severe hypovolemia: give 0.9% saline (osmolality 308 mosm/kg) to restore volume deficit and treat hyperosmolality, followed by 0.45% saline to replace any remaining free water deficit

– Milder hypovolemia: give 0.45% saline and 5% dextrose in water

2) Hypernatremia with euvolemia

– Encourage water drinking or give 5% dextrose and water to cause excretion of excess sodium in urine

– If GFR is decreased, give diuretics to increase urinary sodium excretion; however, diuretics may impair renal concentrating ability, increasing quantity of water that needs to be replaced

3) Hypernatremia with hypervolemia

– Give 5% dextrose in water to reduce hyperosmolality, though this will expand vascular volume

– Administer loop diuretic (eg, furosemide, 0.5–1.0 mg/kg) intravenously to remove excess sodium

– In severe renal injury, consider hemodialysis

Hyperkalemia:

Definition:

- Serum potassium > 5.0 mEq/L ( > 5.0 mmol/L)

- Hyperkalemia may develop in patients taking angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBs), and potassium-sparing diuretics, or their combination, even with no or only mild kidney dysfunction

- The ECG may show peaked T waves, widened QRS and biphasic QRS–T complexes, or may be normal despite life-threatening hyperkalemia

Causes:

1) Spurious

– Leakage from erythrocytes, marked thrombocytosis or leukocytosis

– Repeated fist clenching during phlebotomy

– Specimen from arm with K+ infusion

2) Decreased excretion

– Kidney disease, acute and chronic

– Renal secretory defects, eg, interstitial nephritis, sickle cell disease

– Hyporeninemic hypoaldosteronism (type IV renal tubular acidosis), eg, diabetic nephropathy, heparin, AIDS; adrenal insufficiency

– Drugs that inhibit K+ excretion (spironolactone, triamterene, eplerenone, ACE inhibitors, trimethoprim, nonsteroidal anti-inflammatory drugs)

3) Potassium shift from within the cell

– Burns, rhabdomyolysis, hemolysis, severe infection, internal bleeding, vigorous exercise

– Metabolic acidosis

– Hypertonicity (solvent drag)

– Insulin deficiency

– Hyperkalemic periodic paralysis

– Drugs: digitalis toxicity, -adrenergic antagonists, succinylcholine, arginine

4) Excessive intake of K+

– Ingestion or iatrogenic

Treatment:
(Treatment consists of withholding exogenous potassium, identifying the cause, reviewing the patient’s medications and dietary potassium intake, and correcting the hyperkalemia.)

1) Intravenous bicarbonate,(50 mEq IV over 5 minutes, raises urinary and blood pH. Onset of action within minutes. Only likely to be efficacious if underlying acidosis present.)

2) Calcium (Calcium chloride or calcium gluconate - these are cardioprotective only & don't lower calcium levels. One ampule of calcium chloride has approximately 3 times more calcium than calcium gluconate. Onset of action is < 5 min. Doses should be titrated with constant monitoring of ECG changes during administration; repeat dose if ECG changes do not normalize within 3-5 min.), and

3) Insulin given together with 50% dextrose may be appropriate. (Insulin temporarily shift K+ into cells; Glucose prevents hypoglycaemia.)

Avoid calcium if digoxin toxicity is suspected. Magnesium sulfate (2 g over 5 min) may be used alternatively in the face of digoxin-toxic cardiac arrhythmias. Check out this table for better understanding.

Click here to download

Some examples on how questions should not be answered - from the recent final year IMU examination

2011-03-01T08:13:00.000+08:00

1.

Examiner: So, your patient has diabetes. Ok. Tell me, what is your opinion about his diabetic control?
Student: Um. The patient is asymptomatic; therefore his diabetic control is good.

2.

Examiner: You said the abdominal wall shows guarding. What do you think is the reason?
Student: I think it is because of peritonitis
Examiner: Is the patient able to eat? Does she have vomiting?
Student: No vomiting. The patient is quite comfortable and eats normally.

3.

Examiner: What do you hear on auscultation of the chest?
Student: I hear a pansystolic murmur at the cardiac apex and the same murmur is also heard in the tricuspid area.
Examiner: What is the diagnosis?
Student: Ventricular septal defect.
Examiner: Why do you say so?
Student: Because the murmur is best heard at the cardiac apex.

Did you know?

2011-02-25T13:01:00.000+08:00

No disease in the history of medicine has ever been eradicated by treatment alone. Advances in treatment for diseases do not translate into eradication of diseases in populations. Only measures like improved sanitation and hygiene, improved living spaces, improved economic well being and vaccination have resulted in eradication of diseases.

Knowing the language of a disease

2011-02-03T05:35:00.000+08:00

Rashes

2011-01-22T11:08:00.011+08:00

A raised, reddish, patchy with irregular bordered margins, silvery-whitish scale, over the elbow measuring around 10 cm x 8 cm.

It is important to describe what ever you see in totality. This is just a rough guide - nature of the rash (raised or flat), colour, shape, margins, any characteristic signs/nature of rash that will give away the diagnosis of a particular rash, (for e.g. silvery scale in psoriasis)and site of the rash seen. These are not placed in order and should only be used as a guide. I personally prefer to tell the location of a rash first. (E.g. I see a rash over Mrs. X's elbow. It is a raised, reddish...etc)

While describing a rash seen is VERY important to come to a diagnosis, NEVER forget that the patient's age, gender and presentation of illness are also an EXTREMELY important aid in coming to a diagnosis.
________________________________________________________________________

There is a rash seen on the left, anterior to medial, middle half shin of Mr. X. It is measuring around 8 cm x 7 cm, erythematous, tender (I'm sure it is!), swollen (compare both sides of his leg) with shinny skin (these are the give away, after this...its quite pointless to go on..), with poorly defined margins with some satellite lesions (red round patches seen around the main big patch).

It also gives a BIG plus point if you can add a point or two from your history taking (e.g. the site of the current rash is over a previous wound while Mr. X was gardening, cuts, blisters, burns, insect bites, surgical wounds.) This helps seals the diagnosis of cellulitis.
________________________________________________________________________

This is rash seen all over the back of Mr. Z. It is flat, erythematous (maculopapular rash), typically described as isles of white in a sea of red, that is blanchable (disappears upon pressure). Putting this together with his symptoms of fever, body aches and retro-orbital pain, with the leucopenia and thrombocytopenia, a diagnosis is easily established. Though not shown here, the rash in dengue is usually centipetal. This means that the rash starts on the limbs before "moving" or spreading to the trunk (differentials would be coxsacki virus, secondary syphilis, rRocky mountain spotted fever, smallpox). Centrifugal means the rash starts on the trunk (differentials would be chickenpox, rubella, measles (rubeola), & typhus.

