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59 Cards in this Set

  • Front
  • Back
Lipids
-define
-soluble organic solvents
Lipids found in animals
-Sterols (cholesterol)
-Glycerol esters (triglycerides)
-Fatty acids
-Sphingosenes
-Terpenes (Vits A, E, K)
Lipoproteins
-define
-how cholesterol and triglycerides are transported in serum
Lipoprotein types
-chylomicron
-Very Low Density Lipoprotein (VLDL)
-Intermediate Density Lipoprotein (IDL)
-Low Density Lipoprotein (LDL)
-High Density Lipoprotein (HDL)
Chylomicron
-major lipid
-site of formation
-major site of degredation
-lipid: dietary TG

-site of formation: small intestine enterocyte

-degredation: plasma and hepatocytes
VLDL
-major lipid
-major site of formation
-major site of degredation
-lipid: Hepatic TG

-site of formation: hepatocyte

-degredation: plasma
IDL
-major lipid
-major site of formation
-major site of degredation
-lipid: hepatic TG & cholesterol ester

-site of formation: plasma

-site of degredation: plasma
LDL
-major lipid
-major site of formation
-major site of degredation
-lipid: phospholipid & cholesterol ester

-formation: plasma

-degredation: hepatocytes
HDL
-major lipid
-major sites of formation
-major sites of degredation
-lipid: phospholipid & cholesterol ester

-formation: hepatocyte

-degredation: hepatocyte
Lipoproteins that contribute to serum lactescence
-chylomicron
-VLDL
Major processes that affect [lipoprotein]
-production (of chylomicrons in enterocytes and VLDL in hepatocytes)
-IV processing (LPL catalysed lipolysis on endothelial cell membranes)
-Clearance (hepatocyte)
Lipoprotein lipase
-function
-requirement
-function: breaks down triglycerides into fatty acids
Lipoprotein metabolism (Postprandial)
-describe
-ingested TGs in the presence of LPS and bile acids undergoes lipolysis to form Monoglyceride & Fatty Acid
-MG & FA are reabsorbed by enterocytes and reformed into TG
-Enterocytes assemble TG, CE, phospholipid and apolipoproteins into chylomicrons
-Chylomicrons enter blood via thoracic duct
-With Insulin LPL is activated converting TG into FA for adipocytes or muscle
-Remnant of chylomicron is then removed from the plasma by hepatocytes
Lipoprotein metabolism (Endogenous)
-describe VLDL
-VLDL assembled in hepatocytes
-secreted into sinusoidal blood
-with insulin, LPL is activated converting TG into FA
-VLDL becoms denser as TG is lost --> IDL --> LDL
-LDL delivers cholesterol to many cells for cell membranes or steroid synthesis
-LDL either ends up in cells or is removed by macrophages in liver
HDL function
-serve as apolipoprotein source for other lipoproteins
-accept cholesterol from plasma membranes/lipoproteins and transport it for reutilization or degredation
Triglyceride-rich lipoproteins
-Chylomicron
-VLDL
Cholesterol-rich lipoprotein
-HDL
-LDL
Fate of cholesterol after returned to hepatocytes
-reused in new lipoproteins
-excreted in bile
-degraded to bile acids
Triglyceride
-production in monogastrics
-fasting = hepatocytes
-postprandial = enterocytes
Triglyceride
-production in ruminants
-always producing
TG uses
-tissue/muscle = energy
-adipocytes = storage
Hyperlipemia
-define
-inc. [lipid] in blood
Hyperlipidemia
-define
-inc. [lipid] in blood
Hyperlipoproteinemia
-define
-inc. concentration of lipoproteins in blood
Lipemia
-define
-used to define the turbid or opaque appearance of serum (lactescence)
Hyperlipidemia
-classifications
-physiologic (postprandial)
-Primary (congenital; hereditary)
-Secondary ( acquired)
Physiologic hyperlipidemia
-effect in dogs and cats
-inc. chylomicrons
Physiologic hyperlipidemia
-time for chylomicron clearance in Cats and Dogs
-8-16 hrs
Physiologic hyperlipidemia
-what to think of when there is delayed clearing in cats and dogs
-secondary hyperlipidemia
Pathologic states of hyperlipidemia
-defective clearing by hepatocytes
-defective lipolysis (IV)
-excessive VLDL production
-hormone sensative lipase causing TG--> FA
Hormonal influences causing TG--> FA
-Glucagon
-Epinephrine
-Cortisol

-Insulin (-)
Primary hyperlipidemia
-what is it
-seen in
-cause
-congenital or hereditary defect

