I have a biochem exam tomorrow, and I need to summarize some of my flashcards in different words.  What better place to do it than my blog?  Maybe some people will find the post through google sometime and maybe it will help them out.  Here’s to hoping!

If you aren’t a doctor or a medical student, you won’t understand most of this.  If you are easily offended, please don’t read this, or at least don’t complain to me, because this contains mnemonics.  To remember things, sometimes your words have to be a bit rough.

One last thing, just so you don’t think I’m a wanker.  This is just my last day’s stuff, so don’t assume this is all I know.  I am like Yoda, or House (or at least I want to be).

What is the Function of CN, Azide and CO?

-They prevent electron transfer through complex four

Think of a four bedroom house (complex four), in it someone is getting poisoned with Cyanide and the propane heater is going to kill everyone else with carbon monoxide!!!!

Antimycin A

Prevents Electron transfer through complex three

AAC3….AAC3  Antimycin A Complex 3….stay in my head please!

Rotenone and Amytal

Inhibits transfer of electrons from complex one to ubiquinone

Amy memorizes things by Rote.  Things can be rather ubiquitous in her mind!

Flourine

Besides brittle teeth, what does it do?

It inhibits enolase, thereby preventing 2PG from becoming PEP

You get no pyruvate or final ATP in Glycolysis (which makes glycolysis useless)

Kind of like the government.  They put flouride in your water.  They are useless.  Flourine makes glycoloysis useless…

Arsenate (Arsenic Poisoning)  How does it work?

It inhibits Glyceraldehyde-3-p-dehydrogenase, thus bypassing the dephosphorylation of 1,3-BPG.  Thus, we are not getting our first ATP in glycolysis.  Glycolysis goes on, but it is ineffective.  Then, the rich husband without a prenup dies!

Just think of a hot woman poisoning a rich man to get his money.  Its the first time that has ever happened!

Malonate

Inhibits succinate dehydrogenase

Thus, it prevents succinate from becoming fumarate.  This sucks.

You could also think of a law forbiding oral sex…inhibition of succinate dehydrogenase.  That would be bad (MALonate).

Cori’s Disease

Debranching Enzyme Deficiency…can only break down linear glycogen chains.

Glycogen accumulates in the heart, liver and skeletal muscles.

It leads to stunted growth, hepatomegaly and hypoglycemia

I think of Cori, who was a manager at my first job.  He was a little man who was an alcoholic who couldn’t afford to eat healthy food (hence the hypoglycemia).  He also couldn’t form complex thoughts (i.e. couldn’t break down little chains).  I hated that little man.  He is probably dead or in jail now.

Fluroacetate (Rat Poison!!!)

Inhibits aconitase, preventing the conversion of citrate to isocitrate in TCA.

Flouracetate Preserves Citrate!  Rats keep an orange grove from being harvested!

GLUT-1

RBCs, Brain…uptake

Brain is the first thing that needs glucose.  RBCs need it because they can’t use anythign else.

GLUT-2

Liver and Beta Cells

It goes both ways.

If it goes both ways, it is obviously taking it up the place typically associated with number two.  Any sugars absorbed there must go to the liver.

GLUT-3

Neurons

We give stuff to neurons for free becuase they are special.

GLUT-4

Muscle and Adipose Tissue

Insulin Dependent Uptake

Yeah, Type II diabetics are usally GLUTons 4 lots of stuff that goes into adipose tissue.

GLUT-5

Fructose

Small intestines

Testes

Imagine sperm having so much energy that they can make five babies in one go!

GLUT-7

Gluconeogenic Tissues

Flux Across ER

Think of a 747 flying into the ER (some kind of 9/11 image there)

Von Griek’s Disease (GSD I)

Glucose-6-Phosphatase Deficiency

Gluconeogenesis is inhibited

SEVERE FASTING HYPOGLYCEMIA (they say this is a buzzword!)

Hepatomegaly

So, we have a guy named Von Griek, and he eats all the time because he always has hypoglycemia.  He gets fat, and so does his liver.