_______________________________________________________________________

I'm sorry I can't put up more pictures as there are just too many to mention here. However, I hope that you get the idea of it. :)

Re: Raymond 2

2011-01-08T20:48:00.003+08:00

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Re: Raymond

2011-01-06T21:13:00.002+08:00

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Influenza vaccination, a trick or a treat?

2011-01-03T21:23:00.002+08:00

Suppose a healthy adult comes to you and asks: "Do you think I should take the Influenza vaccine?"; What will you advice? In order to answer that question you will need to know how effective the Influenza vaccine is in protecting people against Influenza, as well as the degree of risk due to the vaccine itself. Reading the article below from the Cochrane Review might help you answer that question.

Link

The Cholera threat...

2010-12-12T13:06:00.003+08:00

There is currently an epidemic of cholera in Haiti. Should all patients with cholera be treated with antibiotics? International guidelines recommend that patients with moderately severe and severe cholera be treated promptly with antibiotics. How do we differentiate between a mild case, a moderately severe case and a severe case of cholera? We can do that by looking at the degree of dehyration. A severe case of cholera is one where the dehyration amounts to 10 percent or more of the body weight. A moderately severe case is one where the dehydration amounts to 5 to 10 percent of the body weight. And a mild case will be one where the dehyration is minimal, less than 5 percent of body weight.

So, what are the antibiotics that can be used for cholera? Doxycycline, Azithromycin or Ciprofloxacin can be used.

Should contacts of cholera patients be given prophylactic antibiotics? The answer is No. Finally, when should a doctor suspect cholera? Cholera should be suspected in any diarrhoeal illness of short duration (less than 24 hours) which is associated with dehydration. Vomiting often accompanies the diarrhoea and there is no fever.

This site has the WHO guidelines for cholera treatment and a good write-up on the antibiotics of choice for the disease.

(NB: Only a single dose of an antibiotic is needed for treatment of cholera. Either 300mg OD Doxycycline or 1gram OD Azithromycin or 1gram OD Ciprofloxacin)

Re: Egbert hee

2010-12-03T10:45:00.003+08:00

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Re: Embert Lee

2010-11-15T02:38:00.004+08:00

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Re: Jason Chan

2010-11-07T21:31:00.015+08:00

Dear Jason Chan,

In response to :"hi there, i saw some article explains that rehydration therapy is divded into phases: phase 1 - 20ml/kg bolus NS or HM for the 1st hr, phase 2 - 2nd-8th hr, give 1/2 of deficit and maintenance then phase 3 give the remaining 50% in the remaining 16 hrs. my question is how can we decide what type of fluid to be introduced into the patient in phase 2 and 3 and when is necessary to give additional KCl? thx"

Yes, well said Jason. The formula that you mentioned is ABSOLUTELY right and is used. However, I have so far seen Neonatologist use that formula more for neonates. I believe it is a very cautious formula and in general peadiatrics, it is a good rule to follow. So, YES. I would encourage you to use the formula.

As for the type, it depends on the purpose of the fluids being used for. To come to an accurate choice requires a good understanding of the contents of each fluids i.e. Normal saline and Hartmann's solution. (which is not explained further here unless requested...:))

Having said that, the use of which type of fluids also varies from hospital to hospital and doctor to doctor. It is personal. In your reading, research & working experience, you'll have to come to a choice of your own. However, generally Normal saline is used for administration of intravenous drugs & quick fluid resuscitation (but there are also doctors who use Hartmann's). Hartmann's is regarded as the solution that most resembles the human plasma electrolyte contents, therefore it is best used to replace any fluids lost i.e. maintenance fluids and (since it has a considerable amount of electrolyte) for raising/maintaining the blood pressure.

As for KCl, it is ultimately given as both the patients' requirements (too sick to eat, losing too much fluids, etc) and either fluids (NS or HM) aren't sufficient. However, it is always wise to take a renal profile to assess the potassium level (as patients with chronic renal failure would have high potassium levels) and proceed as necessary. (the formula to how much KCl to give is not discussed here unless requested. :) )

Does this answer your questions? I hope so. :)

Re: Mark Lee

2010-11-03T20:16:00.004+08:00

Dear Mark Lee,

Basically, the fluid management for children (& elderly) is MORE tedious as compared to an adults'. Having said that, its' not wrong (in fact, it is better) to actually use the formula used for management of fluids in a child on an adult.

However, since adults have a better tolerance of fluids imbalance as compared to a child, they are able to take (slightly) more/less of fluids than the body needs if given by any physician.

Therefore:

1) The clinical manifestations of dehydration can still be used in an adult (the table in my previous pdf file.)

2) However, the initial resuscitation steps for an adult during the ABC need NOT use the 20ml/kg body weight formula. Just run a pint (500ml) of Hartmann's solution or Normal Saline and check for the patients' haemodynamic status after each pint. Repeat this until the patient is stable. (you don't need to count to the exact amount of fluids needed as compared to a child.)

[NB: For extreme ages (children & elderly), the imbalance of fluid tolerance levels are less. This means that for this age groups, it’ll be VERY wise to provide the amount of fluids that is loss or needed, no more or less. So, you'll have to calculate the fluids needed in this age group.]

3) The formula to estimate maintenance requirements still remain the same for an adult as for a child.

[NB: For young adults who you decide to be less accurate in the management of fluids, do LOOK OUT for signs & symptoms of fluid overload, most notably-pleural oedema.]

Re: Rachel

2010-10-24T19:12:00.000+08:00

- All pregnant women should be screened for gestational diabetes unless they are in a low-risk group. (at 28th week)

- Women at high risk for gestational diabetes are those
- >25 years of age;
- those with a body mass index > 25 kg/m2,
- maternal history of macrosomia or gestational diabetes,
- positive diabetes in a first-degree relative;
- high-risk ethnic group (African American, Hispanic, Native American).

- two-step strategy for establishing the diagnosis of gestational diabetes involves
- administration of a 50-g oral glucose challenge with a single serum glucose
measurement at 60 min.
- <7.8 mmol/L (<140 mg/dL) = normal.
- > 7.8 mmol/L (>140 mg/dL) = administration of a 100-g oral glucose challenge
with serum glucose measurements obtained in the
fasting state, and at 1, 2, and 3 h.
- Normal = <5.8 mmol/L (<105 mg/dL), 10.5 mmol/L
(190 mg/dL), 9.1 mmol/L (165 mg/dL), and 8.0
mmol/L (145 mg/dL), respectively.

- Pregnant women with gestational diabetes are at increased risk of:
- preeclampsia,
- delivering infants who are large for their gestational age,
- birth lacerations.
- (after birth) fetuses are at risk of hypoglycemia and birth trauma (brachial
plexus) injury.

