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153 Cards in this Set

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  • Back
What is PKU?
think smelly, retarded babies
What's one reason that binging on booze is a bad idea (aside from the ugly people you might sleep with...)?
alcohol-> increased NADH -> decreased gluconeogenesis -> acidosis -> huge ER bill
What is Kwashiorkor?
think Starvin' Marvin
What's another reason for not being an alky (besides the meetings)?
pellegra- vitamin B3 deficit that gives you a rash, the shits, and altered mental status (even when sober)
Why is my urine black and what the Hell are these black dots on my eyes?!
What is familial hypercholesterolemia?
defective LDL receptors-> accelerated atherosclerosis & xanthomas
Name the fat soluble vitamins, Fat Ass!
think Eating Donuts Adds Kilocalories!
Why could a person be deficient in fat soluble vitamins (esp considering that most of us have plenty of space to store these buggers!)?
think malabsorption- sprue, CF, too much of Mom's mineral oil tx (a spoon a day keeps the enema away!)
What do B vitamin deficiencies result in (other than pernicious anemia)?
dermatitis, glossitis, shits
What is beriberi? Hint: It's not a Voodoo curse.
vitamin B1 deficiency; spell it ber1ber1 (1=i); B1 is required for TPP (generates pyruvate) & transketolase (HMP shunt)
What's the difference b/w wet & dry beriberi (other than that not so fresh feeling)?
dry= polyneuritis, muscle wasting

wet=dilated cardiomyopathy, edema
What happens when you don't get your riboflavin (B2) on?
it's important to have ribo-"flava" (not just b/c the chicks dig it) but FAD & FMN come from it; flava is not just a FAD but a Functionally Mandatory Necessity! not having flava causes angular stomatitis, cheliosis, & corneal vascularization (chicks don't dig this)
What the Hell is Pantothenate? Is that the crap in Pantene that will give my hair lusterous shine upon one washing?
it's B5. it helps make CoA & fatty acid synthase (no wonder why i'm so damn sexy!); lack of B5 gives you dermatitis, enteritis, alopecia & adrenal insufficiency. com'on girls, no guy wants a flaky skinned, bald girlfriend who's adrenal glands don't put out, so take your vitamins!
Was I absent the day we learned about pyridoxine (B6) or do I merely have a B6 deficiency?
I was probably in class the day they taught this but suffering from convulsions/hyperirritablity due to my B6 deficiency brought on by the stresses of med school. it turns out that B6 is needed for ALT, AST (transamination), decarboxylation, & heme synthesis.
Why is B12 important (for the umpteenth thousand time)?
B12 (aka cobalamin)required for homocysteine methylation & methylmalonyl-CoA handling; decreased homocysteine-> decreased methionine-> messed up myelin & increased methylmalonyl-CoA-> increased methylmalonic acid-> messed up myelin; vegetarians eat your heart out (no really, b/c its full of the B12 you'll need to thwart off macrocytic, megaloblastic anemia); US causes are due to malabsorption (vs dietary insufficiency); think sprue, Crohn's, pernicious anemia; do a Schilling test
Why is folic acid so important? Does it justify all of the public service announcements?!
geeze, it's only important if you want to synthesize DNA/RNA! why the concern??
What's biotin? Sounds like some tree hugging herbal medicine crap!
biotin is needed for carboxylating (eg oxaloacetate, malonyo-CoA, methylmalonyl-CoA); deficits lead to dermatitis & enteritis due to antibiotic use or ingesting raw eggs (Rocky must have had some mad IBS!)
Why do we need vitamin D?
b/c we don't want rickets! there is such thing as too much of a good thing, though- too much vitamin D-> hypercalcemia, stupor (think sarcoidosis)
Why does Mom always shove vitamin C down your throat?
no Mom wants a kid w/scurvy unless she's British. vitamin C cross links collagen for healing, facilitates iron absorption, & needed for dopamine synthesis (is this why the British are so static?)
What does vitamin E do?
protects RBCs
What does vitamin K do?