It is inherited as Autosomal Recessive like every other GSD except for Phosphorylase Beta Kinase Deficiencey (which is X linked)

I-Cell Disease (GSD)

Deficiency of the ability to phosphorylate mannose.  Characterized by:  Skeletal abnormalities, restricted joint movement, coarse facial features and death by eight years old (ain’t that nice?)

They can’t phosphorylate mannose on its way to the lysosome

So, some ugly crippled eight year old wants an I-Pod?  Kill him!  He will never be a MAN

Pyruvate Dehydrogenase Deficiency

Congenital Lactic Acidosis.  Brain problems.  Failure to Thrive.  Deprived of Acetyl CoA.

Wow, that just sucks.  I don’t have a way to remember this.  That sucks even more.

Chronic Granulomas

Genetic Defect in NADPH Oxidase

Pyrogenic infections and granulomas

North America Drops Plutonium Hell and its is oxidised into granules.  Yeah, its dumb.  So what, I’ll remember it that way.

Atractylosidase (Plant Toxin)

Disrupts ATP-ADP transport

Prevents proper ATP-ADP transport across membrane

Atractylosidase starts with AT, just like ATP

Glycolytic Enzyme Deficiencies

All of them are autosomal recessive

All of them cause hemolytic anemia

Most common is pyruvate kinase deficiency.

 This is B/C RBCs only do glycolysis, so they die when it doesn’t work.

NADPH-Dependent Xylulose

Defeciency causes “essential pentosuria”.  L-xyulose found in urine.

What is the pH of urine?  It isn’t FIVE!  Xyulose is wierd.  Starts with XY.  Guys are sometimes kind of wierd too.

Pompe’s Disease (GSD II)

Cardiomegaly.  Leads to death.  Can’t break down glycogen.  Lysosomal energy defect.  Normal blood sugar.

Some pompous man has a big heart.  He never dips into his savings, though, and never throws anything away.  He always has a normal amount of cash too.

Glycosyl Phosphate Dehydrogenase Deficiency

This one is X-Recessive!!!!  There is no hexose monophosphate shunt.  There is a defect of NADPH.  Inability to maintain gluthione in RBCs.  Hemolytic anemia.

Womean bleed once per week, and the pH in their vagina is really low.

2,4 Dinitrophenol

Uncouples the ETC.  Makes you BURN UP!

Two nitrus canisters for your car.  Burn baby burn!

Group 3 Splicing Mutations of simple Beta Thalassemias

Exon mutations that affect splice site.  HbE, exon 1, residue 26, GLU–> LYS

Decrease in normal beta globin

Three rhymes with HbE

Digenic Retinitis Pigmentosa

2 mutations on 2 different UNLINKED genes.  Peripherin and Rom1, found it photoreceptor.  You must be HETEROZYGOS for BOTH defects to have the disease.

This one is just…memorable.  Its like I can see it in my head.  Hah!  Folks with Ritinitis Pigmentosa see lots of stuff in their heads!

Enzymes Unique to Gluconeogenesis

Pyruvate Carboxylase, Fl6 Phosphorylase, G6 Phosphatase

Yeah, ok.  Can I have a USB port put into my head so I can remember this???

Congenital Fructose Intolerence “Fructose Poisoning”

Autosomal Recessive.  Aldose B deficiency.  F1P builds up in tissues.  Inhibits glycogenolysis and gluconeogenesis.  Severe Hypoglycemia.

Fructose Poisioning=Aldose B

FPAB

“Frank Porked A Bitch”

Heinz Bodies

In erythrocytes of patients with G6PD deficiency

Impaired ability of RBC to form NADPH.

Heinz….ketchup…contains lots of sodium so it makes you swell, kind of like the RBCs do in this case.

Oxidative drugs and FAVA beans (BUZZWORD), Neonatal Jaundice, Italian People.

  • Share/Bookmark

One Response to “A Bit of Biochemistry Revision”

Leave a Reply

Spam Protection by WP-SpamFree