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Glucose
the body’s main energy source, especially critical for the brain and nervous system, which rely almost exclusively on extracellular glucose
Glycolysis
produce ATP & pyruvate/lactate for immediate energy
Glycogenesis
stores glucose as glycogen(mainly in liver n muscle)
Gluconeogenesis
(formation of G6P from non-carb sources)- liver synthesize glucose from non-carb sources like a.a,lactate, glycerol Liver,pancreas,adrenal glands regulate homeostasis of blood glucos
Glycogenolysis
breakdown of glycogen to glucose for use as energy
ex of monosaccharide
glucose, galactose, fructose
ex of disaccharide
sucrose, lactose
Oligosaccharide
3 to 10 units(glycoproteins)
Polysaccharide
>10 units (glycogen,starch)
Entry step of glucose metabolism
Glucose phosphorylated to glucose 6 phosphate using ATP
saturated lipids
(no double bonds)(straight eq)
unsaturated lipids
(1 or more double bonds)
Triglyceride
3 fatty acids esterified to glycerol backbone
Body's main energy storage form in adipose tissue
Provide insulation n protection of organs
Severely high triglycerides lead to?
acute pancreatitis & atherosclerosis (build up of plaque in arteries)
Phospholipids
Glycerol backbone w/ 2 fatty acids, phosphate group n polar head
Phosphatidylcholine (lecithin-mix of fatty substances)- most common, &phosphatidylethanolamine, sphingomyelin
Hydrophobic tails, hydrophilic head
Structure molecules, forms membranes n lipoprotein surfaces
Cholesterol
4 ringed struc
Amphipathic hydrophobic nucleus n small hydrophilic hydroxyl group→ allows alignment w/ phospholipids(in mem n lipoproteins)
Free cholesterol- in membranes n lipoprotein surfaces
Cholesteryl esters- esterified w/ fatty acids→stored in cells , packed in lipoproteins
Synthesized mainly in liver n intestines from acetyl-CoA
Chylomicrons structure
Sphere w/ core- triglycerides n cholesteryl esters
chylomicrons function
Transports (exogenous)dietary triglycerides from intestines →liver,muscle,adipose tissue
;Hydrolyzed by lipoprotein lipase (LPL), releasing free fatty acids for storage or energy.
whats the chylomicrons surface made of
apolipoproteins, phospholipids, free cholesterol
ApoC-II
(activates LPL)
Apolipoproteins
bind lipids to lipoproteins- enables transport of fats
ApoB-48
(structural)
hyperchylomicronemia
→creamy serum layer after refrigeration
Very low density lipoproteins(VLDL)
Produced by liver to transport endogenous triglycerides(from excess carbs)
[eating too much carbs→liver turn extra verbs into triglycerides→pack in vldl→shipped out]
Delivers triglycerides to muscle(for energy) n adipose tissue(for storage)
Elevated VLDL
→hypertriglyceridemia
IDL
Remnants of VLDL after triglyceride removal by lipoprotein lipase
Normally found briefly in blood(transitional particles (teen stage))
Formed when LPL removes triglycerides from vldl→particle shrinks
elevated idl is uncommon but when it occurs, what is the cause
defective ApoE
LDL
Final version after most triglycerides have been removed, formed from vldl→idl metabolism(sum of chem rxns)
Most of triglyceride is removed , rich in cholesterol esters
Transport cholesterol to peripheral tissue , for mem synthesis n hormone production
Diff sizes n densities , small n dense → atherogenic
lipoprotein(a)
Particles resembles LDL j w/ an additionally ApoA covalently attached to ApoB-100
ApoA has kringles(repeated peptide loops) structurally similar to plasminogen(protease dissolves fibrin clots) interferes w/fibrinolysis; trouble w/ clot break down
Genetically determined unaffected w/ diet or lifestyle
Elevated LpA
→ higher risk of myocardial infarction, stroke, aortic stenosis(narrowing of aortic valve)
HDL
Removes excess cholesterol from tissues n transports back to liver thro reverse cholesterol transport
Smallest n most dense lipoprotein, has more proteins n less lipids
Apo protein A1, A-II, C
Synthesized in liver n intestine
HDL2
larger, rich in cholesterol
HDL3
smaller,denser,less cholesterol
LpX
Abnormal lipoprotein non-atherogenic, rich in phospholipids
Lil triglyceride
In cholestatic liver disease
can produce high cholesterol results
In LCAT deficiency(inability to esterify cholesterol)
when does LpX accumulate
elevated plasma cholesterol which could mislead clinicals; important to differentiate from LDL(contributes to plaque)
what can LpX cause that makes it a problem clinically
gray topped that contain sodium fluoride
specimen collection using what tube
contains an anticoagulant and preservative that inhibits glycolytic enzymes, specifically enolase
whats special with gray topped tubes
Even with fluoride, what must be done ASAP with the plasma
must be separated from cells because the glucose decline in the first hour is virtually identical to tubes without it.
it has a diurnal variation (glucose value can b higher in the morning compared to afternoon)
whats special ab fasting plasma
HbA1c
Formed when glucose binds irreversibly to RBC hemoglobin; a value > 6.5 confirms diabetes.
Fasting Plasma Glucose (FPG)
Normal is 70–99 mg/dL
Prediabetes FPG is
100–125 mg/dL
diabetes FPG is
126 mg/dL.
2-hr oral glucose tolerance test
A value >200 mg/dL indicates diabetes.
