Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
143 Cards in this Set
- Front
- Back
|
where do most lipoproteins, cholesterol and phospholipids form?
|
liver
|
|
|
where are VDls made
|
liver
|
|
|
what are the triglycerides in liver synthesized from
|
CHOS
|
|
|
does HDL form in intestinal epithelium as absoprtion of fatty acid occurs?
|
yes
|
|
|
main function of lipoproteins?
|
transports lipid components in blood
|
|
|
what is added to lipoproteins to make them hydrophilic?
|
apoprotein
|
|
|
when an apoprotein is added to a lipoprotein, it has several functions, name them
|
ligands, cofactors for lipid metabolism, structural stability
|
|
|
in the exogenous pathway, cholesterol + triglycerides absorbed into intestinal mucosa make what?
|
chylomicrons
|
|
|
exogenous pathway: what does the chylomicrons break down to in circulation?
|
Fatty acids and a remnant (mostly cholesterol)
|
|
|
exogenous pathway: fatty acids are converted to what? and then what happens to them?
|
triglycerides, stored in adipose and muscle tissues
|
|
|
exogenous pathway: where does the remnant go and what is it packaged into?
|
liver, VLDLs, then enter blood
|
|
|
endogenous pathway: what are fats in the liver (dietary) and endogenous cholsterol converted to? what do they enter blood as?
|
triglycerides
VLDLs |
|
|
what happens to the Fatty acids in VLDLs?
|
storage in adipose and muscle
|
|
|
what happens to VLDLs remants?
|
converted to IDLs
|
|
|
what happens to IDLs?
|
taken up by liver
lose more triglycerides and become LDLs, then enter liver and non-liver tissues |
|
|
what effect does insulin and T3 have on LDLs ability to bind liver cells?
|
increases
|
|
|
what effects does glucocorticoids have on LDL receptors?
|
decreases ability to bind to cells
|
|
|
where does HDL pick up cholesterol from as its circulating?
|
chylomicron remnants, VLDL remanmts, plasma membranes of body tissues
|
|
|
as HDLS circulate they pick up cholesterol, what then happens to these cholesterol laden HDLs?
|
go to liver - reverse cholesterol transport
some transferred from HDLs -> LDLs by way of VLDLs |
|
|
what are the 2 ways cholesterol can be returned to the liver?
|
HDL and LDL receptor pathways
|
|
|
what is cholesterol?
|
steroid, dervied from lipids, found in all tissues
|
|
|
is cholsterol fat soluble?
|
yes
|
|
|
what does cholesterol control in cell membranes?
|
fluidity and protein fucntion
|
|
|
is cholesterol found in bile acids and steroid hormones?
|
yes
|
|
|
where is most cholesterol in the body from? diet or produced in body?
|
endogenous production
|
|
|
where in the body is cholesterol produced? and from what?
|
liver, acetyl-CoA
|
|
|
where is cholesterol absorbed from and at what speed? then where does it go?
|
slowly from GI tract
into lymphatics |
|
|
what kind of linkages does cholesterol form with FAs?
|
ester linkages
|
|
|
what form is most of the cholesterol in lipoproteins in blood plasma?
|
ester form
|
|
|
name functions of cholesterol...
|
plasma membrane structure, bile salts, formation of steroid hormones, skin - prevent water soluble stuff from entering, help skin produce Vit D, cell membranes- resist temp change, protects and insultates nerve fibers
|
|
|
is cholesterol that is eaten added to bodys cholesterol?
|
yes
|
|
|
what happens to extra FAs eaten?
|
deposited in liver, liver increases acetyl-Coa production, more cholesterol is made
|
|
|
what effect does lack of insulin have on cholesterol?
|
increases plasma [ ]
|
|
|
can there be a genetic component to blood cholesterol level?
|
yes
|
|
|
what problems can high cholesterol lead to?
|
blood vessel blockages, blood clots, hard arteries, MI, strokes
|
|
|
name risk factors for high cholesterol....
|
diet, gender (M), weight (over), old age, genetics, lifestyle (stress, smoking, alcohol), diseases
|
|
|
where is bile produced?
|
liver
|
|
|
where is bile stored?
|
gallbladder
|
|
|
where does bile go after the GB?
|
duodenum - to emulsify fats and absorb fat soluble vtiamins
|
|
|
what is bile made of?
|
bilirubin, cholesterol, bile salts, bile acids, bile pigments
|
|
|
what part of bile is important for lipid transport?
|
bile acids
|
|
|
what mechanism does the body use to get rid of exfess cholesterol?
|
bile acids
|
|
|
what is converted to make bile acids? and where does it happen?
|
liver, cholesterol
|
|
|
what do bile acids do in GB?
|
prevent stone formation from solidification of cholesterol
|
|
|
what do bile acids do in duodenum?
|
emulsify fats so pancreatic ezymes can act, help absorb fat-soluble vitamins
|
|
|
what is the major way to get rid of cholesterol ?
