GIN L45 Lipids
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62 terms
Terms | Definitions |
|---|---|
 ____ are Metabolic fuel: Building blocks for triacylglycerol, phospholipids, and sphingolipids. | Fatty acids |
| ____ are storage depot and major transport form for fatty acids. | Triacylglycerols |
| ___ are soluble metabolic fuel for skeletal, cardiac muscle, kidney, and brain | Ketone bodies |
| ___ are the structural component of plasma memb; precursor to bile acids, vit D, and steroid hormones. | Cholesterol |
| ___ are the major building block of membranes, storage site for poly unsat FAs, and used in signal transduction pathways. | Phospholipids |
| ___ are the structural component of membranes the serve as surface antigens | Sphingolipids |
| Isoprenoid and sterol synth, the early stage of FA synth, occur in the ___. | cytosol |
| Fatty acid oxidation, ketone body synth, acetyl-CoA prod, and FA elongation occur in ___ | mitochondria |
| Phospholipid synth,and late stage sterol synth occurs in the ___ | ER |
| Stigmasterol, stigmastanol, sitostanol, sitosterol, campesterol, demosterol, brassicasterol, and 22,23-dihydrobrassicasterol are ___, which are not normally absorbed. | plant sterols |
| ___ is a rare genetic condition in which people do take up plant sterols and they build up. | β-sitosterolemia |
| Palmitic (pork, C16) and stearic (beef, C18) acids are the two main ___ fatty acids to consider in plants and meat. | saturated |
| ___ is the most common monounsaturated FA. It has a double bond between C9 and 10 (ω-9). It is found in corn and safflower oil, among otherthings. | C18 oleic acid |
| Shelf life of an oil or fat is shortened by ___ | incr number of polyunsaturated acids |
| The ω end of a fatty acid is the ___. | methyl end |
| Linoleic (2), linolenic (3) and arachidonic (4 double bonds) acids are ___ | polyunsaturated |
| Removal of the ___ from the two position of the phospholid starts the IP3 signalling pathway. | arachidonic acid |
| Breast milk provides a bile-salt stimulated lipase that works in the duodenum to ___ | monoglycerides → glycerol and FFA |
| The oral cavity secretes lingual lipase, which acts in the mouth, esophagus, and stomach to ___. | cleave TG at sn-3 |
| The stomach secretes gastric lipase, which acts in the stomach and duodenum to ___. | cleave TG at sn-3 |
| The pancreas secretes pancreatic lipase, which acts in the duodenum to ___. This is clutch. | cleave TG at sn-1 and sn-3 |
| The liver produces bile salts for ___ in the duodenum. | emulsification |
| Exogenous fats are transported from the gut via ___. | chylomicrons |
| Lipoprotein lipase acts on triglycerides and phospholipids of chylomicrons and large VLDL. Where is it produced? | adipoytes of adipose tissue |
| Hepatic lipase acts on triglycerides, phospholipids and small VLDL, IDL, and large HDL. Where is it produced? | striated muscle and liver hepatocytes |
| Lecithin:cholesterol acyltransferase is produced in the liver and acts on ___. | cholesterol and phosphatidylcholine of HDL species |
| In ___, a parasite forms a fistula between the bladder and lymphatics, which causes chyluria (chylomicrons in urine) . | filariasis |
| Pt with massive hyper-TG. What do you check? | • low C-II • LPL |
| The co-factor for LCAT is ___. Without this, there is no esterification, synth of VLDL precursors, or HDL. | apoA1 |
| In the mitochondrion, monounsaturated fatty acids require one enzyme to undergo ___ to create acetyl-CoA. | β-oxidation |
| Polyunsaturated fatty acids require both ____. | isomeras and epimerase |