--> Treatment of gestational diabetes with a two-step strategy of dietary intervention followed by insulin injections if diet alone does not adequately control blood sugar [fasting glucose < 5.6 mmol/L (<100 mg/dL) and 2-h post-prandial <7.0 mmol/L (<126 mg/dL)] is associated with a decreased risk of birth trauma for the fetus. (Usuaully, most pregnant mothers' glucose levels are controlled by diet modification alone. Compliance to these diet restrictions are usually the culprit for high blood sugar.)

- For women with gestational diabetes, within the 10 years after the index pregnancy there is a 80% (Malaysia) risk of being diagnosed with diabetes. All women with a history of gestational diabetes should be counseled about prevention strategies and have an annual screening for diabetes (according to Malaysian CPG).

- In general, during the first trimester, the initial insulin requirement is 0.7 units/kg per d. By late pregnancy, patients generally require 1 unit/kg per d.

--> Generally, 2/3 of the total insulin dose is given in the morning and 1/3 in the evening. Usually, 2/3 of the morning dose consists of NPH (NPH = Humulin N: intermediate type)and 1/3 of regular insulin. The evening dose consists of half NPH and half regular insulin. Determination of the exact amount of insulin for each pregnant woman is done on a case-by-case basis. Start with the safe amount of insulin units by using the formula above (Usually 1 unit/kg per day), and slowly increase/decrease by 4 units if the blood sugar level results are high/low respectively.

--> Usage of metformin:
- Recent evidence suggests that glyburide or metformin are safe and effective
alternatives. However...
- Fetal, neonatal, and maternal outcomes have been evaluated following maternal
use of metformin for the treatment of GDM and type 2 diabetes. Available
information suggests that metformin use during pregnancy may be safe as long as
good glycemic control is maintained; however, many studies used metformin
during the second or third trimester only.
- Therefore, until further research is done (on the 1st trimesters), treatment
with oral hypoglycemics in Malaysia (and many other countries) is NOT advocated
as the routine 1st line treatment(as it increases the risk of congenital
malformations. ), as Insulin is the drug of choice for the control of diabetes
mellitus during pregnancy.

Shock! A brief overview.

2010-09-20T22:40:00.000+08:00

Prof: What is the first line therapeutic strategy for those in shock?
Student: Administration of intravenous fluids.

Prof: That is right. But what if the blood pressure remains low in spite of fluid resuscitation?
Student: Give vasoconstrictors.

Prof: Right again. What are the vasoconstrictors commonly used for shock?
Student: Dopamine, Dobutamine and Norepinephrine.

Prof: Which is better - dopamine or norepinephrine?
Student: I am not sure.

Prof: Vasoconstrictors differ in their degree of alpha adrenergic, beta adrenergic and dopaminergic effects. Dopamine and norepinephrine (noradrenaline) both have alpha and beta adrenergic effects but norepinephrine stimulates alpha adrenergic receptors more than beta adrenergic receptors. Stimulation of alpha receptors will bring up the blood pressure more effectively but at the cost of reduced splanchnic and renal blood flow. Dopamine also stimulates dopaminergic receptors which norepinephrine does not. Stimulation of dopaminergic receptors helps to improve blood flow to the internal organs and kidney but has a deleterious effect on the hypothalamic pituitary axis because it results in reduced prolactin and growth hormone levels. So you can see that there are good and bad points for both norepinephrine and dopamine. A study was published in the March 2010 issue of the New England Journal of Medicine which compared the effect of these two vasoconstrictor agents in shock. You can read the article HERE. You can see from it that both these agents are good as initial therapy for shock. But based on this study it would be preferable to use norepinephrine rather than dopamine for cardiogenic shock.

2 better than 1?

2010-08-16T11:06:00.002+08:00

There is enough evidence to suggest that lowering LDL cholesterol helps decrease the incidence of coronary artery disease. It is a bit of a surprise therefore to learn from the ENHANCE trial that a greater degree of LDL cholesterol lowering with the combination of Ezetimibe and Simvastatin, when compared to Simvastatin alone, did not have any significant impact on the carotid intima-media thickness.

The IMPROVE IT trial is now underway to study if this combination of Ezetimibe and Simvastatin will be better than Simvastatin alone in reducing cardiovascular events.

For now, there is no evidence to recommend that the combination of ezetimibe plus simvastatin is better than a statin alone for patients with elevated LDL cholesterol levels.

Note:
Exetimibe is a drug that lowers LDL cholesterol by reducing intestinal absorption of cholesterol.

Simvastatin is a drug that lowers LDL cholesterol by affecting a key enzyme in the liver.

Carotid intima-media thickness is a marker of atherosclerosis in the carotid artery.

Rosiglitazone, from Hero to Zero.

2010-08-09T11:25:00.011+08:00

In the years that followed the launch of rosiglitazone, there were many papers on its usefulness for patients with diabetes. There were papers that showed the drug’s effectiveness in reducing blood sugar when used alone example and also when used in combination with sulphonylureas example or metformin example . Some other notable trials that showed beneficial effects of rosiglitazone were the DREAM trial and the ADOPT trial. In the DREAM trial investigators showed that rosiglitazone could reduce the development of diabetes in those who had impaired fasting glucose or impaired glucose tolerance while the ADOPT trial showed that rosiglitazone was better than metformin or a sulphonylurea in maintaining glycemic control as monotherapy.

Problems with the drug began to surface in 2007. In early 2007, the first reports that rosiglitazone was associated with osteoporosis and an increased fracture risk appeared - See here. Then, in June 2007 a meta analysis published in the New England Journal of Medicine showed that patients on rosiglitazone had a greater risk of suffering a myocardial infarction - (Read the article).

Food for thought

2010-07-27T01:12:00.002+08:00

Reference: The Lancet

Lung cancer (teratment)

2010-05-08T15:31:00.001+08:00

- The treatment of lung cancer is dependent on the type and stage of cancer.
- The treatment explained here is only a summary:

1) Non-small cell lung cancer

* Stages IA, IB, IIA, IIB & some IIIA :

- basically the tumour is resected with / without removal of the lymph nodes in the mediastinum.
- post-operative radiotherapy is only advocated for selective patients.(with N2 disease if no neoadjuvant chemotherapy)

* Stage IIIA & IIIB

- The treatment for this stage of lung cancer is a little more complicated in that it depends also on the nature of the tumour i.e. bulky, with/without chest wall invasion,etc.
- It is suffice to say that resection of tumour is followed up with chemotherapy or radiotherapy.

* Stage IV & more advanced IIIB

- For this stage, radiotherapy to site of the involved area for relieve of symptoms.
- Chemotherapy for ambulatory patients.
- Resection of primary tumour and tumour spread (metastases) will be considered.

2) Small cell lung cancer

- limited stage (good performance status) : chemotherapy + chest radiotherapy
- Extensive stage (good performance status) : combination chemotherapy
- complete tumour responders (all stages) : consider prophylactic cranial radiotherapy
- Poor-performanc-status patients (all stages) :modified-dose combination, palliative care.