|
liver adds bile acids to bile, leads to relase in feces
|
|
|
can the body totally rid itself of cholesterol?
|
NO
|
|
|
where do statins act?
|
inhibit HMG-coA reducatse, prevents cholesterol synthesis in iliver
|
|
|
what does a typical phospholipid consist of?
|
at least 1 FA, one phosphate, nitrogen base
|
|
|
are phospholipids lipid soluble?
|
yes
|
|
|
what is the main function of phospholipids?
|
cell membranes
|
|
|
name 3 main phospholipids
|
lecithin, cephalin, sphingomyelin
|
|
|
what does lecithin require in the diet?
|
choline
|
|
|
what does cephalin require in diet?
|
inositol
|
|
|
what is a type of sugar used in cell membranes and is important for nerve, brain, mucle fucntion? and is derived from food from plants?
|
Inositol
|
|
|
where are most phospholipids made? where are the rest made?
|
90% in liver
intestinal epithelium |
|
|
major uses of phospholipids in body...
|
precursors to prostaglandins and thromboxanes, regulate membrane enzymes, part of lipoproteins, thromboplastin - blood clotting, myelin production, dontate phosphate radicals, cell membranes
|
|
|
what does DM do to lipid levels?
|
high triglycerides, low HDL, small LDL, trouble clearing VLDLs
|
|
|
what does alcohol do to lipid levels?
|
high triglycerides, stimulates VLDL and FA levels
|
|
|
what does hypothyroidism do to lipid levels?
|
LDL increase d/t lower active LDL receptors
VLDL increase |
|
|
what are metabolic disorders involving elevated plasma lipoproteins?
|
hyperlipoproteinemias
|
|
|
what forms of hypertriglyceridemia are most common?
|
polygenic and familial
|
|
|
what are treatment for high lipids?
|
diet, mono-unsat FAs, antioxidants, statins
|
|
|
what are the major cholsterol carriers in the body? are they associated with atherosclerosis?
|
LDLS
yes |
|
|
what cholsterol provides protection agsinst formation of blockages?
|
HDLs
|
|
|
what cholesterol delivers triglycerides to muscles and adipose? and are then converted to Ldls?
|
VLDLs
|
|
|
are patients with TC >200 at risk?
|
yes
|
|
|
are LDL/HDL and TC/HDL ratios important for determining risk?
|
yes
|
|
|
what are goal levels for HDL?
|
desirable- >45
undesibrale <35, or 40 |
|
|
what are good ratios for LDL/HDL ?
|
3.2 for women
3.5 for men |
|
|
is the TC level a good predicator of ChD?
|
yes
|
|
|
is VLDL a good predictor of CHD?
|
not sure, but VLDLs go to LDLs which are good predictors
|
|
|
is high LDL level good or bad?
|
BAd---CHD
|
|
|
is high HDL good or bad?
|
good - lower risk of CHD
|
|
|
why do you need to fast before having a lipid test?
|
want to measure LDL and HDL not chylomicrons which disappear fast from blood
|
|
|
what is ApoE?
|
protein that helps carry cholesterol and fat in blood
|
|
|
what chromosome is apoprotein E4 on? and what dz is it associated with?
|
CH 19
Alzheimers |
|
|
how many allelic forms of ApoE are there?
|
3
|
|
|
what does E2 do to cholesterol?
|
lowers TC
|
|
|
what does apoprotein E4 do to TC?
|
raises TC
|
|
|
does E4 have an influence on Alzheimers? and what is it?
|
yes, get it earlier
|
|
|
what is olestra?
|
synthetic fat
|
|
|
is olestra safe?
|
dont know, but lipases cant digest it
|
|
|
what happens in Cushing dz?
|
fats called upon to high degree, ketosis
|
|
|
what does hereditary obesity do to lipase?
|
reduces activity
|
|
|
where is carnitine found?
|
muscle and liver cells
|
|
|
what does carnitine do?
|
thyroid inhibitor, stimualtes FA metabolism b/c it an acetyl-carrier in mictochondiral membranes
|
|
|
what happens if carnitine is deficeint?
|
acetyl groups cant go to Krebs
|
|
|
where are carnitine def seen?
|
hemodialysis pts, premies, "organic aciduria"
|
|
|
what are the sx of carnitine def?
|
mild muscle cramps, severe muscle weakness, death
|
|
|
what is the dz that plaques form on inner wall of arteries?
|
atherosclerosis
|
|
|
what causes atherosclerosis?
|
damage to blood vessel's endothelieum - high level of cholsterol and LDL in diet
|
|
|
what peptide hormeone is produced by fat cells and suppresses appetite?
|
Leptin
|
|
|
is there a direct relatiosnhip b/w amt of stored fat and amount of leptin production?
|
yes
|
|
|
leptin stimulates hypothalamic "anoretic cells"...what does this cause?