K is for koagulation (spelling proficiency wasn't a requirement for med school matriculation); intestinal coodies are required for its synthesis (this is why babies & pts on broad spectrum anti-biotics have increased PT & PTT; warfin is it's nemesis (warfin is at war w/ vitamin K)
Who are vitamin K's dependents?
after much investigation, the family court ruled that vitamin K is responsible supporting its progenous clotting factors II, VII, IX, X, & protein C (until age 18 whereby his progeny will bleed to death)
What vitamin keeps your testicles plump and your hair flowing? (Guys, take notes!)
zinc; aside from small balls and baldness, lack of zinc will cause delayed wound healing & predispose you to alcoholic cirrhosis!
Explain ethanol metabolism (and don't say you're too drunk to remember!)
ethanol-> acetaldehyde-> acetate; requires alcohol dehydrogenase, acetaldehyde dehydrogenase, NAD+, NADH; NAD+ is limiting reagent
What gives you a hang-over? Hint: the answer isn't St. Ides Malt Liquor (although this is justifiable).
saturation of acetylaldehyde dehydrogenase; this is how antabuse works
What is marasmus?
tissue/muscle wasting due to energy malnutrition (compare w/Kwashiorkor)
What is a nucleosome?
it's the DNA AND core histones; the "beads" on the string that, altogether, comprise what's called chromatin
What's so cool about H1 (histone 1)?
it's the histone that ties all the nucleosomes together. H1 is a rebel, not part of the core b/c it's too cool for the core.
What is heterochromatin? Hint: chromatin does not have a sexual preference.
this is the transcriptionally abstaining form of chromatin. it's very uptight (looped around histones). it's not promiscuous like that loose slut euchromatin.
Name the purines?
think "pure As Gold"- A,G
What nucleotides bind to which?
G-C (strongest); A-T
What goes into making a good purine?
besides sugar and spice and everything nice, purines require glycine, aspartate, and glutamine
What's this difference b/w a transition mistake & a transversion mistake?
transItion= Identical substitute
transVersion= conVersion b/w types
Why will mother nature never receive a Pulitzer Prize?
b/c her writing is redundant and lacks punctuation. in her defense, her writing is also unambiguous & used universally
What's a silent mutation?
it's more palatable than a missense or nonsense mutation. think "it is better to remain silent & be thought a fool then to speak & remove all doubt". silent mutations are often the result of a tRNA wobble at the 3rd position (damn it tRNA, switch to decaf!)
What is a missense mutation?
it's replacing one aa with a similar aa. kind of like substituting a democrat with a republican.
What is a nonsense mutation?
think stop the nonsense
What is a frame shift mutation?
this is really bad. its when your tRNA starts reading The Oddessy but becomes impatient & settles for the Cliff Notes.
How are DNA topoisomerases & conditioner alike?
they both remove those pesky tangles!
Why is DNA so codependent?
DNA, like many of us, needs the motivation of another to function. primase is the muse of DNA. she (or he) makes the RNA primer on which DNA polymerase III can begin replication.
Does DNA polymerase ever look back?
it may seem that DNA polymerase has no regrets and unaffectedly carries on in his 5'->3' direction. in truth, though, he is very aware of his past mistakes & corrects them in the 3'->5' direction with exonucleases.
What does DNA polymerase I have against RNA primer?
she has always hated that tart, RNA primer. thus she uses her exonucleases to degrade RNA primer at any given chance & fills in the gaps w/DNA (she is much against interrelationships b/w RNA & DNA (she's a deoxyribose supremicist).
What keeps us from getting xeroderma pigmentosa?
we have endonucleases that kick out messed up nucleotides.
Are all bases created equal?
NO! we make a lot of messed up bases that glycolases remove by cutting the base out at a pyramimidic site.
What happens when there're irreconsilable differences b/w nucleotides?
if counseling doesn't work, then your body may hire a mismatch repair attorney. people w/hereditary nonpolyposis colon cancer lack access to litigation.
What are the different kinds of RNA polymerases in eukaryotes?
Which RNA polymerase helps DNA open up?
II=mRNA poly. her nemesis is her mother-in-law alpha-amantin (she thwarts all efforts of mRNA poly by serving her death cap mushrooms at all family get togethers).
When does transcription begin?
in AUG just like school. codes for methionine
When does transcription end (and don't say JUN)?
think U Go Away, U Are Away, U Are Gone (geeze, mRNA can take a hint!).
