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Wednesday, November 23, 2011
Rhaumatoid Arthritis
- 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
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- av Criteria a–d must be present for at least 6 weeks. Criteria b–e must be observed by a physician.
Parkinsonism
- 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 (
- 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) |
Speech disorder
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 | Normal | Normal | |
| Naming objects | Impaired | Impaired | Impaired | Impaired |
| Speech | Telegraphic (staccato speech) | 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
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Knowing the language of a disease
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.
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
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
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
Tuesday, April 19, 2011
HyperNa+ & hyperK+
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
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
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