3) All patients

- radiotherapy for brain metastases, spinal cord compression, weight bearing lytic bony lesions, symptomatic local lesions.
- encourage to stop smoking.
- supportive care during chemotherapy.

Bundle branch block

2010-04-06T18:24:00.002+08:00

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Teratoma

2010-03-23T22:43:00.002+08:00

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Pure Tone Audiometry

2010-03-15T15:46:00.003+08:00

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Lung cancer (Histological classification)

2010-03-09T07:20:00.001+08:00

Bronchogenic carcinomas of primary lung cancers can be classified as follows:

o Non small cell lung carcinomas (NSCLC) : This accounts for 70 -75% of bronchogenic carcinomas and can be further subdivided into:

§ Squamous cell carcinoma (25-30%)

§ Adenocarcinoma (30-35%)

§ Large cell carcinoma (10-15%)

o Small cell lung carcinoma (SCLC) : This chalks up 20 – 25% of bronchogenic carcinomas and comprises mainly of a group of cancers called oat cell carcinomas.

o Combined patterns : this consists of the various types of combinations of NSCLC and SCLC e.g. combined squamous & adenocarcinomas and combined squamous cell carcinomas & SCLC.

Endometriosis

2010-02-19T11:52:00.004+08:00

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Lung cancer (Incidents and risk factors)

2010-02-08T08:54:00.001+08:00

- Lung cancer accounts for around 19% of all cancers and 27% of cancer deaths.

- The incidence is increasing in women (due to the increase in women smokers).

- The major risk factor for lung cancer is cigarette smoking.

- Other risk factors:

o Passive smoking - being near smokers and inhaling the smoke which is being exhaled by smokers increases the risk to twice that of non-smokers.

o Heavy metal exposure - exposure / working with heavy metals e.g. nickel, chromium, vinyl chloride, arsenic for prolonged periods of time.

o Asbestos exposure - increases the risk of non-smokers by 5 fold & 55 times greater in smokers.

o Chronic Obstructive Pulmonary Disease (COPD) (check out my writings on COPD)

o Industrial carcinogens - products from factories that cause cancer e.g. chloromethyl ether.

o Lung scars - e.g. post-tuberculosis infection

o Air pollution - prolonged exposure

o Hereditary - genetic factors

Re: rachel

2010-01-19T08:27:00.003+08:00

Hi rachel, I can't read your lecturer's mind but maybe this is what he's thinking...both asthma and COPD present clinically with breathlessness or acute exacerbations.

However, asthma usually presents with reversible symptoms and interference with normal activity of various degrees i.e. acute exacerbations of breathlessness +/- wheezing and after medication (short acting beta-2 agonist)will be normal.

COPD on the other hand is generally a partially reversible condition (this is a controversial issue for some doctors if you just mention it. You'll have to specify that the improvement of this disease can only be partially achieved if put on long term medication) thus their symptoms are persistent. But what I think your lecturer wants to hear (maybe) is the salient clinical feature of COPD which is the chronic bronchitis of blue bloaters and the emphysematous pink puffers.

A typical blue bloaters (not always seen) have CO2 retention, the picwickian syndrome (obesity, somnolence, hypoventilate, plethoric/red face), short neck, doesn't look breathless, an abnormal ABG (hypercapnic, hypoxic) & shallow breathing.

The pink puffer does not retain CO2, is usually thin, has a long neck, look really breathless, has a normal/ near normal ABG & pursed lips breathing.

That makes all the difference in my opinion for these 2 conditions.

Case report (Kawasaki Disease)

2009-12-31T16:12:00.004+08:00

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Lung Cancer

2009-12-08T10:31:00.000+08:00

- Lung cancers or lung neoplasms can be generally divided into 3 broad categories, namely:

Primary lung cancer (where cancer develops in the lung tissue itself)
Secondary lung cancer (due to deposits of cancer cells originating from other cancer organs)
Mesothelioma (cancer of the layer of tissue (pleura) that surrounds the lung ) - not really a lung cancer per se.

- Primary lung cancers can be further classified into

benign (cancers that do not spread to other organs)
malignant (cancers that do spread)

- More than 20 bengin & malignant primary lung cancers have been identified & classified histologically.

- However, 90 - 95% of these lung cancers are bronchogenic carcinomas.

- About 5% are bronchial carcinoids and 2 - 5% are mesenchymal & other miscellaneous lung cancers.

Re: Manjul Tripathi

2009-12-01T13:53:00.000+08:00

Pharyngitis is one of the leading reason for physician visits by adults world wide. Approximately 10% of adults with pharyngitis who are seen by physicians are infected with group A Streptococcus (GAS)--the only etiology for which antibiotic treatment is currently acceptable. However, almost three-quarters of all patients with pharyngitis who present for medical care continue to receive antibiotics. In addition, doctors frequently prescribe broad-spectrum antibiotics, including the newer macrolides, although GAS remains sensitive to penicillin and is increasingly resistant to macrolides.

Guidelines from expert panels are shifting away from recommending positive culture results before antibiotic treatment and toward using clinical criteria and/or rapid testing for GAS (followed by confirmatory culture if the rapid test is negative). Neuner and colleagues (2003) conducted a cost-effectiveness analysis of five pharyngitis management strategies and studied the impact of a decision rule on those strategies. The five strategies chosen were observation only; empirical treatment with no testing; throat culture for all patients, with treatment for GAS-positive results; optical immunoassay (OIA) rapid testing, culture for negative results, and treatment for any positive result; and OIA alone, with treatment for positive results.

The baseline prevalence of GAS infection in pharyngitis was 9.7%. At this prevalence, the culture strategy was most effective and least expensive; it was followed in efficacy (in order) by OIA/culture, OIA alone, and observation. Empirical therapy was notably less effective than the other four strategies. The OIA/culture strategy was twice as expensive per patient as culture alone. For any prevalence between 6 and 20%, the culture strategy was most effective and least expensive. Only when OIA specificity was >98% did it become the more effective strategy, but culture remained least expensive at all specificity ranges. Only if the prevalence of GAS pharyngitis exceeded 71% would empirical treatment become the least expensive strategy. This point might be relevant if a highly predictive clinical decision rule was first applied to an individual patient.

This study supports the continued use of throat culture before the treatment of pharyngitis in adults as the most effective and least expensive approach. OIA with or without culture is more expensive but clinically effective. Empirical treatment at current prevalence rates of GAS pharyngitis is not recommended.

