Reading about the technical aspects of dialysis. Things that caught my attention
1) Circuit - arterial line - pressure montior- predialysis pressure monitor - kidney - post dialysis pressure monitor - venous side
2) recirculation - happens thru cardiopulmonary circ + at the fistula
3) Temperature fall across the circuit of 1 c can lead to the equivalent of 20% of BMR
4) conductivity/volumetric methods of mixing dialysate
5)batch processing vs. continous flow dialysate
6)effect of reynolds number- type of flow and shear stress
viscosities and flow calculations
Introduction to concept of dialysance.
conductivity for dialysate and how each ion can affect it. donan equilibrium
all these concepts are ringing in the ear all necessitating further reading, ideally fluid dynamics/calculus
Monday, January 25, 2010
Wednesday, January 20, 2010
PD peritonitis
Bear with my typos as I am learning touch typing.
Today talked about PD Peritonitis.
Staph Epi is the most common. Others of note include staph.aureus, strep, enterococci.
Gram negatives are not common and when they occur include E Coli, pseudomonas,acinetobacter etc.
You do not want to see pseudomonas or fungal or TB as they mean Catheter removal, as very difficult to eradicate
In PD fluid, a white cell count of > than 100 and PMN > 50 are needed for diagnosis. Occasionally it can be predominant eosinophilia.
Treatment is initially with Vanc+Gent/ceftaz till organism identified. You can give in every exchange or in 1 bag with a dwell for 6-8 hours.
Secondary peritonitis is from a primary intraabdominal problem like a perforated diverticulum or ischemic bowel etc. and it is polymicrobial in nature. So, on a gram stain if you find both gram+ and gram- think about secondary causes.
Relapse is PD peritonitis with the same organism in less than 4 weeks after finishing therapy
Today talked about PD Peritonitis.
Staph Epi is the most common. Others of note include staph.aureus, strep, enterococci.
Gram negatives are not common and when they occur include E Coli, pseudomonas,acinetobacter etc.
You do not want to see pseudomonas or fungal or TB as they mean Catheter removal, as very difficult to eradicate
In PD fluid, a white cell count of > than 100 and PMN > 50 are needed for diagnosis. Occasionally it can be predominant eosinophilia.
Treatment is initially with Vanc+Gent/ceftaz till organism identified. You can give in every exchange or in 1 bag with a dwell for 6-8 hours.
Secondary peritonitis is from a primary intraabdominal problem like a perforated diverticulum or ischemic bowel etc. and it is polymicrobial in nature. So, on a gram stain if you find both gram+ and gram- think about secondary causes.
Relapse is PD peritonitis with the same organism in less than 4 weeks after finishing therapy
Wednesday, January 13, 2010
Long QT syndrome
What is the basis for a normal action potential in pacemaker cells and normal myocardial cells?
Myocardial cells phase 0 is from rapid entry of sodium channel.Transient phase 1 is due transient outwars potassium current. Phase 2 is due to calcium entry being balanced by potassium exit. Phase 3 is from unbalanced potassium exit.Phase 4 is repolarization phase with mostly Na+K+ ATPase being active and some potassium channel being open with little movement due to compensating electrochemical forces as per Nernst equation.
Pacemaker cells have very small element of Phase 0 sodium activity and is mostly calcium lead.
Why is the T wave not opposite of QRS? and why?
Subendocardial M cells have a longer Action potential when compared with epicardial myocytes. so though they depolarize first, they do not repolarize first.
What is the defect in LQTS?
There are many defects but 3 account for most. Ks accounts for LQTS1, Kr accounts for LQTS2, INa accounts for LQT3
How do the mutations affect the channel function?
Either they interfere with the functioning of normal subdivision or is a production defect by reduced number
What are the T wave patterns in LQTS?
Broad based T in LQTS1, Notched T in LQTS 2 , Tall and Notched in LQTS 3
When do you call the QT as prolonged?
When it is > 430 in makes and > 450 in females .
Patient is dead do you still need to make a diagnosis?
Ofcourse you have the family waiting to die!
What do you ask in family history?
Not just for SCD but for others like deafness/Seizures
What are the other causes of LQTS?
Many drugs and electrolyte imbalances
What about genetic testing?
Can check for the ones you know but a negative doesnot exclude in the presence of other criteria
How is sex going to affect the presentation?
Estrogens block K channels, so prolong APD and hence QT. So prior to puberty males are likely to die more and vice versa afterwards
How about pregnancy?
Increases the risk and the increased risk remains till 6 months postpartum
Is the degree of QT prolongation important?
Yes the longer the QT the more likely for Torsades
What activities precipitate Torsades?
