Lipids Flashcards
lipids
hydrophobic and encased in lipoprotein
4 groups of lipids
-cholesterol esters
-glycerol esters
-fatty acids
-phospholipids
most important lipids
triglycerides and cholesterol
fats help build
structural components
fats specific gravity
<1 = floats to top of water
fatty acids structure
straight chain hydro carbon with carboxyl group
unsaturated
one double bond and at least 1 not saturated with hydrogen
saturated
carbon atom saturated with hydrogen( no double bonds)
all mammals naturally
saturated fatty acids in cis form (allows flexible, bending, even
# carbon atoms)
trans fat
-processing and hardening fatty acids
-poly unsaturated fat
-butter
-from diet
1 fat consumed
triglycerides
esterifed
bound (to be transported); hooks up with cholesterol, glycerol, albumin
body makes majority of fats we needs except
linoleic acid
linoleic acid
essential fatty acid
-from fish
fat is oxidized in
mitochondria- fatty acids converted for energy- either released or stored for ATP
when carbs aren’t readily available goes to
fats then protein
prostaglandins
derivatives of fatty acids
-hormone LIKE in action
-found in almost every tissue- found where needed
all nucleated cells can produce
prostaglandins
ex. of prostaglandins
uterus: aid in contraction
stomach: aid in digestion
platelets: aid in coag
smooth muscle: help with muscle contractions
triglycerides structure
1 glycerol component attached to 3 fatty acids
95% of fat stored is
triglycerides (great energy reservoirs: long term)
where trig from
from diet and produced by liver
forms
from plants= polyunsaturated (cis form)
from animal meat= solid (trans form)
when trig metabolized from fatty acids break apart
fatty acid used for energy
glycerol=
new triglycerides (protect vital organs)
increased trigs=
increased risk of heart attack, pancreatitis, memory loss, foggy brain, xantomas
triglycerides
BAD cholesterol
things that lead to increased trigs
cigarette smoking, obesity, higher carb intake, medications
how long do you need to fast for trig levels
12 hours
cholesterol
found in every cell
90% levels synthesized in liver
cholesterol esterifed amount
80%
cholesterol functions
cellular repair
make and activate vitamin D
precursor for many hormones
recommend daily 300 mg
average american 700 mg
cholesterol levels absorbed by
mucosal cells – chylomicron
if serum looks milky and increased chylomicron is
1 indicator did not fast
excess cholesterol forms
gallstones
gallstones are fixed by
surgery- removal of gallbladder
increased cholesterol liver (parents) can
inherit kids liver with increased cholesterol
what flushed out high cholesterol levels
plant sterols and mucosal cells
stain drugs
composed of plant sterols
after menopause women’s cholesterol levels are
increased (estrogen and cholesterol the same)
normal cholesterol levels after fasting
<200
phospholipids structure
phosphorus group and 2 fatty acids attached to glycerol molecule
make up majority of cell membrane
phospholipids
determine fetal lung maturity
lecithin
lecithin is stable to 35 weeks and after it
increased
what also measures lung maturity (constant throughout gestation)
sphingomyelin
sphingomyelin
produced in myeline sheath, surrong nerves
look at L/s ration for lung maturity
L- increased 35 weeks
S- stays the same
2:1
Diabetic mom= 2.5:1
rare lipid storage disease
nieMann- Pick disease
what occurs in NieMann-pick disease
sphingomyelin accumulation in liver
lipoproteins layers
outer layer with apoprotein
phospholipid
free cholesterol
Inner core: trig and cholesterol esters
function of lipoproteins
transport lipids throughout body and metabolize of lipids
subunits by density lipoproteins
chylomicron
VLDL- very low density
IDL- intermediate
LDL
HDL
FFA- free fatty acids
chylomicron
-least dense ( float to top)
doesn’t move in electrophoresis
-carry exogenous trig.