In an accompanying editorial, Bisno (2003) notes that the American College of Physicians has accepted the use of a clinical algorithm as a substitute for any microbiological testing in making decisions about the treatment of acute pharyngitis in adults. The American Academy of Family Physicians and the Centers for Disease Control and Prevention are supportive of this approach. In the study by Neuner's group, empirical treatment remained less effective and more expensive than other strategies, even when the best algorithm was used. Culture alone was most effective at the present U.S. prevalence of GAS pharyngitis. Because treatment has a minimal impact on clinical symptoms and contagion, and because suppurative or nonsuppurative sequelae are currently rare, the main goal in managing acute pharyngitis in adult patients should be to reduce the inappropriate use of antibiotics, particularly given the trend of physicians to prescribe broad-spectrum antibiotics. The Infectious Diseases Society of America now recommends the use of rapid antigen testing so that a decision regarding antibiotic treatment can be made quickly before the patient leaves the doctor's office. This approach is consistent with the study by Neuner and colleagues, which finds it to be as effective as culture alone, although more expensive. In any event, Bisno concludes that some testing should be performed; if treatment is indicated, penicillin is the drug of choice for nonallergic patients.

Having said the above, if treatment still fails, a re-evaluation of the the patient (in this case, your sister) should be done as the initial diagnosis maybe wrong. A step-wise approach should be taken and investigations retaken. Keep an open mind as to the diagnosis and keep looking out for differential diagnosis, as a once famous professor said - the eyes does not see what the mind does not know. :) Hope this helps and sorry for the extremely late reply. All the best in the recovery of your sister. God bless.

Defeacation reflex

2009-11-12T15:00:00.004+08:00

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Chest tube insertion

2009-10-29T16:49:00.002+08:00

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Malaria

2009-10-28T21:02:00.001+08:00

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Pneumothorax

2009-10-22T09:47:00.002+08:00

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Leptospirosis

2009-10-22T00:28:00.002+08:00

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Re: Yumin

2009-10-19T07:50:00.001+08:00

Hi yumin, you could check out the Natural Guideline Clearinghouse at www.guideline.gov/summary/summary.aspx?ss=15&doc_id=5946&nbr=3915, or you can simply just download the file from http://www.journals.uchicago.edu/doi/pdf/10.1086/425368?cookieSet=1. Its from IDSA website at http://www.idsociety.org/content.aspx?id=4430.

False localising sign & 3rd cranial nerve palsy

2009-10-06T18:55:00.002+08:00

The false localising sigh
• Neurological signs that indicates a pathology far-away from the expected anatomical site.

• Commonest examples are 6th cranial nerve palsy (unilateral or bilateral) and papilloedema secondary to raised intracranial pressure (e.g. chronic meningitis and tumour)

• The reason for false localizing sign in the 6th CNP is due to its’ long intracranial course.

Surgical and medical 3rd nerve palsy
• As the name suggest, the causes of surgical 3rd CNP are compressive lesions (such as aneurysm or tumours)and medical 3rd CNP are those that you’ll see in the medical wards that may involve the course of 3rd cranial nerve.(such as diabetes = most common)

• So, to learn more about the causes of 3rd CNP, you’ll have to cover a wide range of diseases from surgical causes to medical causes that may injure or affect the 3rd nerve anywhere along its’ course. But the important points you’ll need to know are in the ptosis flow chart. 

• Pupillary involvement (dilated pupil that does not react to light shone in either eye) is an important sign differentiating "surgical," including traumatic, from "medical" causes of isolated third nerve palsy. (as shown in my previous flow chart on ptosis)

• Surgical 3rd nerve / Compressive lesions of the 3rd nerve—eg, aneurysm of the posterior communicating artery and uncal herniation due to a supratentorial mass lesion—characteristically have pupillary involvement. Patients with painful acute isolated third nerve palsy and pupillary involvement are assumed to have a posterior communicating artery aneurysm until this has been excluded. Pituitary apoplexy is a rarer cause.

• Medical causes of isolated third nerve palsy include diabetes, hypertension, and giant cell arteritis.

COPD (case presentation)

2009-10-05T07:14:00.002+08:00

click here to download

Re: mishita (Paediatric Protocol for Malaysian Hospital)

2009-09-30T14:34:00.007+08:00

Hey Mishita, I've been asking around and noticed that there are Malaysian protocols on haematological diseases such as the Paediatric Protocol for Malaysian Hospital and they cover heamatological diseases such as anaemia, thalassaemia, ITP, haemophilia and leukeamia. I'm sorry about the previous mistaken information. I have the file with me here and hope this helps. This is the 2008 second edition (the latest I can find) I couldn't find anything for the adults though, but i'll continue to search for it. Hopefully I'll find something useful for you.
click here to download

Re: Mishita

2009-09-18T11:19:00.001+08:00

It's ok.:) As for the other blood disorders, Malaysian MOH per se does not have any CPGs on them. Therefore, u can use any management plan from the text books recommended by your various universities. As a guide, make sure your resources are up to date. By that, it's best to get them from journals or research publications. In view of this, it'll be ridiculous to put up all the literatures available online for this topic. I suggest that u either stick to the text books recommended by your university, ask the lecturers whom u're under and get the name of their referrences, do your own research of the latest updates on the particular topic and make sure u state your sources when asked or if u're working or attached to any hospital - ask them if they have a hospital guideline for the different blood disorders. Hope this helps.

Blood disorders

2009-09-17T16:34:00.004+08:00

Hi Mishita,

There are Clinical Practice Guidelines (CPGs) that u can get from Malaysia Ministry of Health (MOH) website that fit your request of blood diseases such as diagnosis & management of Immune Thrombocytopenic Purpura (ITP) 2006 and diagnosis & management of Chronic Myeloproliferative Disorder 2004. There are no other CPGs by Malaysian MOH on other blood disorders up to 2009. Hope this helps. If u have other request, just let me know. I'll try to help out.

GINA & GOLD guidelines

2009-09-16T12:27:00.003+08:00

Hi Kirara, you can find the GINA guidelines for diagnosis and management of asthma in children 5 years and younger at http://www.ginasthma.com/download.asp?intId=380 and GOLD guidelines for diagnosis, management, and prevention of COPD at http://www.goldcopd.com/download.asp?intId=504

Please take note that these files are not meant for commercial purposes and are strictly for personal, clinical or academic use only.

Speech disorders

2009-09-11T00:54:00.002+08:00

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Fluid management

2009-09-06T23:57:00.002+08:00

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Breathing

2009-09-02T15:26:00.004+08:00

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COPD (treatment)

2009-08-24T10:41:00.001+08:00

Smoking cessation

· Since smoking is the main cause for COPD, stopping is definitely the treatment option. This has proved to prolong the survival in patients with COPD.

· Although lost lung function is not regained, the lung damage stops. (rate of FEV₁ reverts back to that of non-smokers)

· For those who can’t stop smoking without an aid, replacement therapy such as nicotine patch, gum or inhaler helps to some certain extend. (user dependant)

· Oral medication to help smoking cessation is another alternative. (e.g. bupropion)

Bronchodilators

· These are medications used to enlarge a narrow airway by action of relaxing the muscles around the airway.