What is a promoter?
well DNA likes to be recognized for its contributions too. it takes a lot of work to make protein & this should be rewarded. DNA doesn't care about money, having a trust fund an all... DNA is rewarded for its efforts by being somewhat relieved of duty by RNA poly & other transcription factors. this only takes place after DNA has done most of the work & has reached a TATA or CAAT box.
What is an enhancer?
area of DNA that attracts transcription factors that enhance gene expression.
What is an operator?
area of DNA that attracts transcription factors that repress gene expression.
What's the difference b/w an intron & exon?
exons are what contribute to your growth while introns are just interuptions along the way (kind of like your first boyfriends); introns remain in the nucleus.
How does hnRNA become whole in spite of all of her intron baggage?
well differences are the "splice" of life, so hnRNA discovers new meaning by redefining herself via new experiences. she decides to move on w/the aide of her snRP friends, forming a spliceosome alliance. They help her release her intron baggage, thereby allowing her to persue healthy relationships w/exons. happy w/the exons, hnRNA agrees to seal the deal by capping & polyadenylation (huge commitment). she is now referred to as mRNA (she's old fashioned & conceeded to the name change).
What is Pellegra?
think 3D: diarrhea, dermatitis, dementia; caused by niacin (B3) def or a tryptophan def; B3 comes from tryptophan.
Name the Vitamin D forms.
D2= ergocalciferol (drink milk); D3= cholecalciferol (get some sun); 25-OH D3= storage; 1,25 (OH)2 D3= active form-> intestinal absorption of calcium & phosphate.
What is tRNA?
transfer RNA is the pre-aminoacid. the amino acid is covalently attached to its 3' end.
What does tRNA look like?
cloverleaf shape; CCA at 3'end.
what is aminoacyl-tRNA synthetase?
it's the enzyme that makes the amino acid; there's 1 for every kind of amino acid; it is also a proof reader for its amino acid; it requires ATP to make a peptide bond but will read the transcript w/o it.
why does tRNA wobble?
b/c it need only accurately read the first two nucleotides, then it can just insert whatever (hopefully a nucleotide that codes for the proper amino acid).
How is protein synthesis initiated?
a 30S ribosome unit/initiator tRNA are hooked up w/the assistance of initiation factors
what happens during elongation?
1. aminoacyl tRNA binds to A site 2. peptidyltransferase makes a peptide bond & transfers growing polypeptide chain to A site 3. ribosome cruises 3 nucleotides toward 3' RNA while moving peptidyl RNA to P site.
how is protein synthesis terminated?
protein is released from ribosome.
what is the E site of the ribosome?
where tRNA is held while exiting.
what is trimming?
post-translational modification; removal of N or C terminal from a zymogen.
what is a covalent modification?
post-translational phosphor/glycos/hydroxylation.
what does ubiquitin do?
it is the scarlet letter to be worn by defective proteins.
how are cell cycles regulated?
by checkpoints that control the cell phases; regulators include cyclins, cdks, & tumor suppressors.
what's included in mitosis?
PMAT; this is the shortest phase.
what's included in interphase?
G1, S , G2
what's Go? Hint: it's not that lame movie.
it's where permanent cells stay if you refrain from dropping acid. neurons, skeletal mm, RBCs, cardiac mm.
what are stable cells?
although they are compliant w/their Prosac tx, they are also capable of entering G1 if stimulated; otherwise they'll stay in G1; hepatocytes, lymphocytes
what are labile cells?
they never Go; they are always movin' rapidly, though; marrow, gut epithelium, hair
What takes place in the rough ER?
synthesis of exported secretory proteins & N-linked oligosaccharide addition (eg goblet cells & plasma cells are rich w/rough ER).
What tkaes place in the smooth ER?
site of steriod synthesis & detox.
What does the golgi do?
processing & packaging of proteins & lipids from ER to plasma membrane; modifies N-oligosaccharides on asparagine; adds O-oligisaccharides to serine & threonine; adds mannose-6-P; assembles & sulfates proteoglycans & tyrosine.
What is I-cell disease?
when mannose-6-P addition by the golgi doesn't target lysosome proteins to lysosome; coarse face, clouded corneas, restricted jiont movement; high plasma lysosomal enzymes; fatal in childhood.
What is COPI?
vesicular trafficking protein; golgi -> ER (retrograde).
What is COPII?
vesicular trafficking protein; RER -> cis-golgi (anterograde).