-in circulation broken down by lipase
SHOULD BE cleared 12 hours after meal
VLDL- very low density lipoprotein
-contains apo b - bad
-carriers of endogenous trig
-13% cholesterol
VLDL- increase in Cho and trigs
-can dump around body
IDL
not measured
-short lived
LDL- low density lipoprotein
transport cholesterol
most cholesterol rich
LDL transports cholesterol from liver to
tissues in the body
LDL is bad cholesterol because
particles are small and infiltrate into blood vessel walls and have plaque and macrophage foam cells
LDL levels
<100
HDL- high density lipoprotein
-main compent- protein
GOOD cholesterol
-want high levels
>40 men
>50 women
removes excess cholesterol and takes to liver to be broken down
APO A- good
apo lipoproteins
found in outer shell of lipoprotein
-HYDROPHILLIC
enzymatic cofactors in lipid metabolism
Apo
a- good; HDL
b- bad; LDL and VLDL
c-
D-
E- risk factor for alzheimer’s disease; can clear cholesterol from brain and nerve tissue
low values of E can’t do the action
people with alz have
plaque buildup on nerve tissue
another method to see lipoproteins
electrophoresis
for lipid electro. specimen we want
serum or EDTA, fresh
NO heparin or frozen (lipoproteins broken down)
fast for 12 hours
-not on medications for a couple of weeks
specimen for electro. goes into
buffer 8.6 and gives lipid negative charge to migrate
cellulose acetate
stain nice, easy to read
stain for lipids
oil red o
sudan stain
cellulose acetate
point of origin (negative) migrate towards anode
electrophoresis pattern
negative
chylomicron
LDL
VLDL
HDL
Positive
alpha region
HDL (good ch. finish first)
Pre beta range
VLDL
BEta range
LDL
chylomicron stay at point of origin
-seen only after eating
so if seen either didn’t fast or lipid disease
most analyzers calculate indirect LDL
based on other components
Fried Wald Formula
LDL= total cholesterol - (HDL + triglycerides/5)
can’t be used if chylomicron present pr trig >400
Chemical precipitation method
seperate only lipoproteins
-most common HDL
Heparin combined with manganese will precipitate out non-HDL
shows only HDL
hyperlipoproteinemia
abnormal increase in 1 or more lipids (look for trigs or cholesterol)
artheriosclerosis
build up of cholesterol plaque will narrow blood vessels
atherosclerosis
large arteries harden
lipids (esterified cholesterol) gets deposited in artery walls
fatty acid streaks
fatty acid streaks
-excess fat get into macrophage become foam cells
-plaque contain smooth muscle cells, lipids, fibrogenesis tissue and calcified components
-block blood vessels, break off and rupture =thrombo hemolytic event
CRP
inflammation
plaque developing in blood vessels in arms and legs
peripheral vascular disorder
plaque around heart
corney heart diease
plaque around brain
cerebrovascular disease
identify lipid disorders
fredrickson classification scheme (based on serum and lab results)
chylomicrons: 1 and 5 hyperchylomicronemia
won’t be cleared after fast
serum= milky
fat depoisted in tissues; spleen
increase in VLDL, trigs
low fat diets
type 2a and 2b
hypercholesterolemia
2a and 2b
homozygous and heterozygous inherited
-connected to heart disease
-genetic
2a
homozygous inherited; die teenager years with increase lipids
cholesterol >100 always (LDL)
Serum: clear
2b
ethnicity and kids inherit
-defective LDL receptors- can’t get to where need to be : dumped
treatment: stain drugs and diet/ exercise
type 3 and 4
triglyceridemia
secondary disorders -diabetes, pancreatic destruction
serum: turbid/ milky
type 3 and 4 levels
increased LDL
Increased VLDL- carry trig
decreased HDL
type 3 and 4 treatment
1) statin drugs -prevent more cholesterol forming
2) low fat diet
3) nicin treatment
-need high doses
-lots of side effects
-facial flushing
metabolic syndrome
cluster of different conditions when seen together have increased risk of heart attack or stroke
risks factors of metabolic syndrome
increased waist line
>35 women
>40 men
-insulin resistent
-PCOS
-sleep apena
-age
if have any 5= metabolic syndrome
how to decrease metabolic syndrome
diet and exercise