· There are short acting (medication that last only a short period of time after use) & long acting bronchodilators.

· The bronchodilators are in inhaler or oral preparations. (However, inhaled medications have fewer side effects)

· Examples are ipratropium (short acting) and salmeterol (long acting). Theophylline’s use is limited due to its’ narrow therapeutic range. (this means that the individual taking this medication is at a higher risk of getting toxic levels of the medication thus increasing the adverse effects)

Oxygen

· This therapy can be given at home (if the equipment and operator skills are available).

· The therapy shows reduced symptoms & improved survival in patients with COPD. (provided they have stopped smoking)

· The oxygen saturation (Sa_O2) is best kept above 90%.

Lung transplant

· This is only done if all methods of treatment above are tried and have failed & the function of the lung is severely low.(FEV₁ is less than 25%)

Lung volume reduction surgery

· Still another method used to help patients with COPD.

· However, this is a highly specific treatment for a selected group of COPD patients.

COPD (signs & symptoms)

2009-08-17T17:17:00.001+08:00

Do you have COPD?

Symptoms of COPD

- symptom is the change in the body's structure, function, or sensation, experienced by the patient & indicative of disease.

cough with phlegm
breathlessness on mid exertion
wheeze (breathing with difficulty & noisily)

Signs of COPD

- sign is an objective indication of disease, discoverable on examination of the patient (usually) by a physician.

- early signs

wheezing upon exhalation

- late signs

tachypnoea (rapid breathing-the definition varies with the age of the patient)
hyperinflated chest (over expansion / distension of chest)
marked widespread wheeze
'Pink puffers' or 'blue bloaters'

Cardiac murmurs

2009-08-01T15:57:00.005+08:00

Click here to download

COPD & smoking

2009-07-27T15:23:00.002+08:00

Why does smoking causes COPD?

- In a smoker's lung, there are basically two things that take place:

the lung reacts to smoke particles (e.g. nicotine, tar) => know as indirect injury
the smoke particles react to the lung => known as direct injury

- Indirect injury:

In smokers, there is an accumulation of immune cells (immune cells protecting the body are liken to the policemen & soldiers that protect a country) within the alveoli. (remember the tree analogy? These are the leaves)
It is believed that the immune cells (neutrophils and macrophages) are attracted to the lung alveoli by the smoke particles, nicotine. (as an action of local immune cells.)
Of the 2 immune cells, 1 of them (neutrophils) release a variety of protein substances (e.g.neutrophil elastase, proteinase 3 & cathepsin G) finally resulting in lung alveolar damage.
The other immune cell (macrophage) also releases a protein substance calledmetalloproteinase which causes additional damage to the lung alveoli. (It's just like a war occuring within a country's gates. When bullets are fired, innocent people get hurt too.)

- Direct injury:

Smoking plays a role in causing direct injury to the lungs by producing harmful products known as reactive oxygen species / "free radicals".
Free radicals cause lung alveolar damage by destroying the 'guys' that maintain the well-being of the alveoli (known as alpha 1 anti-trypsin)

- All these insults results in the loss of alveolar attachments (supporting structure) & thus acollapse of brochial wall upon breathing. (this is what happens in emphysema)

- The continuous insult in the alveoli causes deposits of hardening tissue (fibrosis) hence thenarrowing of airflow and airway limitation. (this is chronic bronchitis)

COPD (causes)

2009-07-20T13:22:00.002+08:00

Causes of COPD/COAD

- Chronic Obstructive Pulmonary Disease (COPD) commonly occurs in individualsover the age of 35. (It is a progressive disease, therefore it takes time to show physical signs.)

- The single and most inportant cause of COPD is smoking. (Why? check out the next update!!)

- Did you know that in 90% of patients suffering from COPD, it is the result of long-term heavy cigarette smoking? The remaining 10% are non-smokers who develop COPD for which the reason is still uncertain. (medical X-files ^_^)

- In the majority of clinical settings, a patient either has COPD or asthma, not both. However, although asthma (reversible, over-reactive airway) is a distinct disorder, it may be a part of COPD in some patients. (but this is for the respiratory specialist to crack their heads over. ^_^)

- For the past few decades, the increase in smoking, environmental pollutants, and other noxious gas exposures has caused the incidence of COPD to rise dramatically.

-COPD is even ranked in the top 5 causes of morbidity(a diseased state) worldwide.

- Other causes of COPD would include occupational dust exposure (e.g. coal miners) & repeated lung infections. (e.g. tuberculosis)

COPD (Introduction)

2009-07-13T14:39:00.003+08:00

COPD (Chronic Obstructive Pulmonary Disease) / COAD (Chronic Obstructive Airway Disease)

Introduction:

COPD and COAD are the one and the same. The usage of the terms depends on the country you come from. (^_^)

Definition:

- Lung disease are generally grouped into 2 categories, namely obstructive & restrictive diseases.

- Obstructive disease

means - an increase resistance to air flow
due to partial / complete obstruction
at any level of the airway

- Restrictive disease

means - a decrease in the ability of the lung to expand
and - a decrease in the lung's air storage capacity

-COPD falls under the obstructive category of lung diseases. (However, note that there are no absolutes in the medical line. There are COPDs without obstructive elements! )

[NB: a tip for medical or nursing students in answering exam questions - if there is an answer to a question which states words such as ALL or NEVER or anything along that line, the chances that the answer is wrong is certain.(^_^)]

-COPD is a common progressive obstructive disorder ofthe airway with little or no reversibility.

-Clinically, COPD includes a combination of

chronic bronchitis (a person with persistent productive cough for most days, in at least 2 consecutive years)
emphysema (a person with permanent increase of air spaces beyond the normal size, at the level away from the terminal bronchioles-in other words, alveolar region)
Think of the lung as an inverted tree, with it's trunk (trechea) slowly progressing to the leaves. The twigs of the tree are the bronchioles and the leaves are the alveoli / terminal sac.
accompanied by destruction of their walls
with / without obvious deposits of hardening tissue (due to reactive process to the disease).

Ptosis (flow chart)

2009-07-01T23:26:00.006+08:00

Case based learning (Ophthalmology)

2009-06-28T17:25:00.031+08:00

1 case followed by 2 scenarios.

These slides are a compilation of my short and humble experience in various departments. It is also altered slightly for the purpose of case based learning. However, the identity is not revealed for the privacy of the patient.

Case proper

A 45 year old woman came into HTJS accident and emergency department. For the previous 2 days, her left eye had been red and watering. There was slight blurring of vision and the eye was moderately uncomfortable. There was no history of trauma. There right eye was asymptomatic. There was no past eye history. She was fit and well and not taking any pharmacological or traditional medication.

The acute red eye is a common ophthalmological presentation caused by various conditions ranging from trivial to sight-threatening.