Gestational diabetes
Pregnancy hormones (cortisol, estrogen, human placental lactogen, progesterone) antagonize insulin action. Screened via a 1-step (75g) or 2-step (100g) method.
increased insulin resistance
pregnancy leads to what resistance
Diabetes mellitus(DM)
Disorders that r chronic hyperglycemia due to defects in insulin secretion or action
Hexose Monophosphate Shunt(HMP Shunt)
Generates NADPH (for biosynthesis and antioxidant defense) and ribose-5-phosphate (for nucleic acids).
Glucose Oxidase Method
A coupled reaction where peroxidase catalyzes a reaction between hydrogenperoxide(H2O2) and a dye to form a colored compound.
whats significant about Apo A-1 (the primary protein in HDL) in regards to CHD
decreases the risk of coronary heart disease
whats significant about Apo B-100 (found in LDL and VLDL) in regards to CHD
increases risk.
Increased chylomicrons appearance in tube
creamy serum layer; after fatty meal gives plasma milky/turbid appearance
increased VLDL appearance in tube
Cause turbid/cloudy plasma in hyperlipidemia but no creamy layer
a quinoneimine dye
end product of glucose oxidase method
method to measure electrolyte activity
ion selective electrodes (ISE)
Direct ISE
measures undiluted sample (e.g.,blood gas analyzers).
Indirect ISE
measures diluted sample; affected by high lipids/proteins → pseudohyponatremia.
Osmolality
# of dissolved solute particles per kg of solvent, 275–295 mOsm/kg.
dictates water rentention and renin release
normal osmol gap
<10 mOsm/kg
toxic alcohols
an elevated osmol gap indicates unmeasured osmotically active substances in the blood, such as
osmol calculation
2 Na + glucose/20 + BUN/3
Anion gap
Diff of unmeasured anions n cations
High AG=
bicarbonate is being replaced by unmeasured anions; acidosis stuff
ref 8-16mmol/L
AG=Na-(Cl+HCO3)
ref 12-20mmol/L
AG=(NA+K)-(Cl+HCO3)
causes of hypokalemia
Due to GI loss (vomiting, diarrhea)
renal loss (diuretics, Cushing's),
cellular shifts (alkalosis, insulin)
decreased intake
Causes muscle weakness, cramps, and arrhythmias.
Hypokalemia
plasma K con <3.5 mmol/L
causes of hyperkalemia
Due to decreased renal excretion (renal failure, Addison's)
cellular shifts (acidosis, tissue injury)
artifactual errors (hemolyzed sample, prolonged tourniquet, fist clenching).
hyperkalemia
plasma K con >5.1 mmol/L
Pseudohyperkalemia
is a pre-analytical error caused by a hemolyzed sample, prolonged tourniquet use, or fist clenching
high osmolality
Na is high n water is low
low osmol
Na is low n water is high
Hyponatremia
Caused by losing sodium or retaining too much water.
kidney disease
heart failure
diuretics
vomit, diarrhea
Hypernatremia
caused by excess water loss, decreased water intake, or increased sodium retention
dehydration
sweating
diarrhea
chloride
what electrolyte is always evaluated alongside bicarbonate to maintain electroneutrality
Hypochloremia
Strongly associated with prolonged vomiting (loss of gastric HCl) or high bicarbonate states (metabolic alkalosis)
Hyperchloremia
Associated with GI bicarbonate loss (diarrhea) or renal tubular acidosis(metabolic acidosis)
henderson hasselbach
what eq defines the relationship between pH, the metabolic component (bicarbonate), and the respiratory component (pCO2).
the pancreatic islets of Langerhans
insulin is produced by beta cells of
anaerobic glycolysis
Severe anemia decreases oxygen to tissues, leading to
high anion gap metabolic acidosis
anaerobic glycolysis this generates lactic acid, resulting in a
Intravenous (IV) Fluid Therapy
Drawing blood proximal to (above) a running IV line causes massive pre-analytical errors. The sample is contaminated by the IV fluid, causing the analytes in the fluid (like Na and Cl in normal saline) to read critically high, while all other analytes are artificially diluted
collecting sample before giving patient IV to not impact electrolytes
Pediatric dyslipidemia
is an important predictor of future cardiovascular disease
dyslipidemia
abnormal level of lipids
calcium and phosphorus
Parathyroid hormone (PTH) directly controls
PTH in kidney does what
it promotes Ca reabsorption in distal tubule
excretion of HPO4
activation of renal 1-alpha-hydroxylase
these actions are direct
P
to be excreted by the kidneys
role of PTH for Mg
enhances renal reabsorption and intestinal absorption
RAAS (blood vol regulation)
Renin (kidney) → Angiotensin II (vasoconstrictor) → Aldosterone (Na reabsorption, water follows
severe anemia
In addition, the accuracy of pulse oximetry can be compromised by many factors, including poor perfusion and
greater
As lipoprotein particles become smaller and denser, their relative protein content generally becomes
ABCA1 transporter
active transfer of cholesterol to ApoA-1
LCAT enzyme (lecithin-cholesterol acyltransferase)
esterifies free cholesterol so it can b stored in HDL
chol value
<200mg/dL
LDL value
100
HDL value
>40 for men
>50 for women
triglycerides value
<150
Secondary dyslipidemia
Caused by another disease, lifestyle factor, or medication.
Tangier disease
a rare inherited disorder involving defects in the ABCA1 transporter, which normally transfers cholesterol to Apo A-I. (impairment of HDL formation)