Hello everyone!
Click here to read about Lipoproteins and apoproteins if you need a quick revision before we get started :)
In this blog post, I'll be talking about lipoprotein disorders, how to remember them and some facts that you need to know about the disorders.
Type I hyperlipoproteinemia
Chylomicrons increased in childhood.
VLDL increased later in life.
Lab findings: Increase in serum triglycerides.
Why?
CPL (Capillary lipprotein lipase) hydrolyzes triglycerides in lipoproteins.
It requires apo-CII as a co-factor.
Clinical findings: Acute pancreatitis (Pancreatic vessels filled with chylomicrons rupture), eruptive xanthomas.
Type II hyperlipoproteinemia
Serum LDL is increased.
Lab findings:
In IIa, only cholesterol is increased.
Why?
Liver cholesterol synthesis is deprived of negative feedback.
In IIb, cholesterol and triglycerides are increased.
Why?
Liver overproduces VLDL in IIb
Acquired causes: Primary hypothyroidism, nephrotic syndrome, extrahepatic cholestasis.
Clinical findings: Tendon xanthomas, Xanthelasma, premature coronary artery disease and stroke.
Type III hyperlipoproteinemia
This dysbetalipoproteinemia is also known as "remnant disease".
Lab findings: Elevation in cholesterol and triglyceride levels.
Why?
Apo E is required to remove chylomicron remnants and IDL (remnant of VLDL).
Clinical findings: Palmar xanthomas, increased risk for coronary artery and peripheral vascular disease.
Type IV hyperlipoproteinemia
Increase in VLDL.
Lab findings: TG accumulates
in preference to cholesterol, like IIb.
Acquired causes: Excess alcohol, OCPs, Diabetes mellitus, chronic renal failure, thiazides, beta blockers.
Clinical findings: Eruptive xanthomas, increased risk for coronary artery and peripheral vascular disease.
For the sake of completion, I'd like to add another disease -
Tangier disease is due to lack of ABC1 cholesterol transporter gene.
Cholesterol accumulates inside cells. Blood HDL and cholesterol are low.
The disease is characterized by atherosclerosis, hepatosplenomegaly, polyneuropathy and orange tonsils.
*phew* That's all!
Like I always say, if you stare at a word long enough, you find the mnemonic in the word itself :P
I made these myself, hope you find them helpful ^__^
Happy Indian Independence Day :)
-IkaN
Click here to read about Lipoproteins and apoproteins if you need a quick revision before we get started :)
In this blog post, I'll be talking about lipoprotein disorders, how to remember them and some facts that you need to know about the disorders.
Type I hyperlipoproteinemia
Chylomicrons increased in childhood.
VLDL increased later in life.
Lab findings: Increase in serum triglycerides.
Why?
CPL (Capillary lipprotein lipase) hydrolyzes triglycerides in lipoproteins.
It requires apo-CII as a co-factor.
Clinical findings: Acute pancreatitis (Pancreatic vessels filled with chylomicrons rupture), eruptive xanthomas.
Type II hyperlipoproteinemia
Serum LDL is increased.
Lab findings:
In IIa, only cholesterol is increased.
Why?
Liver cholesterol synthesis is deprived of negative feedback.
In IIb, cholesterol and triglycerides are increased.
Why?
Liver overproduces VLDL in IIb
Acquired causes: Primary hypothyroidism, nephrotic syndrome, extrahepatic cholestasis.
Clinical findings: Tendon xanthomas, Xanthelasma, premature coronary artery disease and stroke.
Type III hyperlipoproteinemia
This dysbetalipoproteinemia is also known as "remnant disease".
Lab findings: Elevation in cholesterol and triglyceride levels.
Why?
Apo E is required to remove chylomicron remnants and IDL (remnant of VLDL).
Clinical findings: Palmar xanthomas, increased risk for coronary artery and peripheral vascular disease.
Type IV hyperlipoproteinemia
Increase in VLDL.
Lab findings: TG accumulates
in preference to cholesterol, like IIb.
Acquired causes: Excess alcohol, OCPs, Diabetes mellitus, chronic renal failure, thiazides, beta blockers.
Clinical findings: Eruptive xanthomas, increased risk for coronary artery and peripheral vascular disease.
Type V hyperlipoproteinemia
Increase in chVlomicrons and VLDL.
It is a mixture of types I and IV familial dyslipidemias.
Lab findings: TG levels are high, whereas cholesterol concentration increases only moderately.
Clinical findings: Like type I, but unlike type IV, there is no major risk of atherosclerosis, so that pancreatitis and eruptive xanthomas remain the main complications.
Here is a summary table :)
For the sake of completion, I'd like to add another disease -
Tangier disease is due to lack of ABC1 cholesterol transporter gene.
Cholesterol accumulates inside cells. Blood HDL and cholesterol are low.
The disease is characterized by atherosclerosis, hepatosplenomegaly, polyneuropathy and orange tonsils.
*phew* That's all!
Like I always say, if you stare at a word long enough, you find the mnemonic in the word itself :P
I made these myself, hope you find them helpful ^__^
Happy Indian Independence Day :)
-IkaN
really thanks a lot
ReplyDeletevery creative dude!
Aww.. Thank you :) Glad it helped ^__^
Deletei came to know that u have a immunology blog too...
Deletei have a doubt ...
does dendritic cells exhibit both mhc 1 and mhc 2?
i have studied that all nucleated cells express mhc 1
Oh yes, I do.
DeleteHere's the link to the answer:
http://immense-immunology-insight.blogspot.in/2013/10/question-which-cells-have-which-mhc.html
Thanks for asking =)
thnx for clearing my doubt!
Deletethat too in ur sTyLe ! :-)
may i know the source from where u got the answer for my question?
DeleteUmm.. I kinda knew this from before. Can I state the reference as my brain? =P
DeleteA similar question was asked here: http://answers.yahoo.com/question/index?qid=20110622181149AAtQqYh
Hope it helps! :)
no probs :)
Deletebut since i am appearing for my post graduate exam entrance exam i needed a reliable answer thats it!!
thnx again !!!!! :-)
Ohh, that way.. You may refer to the book Janeway's Immunobiology 8th Edition, Fig 9.2, it's giving there. I can not paste the info here due to copyright issues =)
DeleteAlmost all nucleated cells express MHC class I receptors, including professional APCs.
DeleteIf a virus infects a macrophage or dendritic cell, it will try to promote its own destruction through cytotoxic T cells.
However, dendritic cells can ingest viruses through pinocytosis and therefore activate the adaptive immune response to create antibodies for the virus through class II MHC receptors.
Source: Wikipedia http://en.wikipedia.org/wiki/Antigen-presenting_cell
i d like to markawesome a hundred times for that.
ReplyDeleteAw that's so sweet.
DeleteLove x100 times for you!
You are awesome. Never forget that. :)
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DeleteSuperb!!!!
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DeleteU made it so simple, love it, tnx dr
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DeleteI was having a hard time with these... not anymore! Thanks so much!
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ReplyDeleteThank you .. I was really having hard time with this topic .
ReplyDeleteThank you very much :)
Thanks!! It really helped me a lot..you are awesome!
ReplyDeleteThank you!! This is great!
ReplyDeleteThanks so much, mnemonics on these are hard to find!!! Think I finally have them down.
ReplyDelete