Hey guys, we started Internal Medicine Last week, so we were
studying about different types of skin lesion as in rashes in Harrison’
Internal Medicine 19e. So I made little chart myself to memorize it.
So I thought to share it with you all.
Tuesday, August 16, 2016
Sunday, August 14, 2016
Polymyalgia rheumatica and giant cell arteritis mnemonic
Here's a mini post for the day!
What are the symptoms of Polymyalgia rheumatica? What is it associated with?
Saturday, August 13, 2016
#AnswerTime: A patient with delusion
Here's the answer to a question we posted earlier: http://www.medicowesome.com/2016/08/quiztime-patient-with-delusion.html
Answer:
#QuizTime: A patient with delusion
#QuizTime
A 32 year old male patient came to the Psychiatry OPD complaining that his wife wanted to kill him. He was asked why he didn't report to the police , to which he said they were not ready to believe him.
He was suspected of having a delusion of persecution.
A 32 year old male patient came to the Psychiatry OPD complaining that his wife wanted to kill him. He was asked why he didn't report to the police , to which he said they were not ready to believe him.
He was suspected of having a delusion of persecution.
Saturday, August 6, 2016
Correction of hyponatremia and hypernatremia mnemonic
Hello!
Never correct sodium too quickly.
If you correct hypernatremia too fast, it'll result in cerebral edema. Why?
When hypernatremia is corrected too rapidly, cerebral edema results because the relatively more hypertonic ICF accumulates water.
If you correct hyponatremia too fast, it'll result in central pontine myelinolysis (CPM) aka osmotic demyelination syndrome. Why?
Chronic hyponatremia is associated with the loss of osmotically active organic osmolytes (such as myoinositol, glutamate, and glutamine) from astrocytes, which provide protection against brain cell swelling.
However, organic osmolytes cannot be as quickly replaced when the brain volume begins to shrink in response to correction of the hyponatremia. As a result, brain volume can fall from a value that is initially somewhat above normal to one below normal with rapid correction of hyponatremia.
The mechanism by which a rapid fall in brain volume results in demyelination has not been established.
How do I remember this?
Here's another mnemonic:
From low to high, your pons will die (CPM)
From high to low, your brain will blow (Cerebral edema, herniation)
That's all!
-IkaN
Never correct sodium too quickly.
If you correct hypernatremia too fast, it'll result in cerebral edema. Why?
When hypernatremia is corrected too rapidly, cerebral edema results because the relatively more hypertonic ICF accumulates water.
If you correct hyponatremia too fast, it'll result in central pontine myelinolysis (CPM) aka osmotic demyelination syndrome. Why?
Chronic hyponatremia is associated with the loss of osmotically active organic osmolytes (such as myoinositol, glutamate, and glutamine) from astrocytes, which provide protection against brain cell swelling.
However, organic osmolytes cannot be as quickly replaced when the brain volume begins to shrink in response to correction of the hyponatremia. As a result, brain volume can fall from a value that is initially somewhat above normal to one below normal with rapid correction of hyponatremia.
The mechanism by which a rapid fall in brain volume results in demyelination has not been established.
How do I remember this?
 |
| Central pontine myelinolysis* mnemonic |
From low to high, your pons will die (CPM)
From high to low, your brain will blow (Cerebral edema, herniation)
That's all!
-IkaN
Study group discussion: Widow makers artery
Does anyone know why left anterior descending artery is called widow's artery?
Tuesday, August 2, 2016
Approach to acid base disorders: Metabolic alkalosis notes
In suspected metabolic alkalosis, always check urinary chloride levels.
Metabolic alkalosis associated with a reduction in the ECV (Vomiting, diuretics):
There will be a stimulus for Na and Cl reabsorption to replenish extracellular volume.
Urinary Cl is very low ( < 25 meq/L).
Administration of NaCl and water leads to correction of the metabolic alkalosis.
Such causes of metabolic alkalosis are said to be saline responsive.
Metabolic alkalosis associated with a reduction in the ECV (Vomiting, diuretics):
There will be a stimulus for Na and Cl reabsorption to replenish extracellular volume.
Urinary Cl is very low ( < 25 meq/L).
Administration of NaCl and water leads to correction of the metabolic alkalosis.
Such causes of metabolic alkalosis are said to be saline responsive.
Approach to acid base disorders: Metabolic acidosis notes
Hello!
I made these notes while studying acid base disturbances. Now they might not make sense to someone who has never studied this topic before.. But for those who have read about it, this should be excellent for revision.
Calculation of anion gap:
ALWAYS calculate the anion gap first.
Anion gap = [Na+] − ([Cl-] + [HCO3−])
Normal anion gap = 8 - 16 mEq / L
I made these notes while studying acid base disturbances. Now they might not make sense to someone who has never studied this topic before.. But for those who have read about it, this should be excellent for revision.
Calculation of anion gap:
ALWAYS calculate the anion gap first.
Anion gap = [Na+] − ([Cl-] + [HCO3−])
Normal anion gap = 8 - 16 mEq / L
Monday, August 1, 2016
Envelope shaped crystals in urine: Calcium oxalate mnemonic
Heyyyyyy!
X in oXalate looks like an envelop to me :D
X in oXalate looks like an envelop to me :D
Drugs causing crystal induced AKI mnemonic
Hello!
So today I was reading about acyclovir and crystal induced acute kidney injury.
Acyclovir is rapidly excreted in the urine (being both filtered and secreted) and has a relatively low solubility. Intravenous (IV) therapy may lead to the deposition of acyclovir crystals in the tubules if the patient is volume depleted. This results in intratubular obstruction and foci of interstitial inflammation.
So today I was reading about acyclovir and crystal induced acute kidney injury.
Acyclovir is rapidly excreted in the urine (being both filtered and secreted) and has a relatively low solubility. Intravenous (IV) therapy may lead to the deposition of acyclovir crystals in the tubules if the patient is volume depleted. This results in intratubular obstruction and foci of interstitial inflammation.
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