What is clathrin?
vesicular trafficking protein; trans-golgi -> lysosomes, plasma membrane -> endosomes.
What are microtubules?
polymerized dimers of alpha/beta-tubulin; 2GTP bound/dimer; part of flagella, cilia, & spindles.
Name 5 drugs that act on microtubules?
mebendazole, taxol, griseofulvin, vincristine, colchicine.
What is Chediak-Higashi syndrome?
microtubule polymerization defect.
What are cilia made of?
microtubule doublets (9 +2)linked by dynein ATPase.
What is Kartagener's syndrome?
defective dynein resulting in defective cilia.
What is the plasma membrane made of?
cholesterol, phospholipids, sphingolipids, glycolipids, proteins.
What is phosphatidylcholine(aka lecithin)?
component of RBC membrane, myelin, bile, & surfactant; esterfies cholesterol (eg LCAT).
Name 2 drugs that inhibit the sodium pump?
ouabain binds K+ site; cardiac glycosides inhibit Na+/K+ATPase.
Name the 4 types of collagen.
type 1= bone, skin, tendon, cornea; type II= catilage; type III = reticulin; type VI= basement membrane.
What cells make collagen?
How is collagen made?
preprocollagen synthesized in RER-> hydroxylation (req Vitamin C)-> glycosylation in golgi & synthesis of procollagen; exocytosis; proteolysis into tropocollagen; crosslinking forms collagen fibrils.
What is Ehlers-Danlos syndrome?
defective collagen synthesis; hyperextendible skin, bruising, hypermobile joints; assoc w/berry aneurysms; inherited.
What is osteogenesis imperfecta?
abnormal type I collagen synthesis; autosomal dominant; fractures, blue sclerae, hearing loss, dental problems.
What is Marfan's syndrome?
defective fibrillin.
What is elastin made of?
non-hydroxylated proline & lysine; elastin= tropoelastin + fibrillin scaffolding; elastase allows relaxed form; alpha1-antitrypsin inhibits elastase.
What happens in the mitochondria?
beta-oxidation, acetyl-CoA production, Kreb's cycle.
What happens in the cytoplasm?
glycolysis, fatty acid synthesis, TTP shunt, protein synthesis (RER), steroid synthesis (SER).
What happens in both the mitochondria & the cytoplasm?
gluconeogenesis (hepatocytes), urea cycle, heme
What is S-adenosyl-methionine (aka SAM)?
ATP + methionine; transfers methyl units; relies on B12.
What is NADPH?
electron acceptor used in anabolic processes (eg steroid synthesis), respiratory burst, & P-450; comes from the TPP shunt.
What is chronic granulomatous disease?
deficit of NADPH oxidase (makes bleach out of O2); neutrophils can't kill bugs
What blood problem is commonly assoc. w/a glycolytic enzyme deficiency?
hemolytic anemia b/c RBC's rely on glycolysis for energy.
What is the pyruvate dehydrogenous complex?
the enzyme + vitamins B1,2,3,5, + lipoic acid; makes pyruvate into acetyl-CoA; activated by excercise.
What happens when you have a pyruvate dehydrogenase deficiency?
lactic acidosis, neurologic defects; tx w/ketogenic nutrients.
How many ATP does 1 NADH make per turn?
How many ATP does 1 FADH2 make per turn?
Name 8 ox-phos poisons.
rotenone, CN-, antimysin A, CO (e- transport inhibitors); oligomycin (ATPase inhibitor); UCP, 2,4-DNP, aspirin (uncouplers).
What happens when you have a glucose-6-P deficiency?
cannot generate G6PD that is required to reduce glutathionine that detoxifies the free rads & peroxides; RBC's are especially susceptible to oxidizing agents & will form hemoglobin precipitates (Heinz bodies); Blacks; X-linked recessive.
What happens when you have an aldolase B deficiency?
recessive; fructose accumulation; inhibition of glycogenolysis & gluconeogenesis; hypoglycemia, jaundice, cirrhosis, vomiting.
What is essential fructosuria?
deficient fructokinase; benign.
What is galactosemia?
autosomal recessive; absence of galactose-1-P uridyltransferase; accumulation of toxins (eg galactitol); cataracts , hepatosplenomegaly, mental retardation
Name the essential aminoacids.