LQT1 - Physical exp swimming
LQT2- sudeen loud noise alarm clock
LQT3-no arousal needed
Does the type of mutation matter?
Yes it does - depending on which domain is affected the pore part/ the cytoplasmic domain or extracellular
dominant negative versus haploinsufficiency
What are the treatments that can be used?
Beta blocker,LCDS,AICD
Once AICD is it a done deal?
Still have to use beta blocker and also avoid major physical activities
Is AICD cost effective in LQTS?
It is at least 10-20 times cheaper per life saved when compared with CHF
What is electrical storm?
> 2 shocks in < 24 hours
Why does mexileten or lidocaine make sense?
How does a prolonged QT lead PVT?
Where do the antiarrhytmics act?What are the subtyeps in 1?
What are the other congenital syndromes that we need to remember for sudden death?
Are the capacitators already charged ready to go in AICD?
Does the AICD always need to shock to terminate VT? and how can it do it?
How does hypokalemia cause PVT IN long QT?
what is the problem with bazett's ? undercorrects at tachy and over corrects at brady.
Myocardial cells phase 0 is from rapid entry of sodium channel.Transient phase 1 is due transient outwars potassium current. Phase 2 is due to calcium entry being balanced by potassium exit. Phase 3 is from unbalanced potassium exit.Phase 4 is repolarization phase with mostly Na+K+ ATPase being active and some potassium channel being open with little movement due to compensating electrochemical forces as per Nernst equation.
Pacemaker cells have very small element of Phase 0 sodium activity and is mostly calcium lead.
Why is the T wave not opposite of QRS? and why?
Subendocardial M cells have a longer Action potential when compared with epicardial myocytes. so though they depolarize first, they do not repolarize first.
What is the defect in LQTS?
There are many defects but 3 account for most. Ks accounts for LQTS1, Kr accounts for LQTS2, INa accounts for LQT3
How do the mutations affect the channel function?
Either they interfere with the functioning of normal subdivision or is a production defect by reduced number
What are the T wave patterns in LQTS?
Broad based T in LQTS1, Notched T in LQTS 2 , Tall and Notched in LQTS 3
When do you call the QT as prolonged?
When it is > 430 in makes and > 450 in females .
Patient is dead do you still need to make a diagnosis?
Ofcourse you have the family waiting to die!
What do you ask in family history?
Not just for SCD but for others like deafness/Seizures
What are the other causes of LQTS?
Many drugs and electrolyte imbalances
What about genetic testing?
Can check for the ones you know but a negative doesnot exclude in the presence of other criteria
How is sex going to affect the presentation?
Estrogens block K channels, so prolong APD and hence QT. So prior to puberty males are likely to die more and vice versa afterwards
How about pregnancy?
Increases the risk and the increased risk remains till 6 months postpartum
Is the degree of QT prolongation important?
Yes the longer the QT the more likely for Torsades
What activities precipitate Torsades?
LQT1 - Physical exp swimming
LQT2- sudeen loud noise alarm clock
LQT3-no arousal needed
Does the type of mutation matter?
Yes it does - depending on which domain is affected the pore part/ the cytoplasmic domain or extracellular
dominant negative versus haploinsufficiency
What are the treatments that can be used?
Beta blocker,LCDS,AICD
Once AICD is it a done deal?
Still have to use beta blocker and also avoid major physical activities
Is AICD cost effective in LQTS?
It is at least 10-20 times cheaper per life saved when compared with CHF
What is electrical storm?
> 2 shocks in < 24 hours
Why does mexileten or lidocaine make sense?
How does a prolonged QT lead PVT?
Where do the antiarrhytmics act?What are the subtyeps in 1?
What are the other congenital syndromes that we need to remember for sudden death?
Are the capacitators already charged ready to go in AICD?
Does the AICD always need to shock to terminate VT? and how can it do it?
How does hypokalemia cause PVT IN long QT?
what is the problem with bazett's ? undercorrects at tachy and over corrects at brady.
Tuesday, January 12, 2010
Polycystic Kidney disease
Attended a grand round on polycystic kidney disease. Left with a lot more questions than I entered with.
OK Polycystin is a part of cilia and it detects motion. If it is screwed up as it does in PKD, you get cysts.
The organs affected like Kidney, liver(Bile), colon (Feces), lung - bronchiectasis(Air) , seminal vesicles(semen) have some thing flowing in a direction.
Only in the CVS it is kind of funky in that
1)Why is it only the circle of willis is affected? Has it got to do with the fact that blood flow can reverse its direction in COW unlike other systemic blood vessels and needs polycystin to detect the direction of blood flow, so that it can make the needed adjustments in flow so that the brain gets it's blood supply.
What about MVP and AR? Is there a role for polycystin here as well as it is the place where you want the blood to flow in one direction.