| The end-product of odd carbon chain fatty acid oxidation is ___. | propionyl-CoA |
| In an ATP-dependent process, propionyl-CoA is converted into methylmalonyl-CoA. Then, requiring ___, it is converted into succinyl-CoA for use in the TCA cycle. | B12 |
| Type I hyperlipidemia refers to ___. | exogenous hyperlipidemia, with elevation of chylomicrons |
| Type IV hyperlipidemia refers to ___ | endogeous hyperlipidemia with VLDL elevation |
| Type V hyperlipidemia refers to ___. | mixed (VLDL & chylomicrons) |
| Type II-a hyperlipidemia refers to ___. | hypercholesterolemia (LDL) |
| Type II-b hyperlipidemia refers to ___. This is the most common. | combined hyperlipidemia (LDL & VLDL) |
| Type III hyperlipidemia refers to ___ | remnant hyperlipidemia (β-VLDL) |
| What are some primary type I (exogenous) hyperlipidemias? | • familial lipoprotein lipase deficiency • C-II apolipoprotein deficiency |
| What are some secondary type I (exogenous) hyperlipidemias? | • dysglobulinemia • SLE |
| What are some primary type IV (endogenous) hyperlipidemias? | • familial hypertriglyceridemia (mild form) • familial multiple-lipoprotein-type hyperlipidemia • sporadic hypertriglyceridemia • Tangier dz |
| Sporadic hypertriglyceridemia is associated with ___. | gout |
| What are some secondary type IV (endogenous) hyperlipidemias? | • dysglobulinemias • SLE • diabetic hyperlipidemia • glyocogenosis type I • lipodystrophies • uremia • hypopituitarism • nephrotic syndrome |
| Primary Type V (mixed) hyperlipidemias? | • familial hyper-TG (severe form) • familial lipoprotein lipase deficiency • C-II apolipoprotein deficiency |
| Handful of primary type II-a (LDL) hyperlipidemias? | • familial hyper-chol (LDL-R defect) • familial mult lipoprotein0type hyperlip. • polygenic hyperchol (incl exogenous hyper-chol) |
| Secondary type II-A (LDL) hyperlipidemias? | • nephrotic syndrome • hypothyroidism • dysusglobulinemias • Cushing syndrome • acute intermittent porphyria |
| ___ is a primary Type II-b (combined VLDL and LDL) hyperlipidemia. | familial multiple lipoprotein-type hyperlipidemia |
| Type II-b (combined VLDL and LDL) hyperlipidemia can be a 2º d/o of: | • nephrotic syndrome • hypothyroidism • dysglobulinemias • Cushing syndrome • glucocorticoid use, stress |
| Type III hyperlipidemia (remnant, β-VLDL) is 1º in ___. | familial dysbetalipoproteinemia |
| Type III hyperlipidemia (remnant, β-VLDL) is 2º in___. | hypothyroid, SLE |
| Key finding in Type III hyperlipidemia? | palmar xanthomas |
| Familial lecithin:cholesterol anyltransferase (LCAT) deficiency is a 1º cause of ___. | lamellar hyperlipoproteinemia (vesicular and discoidal proteins) |
| Lamellar hyperlipoproteinemia (vesicular and discoidal proteins) can occur 2º to ___. | cholestasis (with LP-X), hepatic fail (with lamellar HDL) |
| Apolipoprotein d/o, enzyme d/o, receptor d/o, transfer/transport protein d/o are types of ___. | monogenic d/o of plasma lipoproteins |
| ApoE deficiency leads to ___ | hyper-VLDL |
| ___ is a type of LCAT dz that cuases corneal opacities. | Fish-eye |
| Classic abetalipoproteinemia is caused by ___, resulting in a total absence of plasma LDL. | microsomal triglyceride transfer protein |
| In a ___ deficiency, HDL cannot pick up cholesterol from tissues. | ABC1 |
| Insufficient chol in RBCs causes ___. | acanthocytosis |
| In the clinical lab, three lipid values are measured from which the others are derived. They are: | Total chol, TG, and LDL |
| ___ is usually 20% of TG. | VLDL |
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