What are the important causes of red eye do you know of?

Answer: (Please click & drag the empty section below to reveal the hidden answer. ^_^)

Are you contented with the history taken?

If yes, justify your statement.

If no, what further questions would you have asked her?

Suggest some physical examination you would carry out in this patient to aid in your diagnosis and their expected findings.

Answer: (Please click & drag the empty section below to reveal the hidden answer. ^_^)

¨ recent upper-respiratory tract infection

¨ direct contact with an infected person

¨ onset (abrupt / insidious)

¨ type of visual blurring (isolated fields/all fields)

¨ photophobia (secondary iritis)

¨ rash (herpes simplex)

¨ headache

¨ Examine the eye with its adnexa. (also with fluorescein stain)

¨ Direct ophthalmoscope

¨ Visual acuity & visual field

¨ Lymph node palpation

With the symptoms she had, what is the most likely diagnosis?

Answer: (Please click & drag the empty section below to reveal the hidden answer. ^_^)

Acute viral conjuctivitis

Dr. Ceccilia of the A&E department diagnosed her to be viral conjunctivitis and commenced a broad spectrum topical antibiotic, arranging a routine review appointment in 3 days but warning the patient to return urgently prior to this if the symptoms worsened.

Do you agree with this method of management?

What would be your management for her?

Answer: (Please click & drag the empty section below to reveal the hidden answer. ^_^)

Management for viral conjunctivitis is supportive and no specific treatment is available.

¨ Topical antiviral agents (e.g. aciclovir, trifluorothymidine) are effective against herpes simplex.

¨ Vasoconstrictors/ antihistamine may reduce symptoms.

¨ Artificial tears are used for soothing effect.

¨ Antibiotics are prescribed only when diagnosis is in doubt.

¨ Topical steroids reduces symptoms but should be used when diagnosis is certain & under ophthalmological supervision.

¨ Antihistamines

¨ Levocabastine HCl 0.05% ophthalmic solution (Livostin)

¨ 1 drop four times daily (up to 2 weeks)

¨ Emedastine difumarate 0.05% solution (Emadine)

¨ 1 drop four times daily

¨ Mast cell stabilizers

¨ Cromolyn sodium 4% solution (Crolom)

¨ 1 drop four to six times daily

¨ Ketotifen fumarate 0.025% solution (Zaditor)

¨ 1 drop two to four times daily

¨ Lodoxamide tromethamine 0.1% solution (Alomide)

¨ 1 or 2 drops four times daily (up to 3 months)

¨ Nedocromil sodium 2% solution (Alocril)

¨ 1 drop twice daily

¨ Olopatadine hydrochloride 0.1% solution (Patanol)

¨ 1 drop twice daily

Sccenario 1

The patient returned to the hospital later the same day complaining that the pan in the left eye had become severe. There was now frontal headache and malaise. The vision in the eye had become much worst (counting fingers only). The eye was very inflamed and the cornea looked hazy. The pupil was oval in shape and failed to react to direct and consensual light stimulation. There was left relative afferent pupillary defect.

What is the most likely diagnosis? What features of the history and examination lead you to this conclusion?

Answer: (Please click & drag the empty section below to reveal the hidden answer. ^_^)

¨ Acute angle closure glaucome

¡ Unilateral eye pain

¡ Often with headache

¡ Poor vision

¡ Hazy cornea (due to oedema)

¡ Oval mid-dilated fixed pupil

¡ Haloes around lights (corneal oedema)

¡ Loss of red reflex

¡ Hypermetropia

¡ Previous symptoms of similar attack

¡ Nausea, vomiting

What is the differential diagnosis and why?

Answer: (Please click & drag the empty section below to reveal the hidden answer. ^_^)

¨ Iritis is the main differential diagnosis, but few other conditions cause such pain with visual loss.

¨ Conjunctivitis and blepharitis cause disconfort only.

¨ Acute corneal problems may cause pain but usually there is a history of trauma or an obvious ulcer on staining with fluorescein.

How would you manage this patient?

Answer: (Please click & drag the empty section below to reveal the hidden answer. ^_^)

¨ Urgent referral to an ophthalmologist is necessary, as permanent visual loss can rapidly occur if untreated.

¨ Initial treatment is to lower the intraocular pressure using

¡ β-blocker :Timolol, 0.5%, 1 drop in the affected eye

¡ Cholinergic :Pilocarpine, 2% eyedrops, two drops every 15 minutes for 2–3 hours

¡ Carbonic A.I. :Acetazolamide, 500 mg orally or 250 mg intravenously

¡ α-adrenergic :Apraclonidine, 1%, one drop every 12h)

¡ Oral agents :glycerol, 1.0 to 1.5 g/kg in a 50% solution

ú oral isosorbide can be substituted (1.5 to 2.0 g/kg).

¡ Intravenous :mannitol (20% solution, 2 g/kg given over 30 min)

¨ Give sedation, antiemetics, and analgesics as necessary to control pain nausea and agitation.

¨ peripheral iridotomy, which establishes a communication between the posterior and anterior chambers & prevent further occurance. (argon or Nd:YAG laser)

¨Rarely, surgical peripheral iridectomy is required.

Scenario 2

The patient attended the next appointment as scheduled, but the left eye was now considerably more uncomfortable and visual acuity was reduced to 6/18. Photophobia was a prominent feature. Dr. Cecilia suspected acute glaucoma. The appearance of the left eye is as below.

Describe the abnormality seen here and suggest the diagnosis.

Answer: (Please click & drag the empty section below to reveal the hidden answer. ^_^)

This is acute uveitis. The episcleral vessels are dilated (ciliary fluch), the corneal appears misty (endothelium is covered with inflammatory precipitates), and the iris is indistinct due to the anterior chamber cellular reaction. There is a mixed hypopyon (layered white blood cells) and hyphema (hemorrhage) within the inferior anterior chamber. The pupil has scarred in places to the lens by posterior synechiae, which causes the irregular appearance of the pupil.

What is the management of this condition?

Answer: (Please click & drag the empty section below to reveal the hidden answer. ^_^)

¨ Topical steroids are the main treatment. A dilating drop such as atropine, cyclopentolate or homatropine can also be prescribed: as this eases the pain and helps stop the formation of permanent posterior synechiae (adhesions between the iris and lens)

What are the systemic associations of this disorder?

Answer: (Please click & drag the empty section below to reveal the hidden answer. ^_^)

¨ ¾ of all cases are idiopathic. Ankylosing spondylitis, Reiter’s syndrome, psoriatic arthritis, arthritis of inflammatory bowel diseases (Crohn’s disease, ulcerative colitis), sarcoidosis, juvenile chronic arthritis are the most frequently identified associations.