2) What is the role of estrogen in altering the function of polycystin?
3) If PKD was so bad, how did it survive evolution ? Was it a case of positive selection or Was it a case of a recent mutation that has not entirely gone through the rigor of evolution?
If it was a case of positive selection, under what conditions was it selected and what are the benefits of PKD?
More reading to do!!!
OK Polycystin is a part of cilia and it detects motion. If it is screwed up as it does in PKD, you get cysts.
The organs affected like Kidney, liver(Bile), colon (Feces), lung - bronchiectasis(Air) , seminal vesicles(semen) have some thing flowing in a direction.
Only in the CVS it is kind of funky in that
1)Why is it only the circle of willis is affected? Has it got to do with the fact that blood flow can reverse its direction in COW unlike other systemic blood vessels and needs polycystin to detect the direction of blood flow, so that it can make the needed adjustments in flow so that the brain gets it's blood supply.
What about MVP and AR? Is there a role for polycystin here as well as it is the place where you want the blood to flow in one direction.
2) What is the role of estrogen in altering the function of polycystin?
3) If PKD was so bad, how did it survive evolution ? Was it a case of positive selection or Was it a case of a recent mutation that has not entirely gone through the rigor of evolution?
If it was a case of positive selection, under what conditions was it selected and what are the benefits of PKD?
More reading to do!!!
Thursday, January 7, 2010
Tumor lysis in renal cell carcinoma
Doing a morning report on RCC on being treated with Sunitinib lead to AKI.
What is Sunitinib?
A molecule(not antibody) which inhibits multiple tyrosine kinase motifs of second messenger systems of chemokines like VEGF.
It has some crazy side effects like
1) Hypothyroidism
2) Cardiac failure
3) HTN/Proteiuria a.k.a Bevacizumab like
4) Pancreatitis
Only one report of TLS
Coming to TLS
Criteria does not have creatinine!!!
Has uric acid>8
potassium>6
Calcium< 7
Phosphate> 4.5
If preexisting abnormalities in the above values due to some other pathologies take a 25% change.
If cr >1.5x of previous it becomes clinical TLS
TLS most commonly happens in rapidly proliferating tumors.
Why?
They need all the purines for the DNA/RNA for them to grow and when it breaks down as we all know what we get is uric acid
Rapidly proliferating leukemias and lymphomas are the ones at highest risk
TLS happens within 48 hrs of chemo and anything beyond is unlikely from TLS
Why do the electrolyte changes happen?
Potassium is intracellular and when the chemo lyses the cell it comes out
same applies to phosphate/urate
calcium goes down due to phosphate binding with it
How is the kidney affected?
Uric acid precipitates and blocks up the nephrons
What do we do about TLS
1) Prevent it by
- IV fluids - keep the uric acid low in concentration in the kidney
- Allopurinol - only useful preemptive and does not prevent xanthine and hypoxanthine from precipitating!
- Uricase - melt the uric acid simple
Bicarbonate is unproven as it will make uric acid soluble but calcium phosphate insoluble:(
2)Treat
- HD - Takes out uric acid
- Uricase
What is Sunitinib?
A molecule(not antibody) which inhibits multiple tyrosine kinase motifs of second messenger systems of chemokines like VEGF.
It has some crazy side effects like
1) Hypothyroidism
2) Cardiac failure
3) HTN/Proteiuria a.k.a Bevacizumab like
4) Pancreatitis
Only one report of TLS
Coming to TLS
Criteria does not have creatinine!!!
Has uric acid>8
potassium>6
Calcium< 7
Phosphate> 4.5
If preexisting abnormalities in the above values due to some other pathologies take a 25% change.
If cr >1.5x of previous it becomes clinical TLS
TLS most commonly happens in rapidly proliferating tumors.
Why?
They need all the purines for the DNA/RNA for them to grow and when it breaks down as we all know what we get is uric acid
Rapidly proliferating leukemias and lymphomas are the ones at highest risk
TLS happens within 48 hrs of chemo and anything beyond is unlikely from TLS
Why do the electrolyte changes happen?
Potassium is intracellular and when the chemo lyses the cell it comes out
same applies to phosphate/urate
calcium goes down due to phosphate binding with it
How is the kidney affected?
Uric acid precipitates and blocks up the nephrons
What do we do about TLS
1) Prevent it by
- IV fluids - keep the uric acid low in concentration in the kidney
- Allopurinol - only useful preemptive and does not prevent xanthine and hypoxanthine from precipitating!
- Uricase - melt the uric acid simple
Bicarbonate is unproven as it will make uric acid soluble but calcium phosphate insoluble:(
2)Treat
- HD - Takes out uric acid
- Uricase
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