Hint: PriVaTe TIM HALL.
phe, val, thr, trp, ile, met, his, arg, leu, lys
What is hyperammonemia?
can be acquired (eg liver damage) or hereditary (eg ornithine transcarbamoylase def); excess NH4+ -> inhibition of Kreb's cycle; tremor, slurring, vomiting, cerebral edema, blurred vision, somnolence.
Why do we need insulin?
allows entrance of glucose into adipose & muscle cells.
What does insulin inhibit?
glucagon release by alpha pancreas cells.
What does insulin do?
increases: glucose transport, glycogen synthesis/storage, TG synthesis/storage,Na+ retention, protein synthesis (muscles).
What cells don't require glucose? Hint: BRICK L
brain, RBCs, intestine, cornea, kidney, liver.
What role does adrenaline (aka epinephrine) play in glycogenensis & glycogenolysis?
glycogenesis = (-)
glycogenolysis = (+)for both muscle & liver glycogen stores.
What's the difference in glycogen response for muscle vs liver?
muscle metabolizes glucose fast; the liver acts to maintain blood sugar levels.
How do you synthesize fat?
acetyl-CoA (mitochondria)-> citrate shuttle (matrix)-> acetyl-CoA + biotin (cytoplasm)-> malonyl CoA-> FA
How do you burn fat?
FA + CoA-> acyl-CoA (cytoplasm)-> carnitine shuttle (matrix)-> acyl-CoA which is beta-oxidized into acetyl-CoA groups.
What are ketone bodies?
FA + aminoacids in the liver -> acetoacetate + beta-hydroxybutyrate. these products can be used in leiu of glucose during fasting & diabetes for the brain & muscle; fruity breath.
How do you make cholesterol?
HMG-CoA reductase is the rate limiting step; converts HMG-CoA to mevalonate; most cholesterol gets esterfied by LCAT.
What drug inhibits cholesterol synthesis?
lovestatin inhibits HMG-CoA reductase.
What are the essential fatty acids?
linoeic & linolenic acid. eicosanoids rely on these babies!
What does pancreatic lipase do?
degrades TG in small intestine.
What does lipoprotein lipase do?
degrades TG in chylomicrons & VLDLs.
What does hepatic TG lipase do?
degrades TG in IDL.
What does hormone sensitive lipase do?
degrades TG in adipocytes.
What does LCAT do?
esterfies cholesterol.
What does CEPT do?
transfers cholesterol esters to other lipoproteins.
What does A1 do?
activates LCAT.
What does B-100 do?
binds to LDL receptor & mediates VLDL secretion.
What does CII do?
it's a cofactor for lipoprotein lipase.
What does B-48 do?
mediates chylomicron secretion.
What does E do?
mediates extra remnant uptake.
What are lipopriteins made of?
cholesterol, TG, phospholipids.
What do chylomicrons do?
takes TG from intestine to peripheral tissues & cholesterol to liver.
Which lipoproteins do chylomicrons need?
B-48, A,C,E.
What does VLDL do?
takes liver TGs to peripheral tissues.
Which lipoproteins do VLDLs need?
B-100, C-II, E
What does IDL do?
comes from VLDL degradation. takes TGs & cholesterol to liver to process into LDL.
What lipoproteins does IDL need?
B-100, E.
What does LDL do?
takes liver cholesterol to peripheral tissues; formed from VLDL via lipoprotein lipase in peripheral tissue.
What lipoproteins does LDL need?
What does HDL do?
takes peripheral cholesterol to liver; also a storage for apoC & apoE for chylomicron & VLDL metabolism; secreted by liver & intestine.
How is heme broken down?
heme-> biliverdin-> bilirubin -> liver -> bile.
What is heme made of?
2 alpha + 2 beta polypetide subunits.
Explain R vs T forms of heme.
T = low O2 affinity; R= high O2 affinity. T unloads!
What favors T form over R form heme?
increased: Cl-, H+, CO2, 2,3-BPG, temperature favor O2 unloading; shifts curve right.
What happens to CO2?
travels as bicarbonate in blood to lungs; binds to globin (not heme); favors T form of heme.
What is methemoglobin?
this is oxidized hemoglobin (Fe3+) that prefers CN- over O2; push nitrates!
What is carboxyhemoglobin?
hemoglobin has a fettish for CO.