-seen in Miniature Schnauzers

-cause: dec. production of LPL --> defective lipoprotein lipolysis
Secondary Hyperlipidemia
-causes (most common*)
-Hypothyroidism (*)
-Diabetes mellitus (*)
-Acute pancreatitis
-Cholestasis
-Hyperadrenocorticism
-Nephrotic Syndrome & PLN
-Equine hyperlipemia (*)
-
Hyperlipidemia caused by hypothyroidism
-what is expected to increase
-reasons why
-inc. cholesterol

why:
-dec. hepatic lipase ---> dec. clearance of LDL
-dec. thyroxine --> dec. LPL activity
Hyperlipidemia caused by diabetes mellitus
-what is expected to increase
-reasons why
-inc. TG

why:
-dec. insulin --> dec. LPL activity
-inc. VLDL synthesis from influx of FAs
Hyperlipidemia caused by Acute Pancreatitis
-what is expected to increase
-reasons why
-Inc. TG

why:
-dec. insulin --> dec. LPL activity
-inflammatory cytokines
-cholestasis
Hyperlipidemia caused by cholestasis
-what is expected to increase
-reasons why
-inc. cholesterol

why:
-dec. cholesterol biliary excretion
-effector --> inc. cholesterol synthesis
Hyperlipidemia caused by hyperadrenocorticism
-what is expected to increase
-reasons why
- inc. cholesterol

why:
-stimulation of VLDL synthesis
-inc. hormone sensitive lipase --> inc. FA reflux
-antagonize insulin --> dec. LPL activity
Hyperlipidemia caused by Nephrotic Syndrome & PLN
-what is expected to increase
-reasons why
-inc. cholesterol

why:
-stimulate VLDL synthesis in hepatocytes
-dec. intravascular processing
Hyperlipidemia caused by Equine Hyperlipemia
-what is expected to increase
-reasons why
-inc. TG

why:
-anorexia, obesity, pregnancy, lactation, renal failure, endotoxemia
-neg. energy balance --> mobilization of FAs --> inc. synthesis in hepatocytes --> inc. VLDL
Hyperthyroidism causing hyperlipidemia
-pathogenesis
Dec. triiodothyronine (T3)
-dec. hepatic lipase activity
--dec. clearance of LDLs
---hypercholesterolemia

Dec. Thyroxine (T4)
-dec. LPL activity
--dec. intravascular processing (possible mild inc. in [TG])
---hypercholesterolemia
Nephrotic syndrome causing hyperlipidemia
-pathogenesis
-dec. Lipolysis of lipoproteins with apoprotein B
--hyperlipoproteinemia (hypercholesterolemia)

Possibly linked to PLN causing a loss of protein to bind to LPL
Postprandial cause of hyperlipidemia
-pathogenesis
Ingest a TG containing meal
-inc. formation of chylomicrons
--chylomicrons enter lacteals
---chylomicrons enter blood
----hypertriglyceridemia
Main reason for delayed clearing of chylomicrons
-any condition with dec. LPL activity
Diabetes Mellitus causing hyperlipidemia
-pathogenesis
Insulin deficiency
-dec. LPL activity
--dec. intravascular lipolysis
---hyperlipoproteinemia (hypertriglyceridemia, hypercholesterolemia)
-inc. mobilization of feuls
--inc. production of VLDLs
---hyperlipoproteinemia (hypertriglyceridemia)
Pancreatitis causing hyperlipidemia
-pathogenesis
-dec. insulin ---> dec. LPL
-inc. TNF
--inc. production of VLDLs
Equine hyperlipidemia causing hyperlipemia
-pathogenesis
Anorexia, Pregnancy, Lactation, Renal Failure, dec. Insulin...
-neg. energy status
--inc. glucagon
---inc. lipolysis of TG in adipocytes
----inc. FAs to liver
-----inc. TG synthesis in liver
------inc. VLDL production
-------hyperlipidemia (inc. TG)
Causes of secondary hyperlipidemia that can result in Lipemia
-Postprandial
-Diabetes mellitus
-Pancreatitis
-Equine hyperlipidemia
Portosystemic shunt/Liver failure causing hypolipidemia
-pathogenesis
Dec. functional hepatic mass
-dec. production of cholesterol, TG, apoproteins, phospholipids
--dec. production of VLDLs
---dec. plasma lipoproteins
----hypocholesterolemia
Hypercholesterolemia
-causes
-inc. cholesterol production
-dec. lipolysis of intravascular processing of lipoproteins
-unknown/multiple mechanisms
Inc. cholesterol production
-caused by
-by hepatocytes due to nephrotic syndrome or PLN
-by enterocytes due to postprandial hyperlipidemia
Dec. lipolysis of intravascular processing of lipoproteins
-causes
-hypothyroidism
-Nephrotic syndrome or PLN
Unknown mechanisms causing hypercholesterolemia
-causes
-obstructive cholestasis
-diabetes mellitus
Hypertriglyceridemia
-causes
-inc. triglyceride production
-dec. lipolysis or intravascular processing of lipoproteins
-unknown/multiple mechanisms
Inc. triglyceride production
-causes
-by hepatocytes due to Equine hyperlipemia/hyperlipidemia
-by enterocytes due to postprandial hyperlipidemia
Unknown mechanisms causing hypertriglyceridemia
-causes
-acute pancreatitis
-daibetes mellitus
TG & Cholesterol in chylous effusion compared to plasma
-TG: inc.
-Cholesterol: ok-inc.
-Chol:TG : dec.
Standing plasma test for chylomicrons
-describe
Visual lipemia when the plasma stands for 16 hrs
-creamy layer on top --> chylomicrons
-creamy layer not present --> chylomicrons are or are not present
Cholesterol lowering drugs in humans
-bile acid sequestrants
-statins
-inhibit pancreatic lipase
-inhibit cholesterol absorption