Sore throat (treatment)

2009-06-28T13:35:00.000+08:00

- Most common (more than 90%) type of sore throat is viral pharyngitis. (virus causing inflammation to the throat/viral sore throat)

- How do you know if you’ve got a viral or bacterial sore throat?

o In bacterial sore throat, these are the signs & symptoms. (These suggest the presence of bacterial infection, and are not diagnostic in nature.)

§ Absence of cough

§ Tender cervical lymph nodes (painful lumps around the neck region upon pressing)

§ Enlarged tonsil with exudates

§ High grade fever ( more than 38⁰C )

o In viral sore throat, the symptoms are the direct opposite of the above, namely:

§ Presence of cough

§ Non-tender cervical lymph nodes

§ No enlarged tonsils

§ Low grade fever (<38⁰c)

- However, please note that with the presence of ALL 4 of the above signs and symptoms for bacterial sore throat, the chances of ACTUALLY having a bacterial sore throat is only about 50%(52.8%) according to research. (This is as good as tossing a coin to determine heads or tails. J) This percentage decreases with reduce in the number of signs and symptoms. Therefore, if you’ve only have 1 symptom among the 4 (mentioned above), the chances are slightly below 10% that you’ve got a bacterial infection.

- Other clues to help you determine if its viral or bacterial are: (This is not absolute)

o If you’ve been around people who cough or sneeze (at work or school) and subsequently (you and other healthy people exposed) get it within a matter of hours, it is most likely viral. (As viral sore throat is highly contagious, it spreads easily through contact of bodily fluids e.g. mucus or saliva) Bacterial sore throat usually takes hours to days to develop. Therefore, the best way to prevent sore throat is to avoid people who are sick, frequent effective hand washing technique and a healthy living.

o If you’ve been having it for more than a week (without the exposure to a constant source of new infected people), it is most likely bacterial. (A single episode of viral sore throat usually last for 3 to 7 days, but a bacterial last longer than a week. This is with the exception that you do not get repeated viral infections (e.g. being in a classroom full of students who are also coughing) as this might make it seem like a bacterial sore throat.)

- In light that most sore throat cases are viral infections rather than bacterial, what is the treatment for viral sore throat?

o Antivirals are effective in preventing and treating viral sore throats but are rather expensive and are not used for treatment of the ‘patty’ sore throat.

o If you can’t afford / get antivirals, there is only supportive therapy. (This means that you can only treat the symptoms individually i.e. bring down the fever by giving paracetamol (panadol) or relieve the pain by giving analgesics (pain-killer). However, this does NOT cure the root cause of the problem, but ONLY relieves the patient of his/her complaints! )

o The use of antibiotics is a clinically controversial issue.

o Theoretically, the use of antibiotics for viral sore throat is not encouraged. Reasons being:

§ There are no bacteria to kill, why use anti-bacteria? J (Please keep in mind that there are cases though no bacterial infection is detected, a high clinical suspicion for a potentially harmful bacterial infection is favoured and treated to prevent the unwanted side effects. Therefore, experience is needed for these.)

§ Widespread usage of antibiotics causes the emergence of anti-bacterial resistant bacteria. (most famous bacteria are MRSA / Methicillin-Resistant Staphylococcus Aureus & tuberculosis /TB bacteria – Mycobacterium tuberculosis)

§ Induction of bacterial infection. (The prolonged use of antibiotics will kill the local bacterial flora / “good bacteria” and this makes room for pathogenic bacteria / “bad bacteria” to colonise the free spaces that was made available for them.)

§ There are indications for antibiotic use in sore throats that are approved by WHO, but these are mainly for bacterial use.

o How about traditional medicine or home remedies?

§ Most of these methods are either passed down from generation to generation or from wise sayings / observations done by our ancestors. Though it might work for some, it is also true that it might not work for others. If it’s harmless, why not try it? J

§There are no scientific research done on most of these treatments, therefore no substantial proof can be used to backup the usage of these methods.

Karposi sarcoma (throat)

2009-06-27T16:46:00.001+08:00

This is Karposi sarcoma (spot diagnosis-can't miss this)

Notice:

-a well elevated, round, purplish nodule just behind the right upper molar tooth.

-if you see this, think of retroviral infections (e.g. HIV)

-the dental fills are normally seen in most people

Streptococcal tonsillopharyngitis

2009-06-27T16:40:00.001+08:00

This is a picture of Streptococcal tonsillopharyngitis:

Notice:

-severe inflammation involves both tonsils and pharynx with marked redness, swelling and exudate.

Follicular pharyngitis

2009-06-27T16:37:00.001+08:00

This is Follicular pharyngitis due to Streptococcus pyogenes:

Notice:

-bilaterally enlarged and injected tonsils with pockets of yellowish exudates.

-non-injected palate (normal la...)

Ebstein-Barr Mononucleosis

2009-06-27T16:31:00.001+08:00

This is a picture of Ebstein Barr Mononucleosis (EBM).

Notice:

-bilaterally enlarged tonsils but with whitish exudates.

-petechiae on soft palate. (tiny bleeds from vessels underneath the skin)

-lymph node enlargement (not seen in this picture but should be examined to help come to a diagnosis ^_^)

Quincy / Peritonsillar abscess

2009-06-27T16:27:00.001+08:00

This is Quincy / Peritonsillar abscess.

Notice: (as the labels will show)

-the left tonsil is enlarged as compared to right.

-uvula is deviated to the right.

-a reddish area on the soft palate (abscess)

-this is seen in patient who usually have reccurent throat infections.

Orasl thrush

2009-06-27T16:22:00.001+08:00

This is a typical picture of candida infection of the throat (or known as oral thrush).

Notice:

-small patches of whitish-yellow exudate on the palate, dorsum of tangue, pharynx and mucosa. (fungus growth)

-reddish patches surrounding the fungus growth.

-this is not common in a healthy individual, but often seen in patients with AIDS, severe uncontrolled diabetes mellitus.

Viral pharyngitis (pic)

2009-06-27T16:11:00.001+08:00

This is a typical picture of viral pharyngitis.

Notice:

-slight post nasal drip (saliva + air blubbles behind the uvula)

-injected oropharynx (red throat wall)

-lymphoid enlargement (small swellings behing the throat wall)

Sore throat (physical examination)

2009-06-27T15:59:00.002+08:00

•Inspection

–General appearance

–Nutritional status

–Hydration status

–Hoarseness of voice

•Hands

–Clubbing

–Nail changes

•Face

–Pallor

•Neck

–Thyroid enlargement ortendness

–Lymphadenopathy

•Inspection of oral cavity and pharynx

–Lips

–Angle of the mouth

–Halitosis

–Ulcers

–Abnormal masses

–Exudates

–Uvula

–Soft palate

–Tonsils

–Tongue

•Also inspect

–Ear for infections

–Ear pain

•Palpate

–Neck for cervical lymphadenopathy

–Sinus for tenderness

–Thyroid