|
cells release appetite-suppressing neuropeptide
|
|
|
leptin also inhibits cells called "orexigenic cells that normally release appteptite- stim peptide..so what happens when leptin is present?
|
the appetite stim peptide is NOT released, so appetite is suppressed
|
|
|
are obese pts more likely to develop blood clots? heart attacks and strokes?
|
yes
|
|
|
names diffrent types of proteins..broad categories
|
enzymes, structural, nucleoproteins, O2 transport proteins, contractile, other
|
|
|
what is the basic building block of proteins?
|
amino acids
|
|
|
how are proteins synthesized?
|
peptide bonding b/w amino acids
|
|
|
what are on the ends of a polypeptide?
|
carboxyl and amino group
|
|
|
what process forms polypeptides?
|
removal of H20
|
|
|
what process digests a protein?
|
hydrolysis + addition of H2O
|
|
|
how does GH affect protein metabolism?
|
increase rate of synthesis
|
|
|
how does thyroxine affect protein met.?
|
indirectly inxcreases protein met.
|
|
|
how do glucocorticoids affect protein synthesis?
|
decrease presence of cellular proteins, rise in plasma amino acids
|
|
|
how does insulin affect protein synthesis?
|
if deficeint, syn goes to near zero
|
|
|
how do testosterone and estrogen affect protein syn?
|
deposition of proteins, estrogen not as much
|
|
|
does the type and [amino acids] depend on diet?
|
yes
|
|
|
why are amino acids failry strong acids?
|
occur in blood as ionized (charged) state
from removal of a H+ from amino group |
|
|
what happens to amino acids after a meal?
|
absorbed over 2-3 hrs from GI tract
|
|
|
how quick does the body absorb amino acids once they are in the blood?
|
w/in 5-10 mins
|
|
|
how do amino acids get into cells?
|
active transport - facilitated
|
|
|
why arent amino acids stored in large amts?
|
when aa enter cells, they recombine into proteins that can be stored
|
|
|
what directs the recombination of amino acids?
|
m-RNA and ribosomes
|
|
|
can proteins be catabolized back into amino acids?
|
yes
|
|
|
what enzyme does this?
|
lysozyme
|
|
|
what happens to excess amino acids
|
degraded and used for energy, converted to fat or glycogen and stored
|
|
|
is there a homeostasis b/w plasma and cellular proteins?
|
yes
|
|
|
proteins can be broken down into amino acids...expalin why this happens
|
if cells need a certain protein, amino acids in blood are used to make it - these amino acids are replaced by degrading other proteins in cells
|
|
|
does cancer deplete amino acids in body cells?
|
yes
|
|
|
what are the 3 major kinds of proteins in plasma?
|
albumin, globulins, fibrinogen
|
|
|
what is a major fucntion of albumin?
|
colloid osmotic pressure in plasma
|
|
|
what are globulins responsible for?
|
natural and acquired immunity
|
|
|
what are the proteins that are long-fiber like threads that form during blood clotting?
|
fibrinogen
|
|
|
all of albumin and fibrinogen, most globulins are produced where?
|
liver
|
|
|
where are the rest of the globulins produced?
|
lymphoid tissues
|
|
|
what is an essential amino acid?
|
cant be made in the body, must eat
|
|
|
what is a non-essential amino acid??
|
produced in large amts in the body
|
|
|
do amino acids contain nitogen?
|
yes
|
|
|
what metabolic processes can proteins be used in?
|
gluconeogenesis, ketogenesis
|
|
|
if body has enough protein, what does it do with the rest?
|
stored as fat &/or glycogen or altered by deamination or transamination
|
|
|
do proteins produce more or less ATp than CHO and lipids?
|
less
|
|
|
obligatory protein loss is...
|
amt lost each day regardless ~20-30g/day
|
|
|
what happens if you dont eat enough protein to make up for obligatory loss?
|
digest muscles, structures
|
|
|
what can happen when the liver is not working properly and cant change NH3 into urea during deamination?
|
hepatic coma
|
|
|
is NH3 toxic?
does it buildup? what is it most toxic to? |
yes
yes brain |
|
|
can the liver produce protein when it is being lost d/t some condition?
|
yes up to 30g per day
|
|
|
what is the best tx for severe protein def?
|
plasma protein IV
|
|
|
results from damage to glomeruli of kidneys, leads to lowered BP, increased protein in urine, leads to edema, dx done by urine test or electrophoresis...
|
nephrotic syndrome
|
|
|
abnormal collagen, autosomal dom or recessive, joint and skin manifestations, skin hyperextensilbe, joints are hypermobile
|
Marfans
|
|
|
not common in US, VIt C def, Sx: weak collagen tissue, petechiae, bruises, hemorrhage
|
Scurvy
|
|
|
methods of protein analysis
|
gel electrophoresis, rate of enzyme activity
|
