P42 - Lipids Flashcards

1
Q

lipids are soluble in ____ and relatively insoluble in ___

A
  • organic solvents

- H2O

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2
Q

cholesterol is mostly produced in ____

A
  • hepatocytes
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3
Q

cholesterol is liberated from _____

A
  • lipoproteins
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4
Q

triglycerides are in _____

A
  • lipoproteins
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5
Q

triglycerides are produced in (monogastric) in fasting and postprandial situation

A
  • hepatocytes

- enterocytes

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6
Q

FA (fatty acids) attached to alcohol is an

A
  • esterified fatty acid
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7
Q

hyperlipemia and hyperlipidemia are increase in

A
  • lipids
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8
Q

hyperlipoproteinemia is increase in

A
  • lipid proteins
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9
Q

expected clearing of chylomicrons in dogs and cats is 8 hours - if delayed think

A
  • secondary (acquired) hyperlipidemia
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10
Q

how does hypothyroidism cause an increase in cholesterol

A
  • decrease hepatic lipase -> decrease clearance of LDL

- decrease thyroxine -> decrease LPL activity

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11
Q

how does diabetes mellitus cause an increase in TG

A
  • decrease insulin -> decrease LPL activity

- increase VLDL synthesis (influx of FA)

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12
Q

how does equine hyperlipemia cause an increase in TG

A
  • anorexia, obesity, pregnancy, lactation, renal failure, endoteoxemia
  • > negative energy balance -> mobilization of FA -> increase synthesis of TG in hepatocytes -> increase VLDL (increase [TG])
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13
Q

values of [cholesterol] and [triglyceride] in hypothyroidism dog (also know mechanism)

A
  • increase to highly increase

- increase

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14
Q

values of [cholesterol] and [triglyceride] in portosystemic shunt dog (also know mechanism)

A
  • decrease

- WRI

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15
Q

values of [cholesterol] and [triglyceride] in hepatic failure dog (also know mechanism)

A
  • decrease

- WRI

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16
Q

values of [cholesterol] and [triglyceride] in postprandial cat or dog (also know mechanism)

A
  • WRI - increase

- increase to highly increase

17
Q

values of [cholesterol] and [triglyceride] in diabetes mellitus cat or dog (also know mechanism)

A
  • increase

- increase to moderate increase

18
Q

values of [cholesterol] and [triglyceride] in equine hyperlipidemias in horse (also know mechanism)

A
  • WRI - increase

- increase to highly increase

19
Q

increase cholesterol production by what 2 things and why

A
  • hepatocytes - nephrotic syndrome or protein-losing nephropathy
  • enterocytes - postprandial hyperlipidemia
20
Q

hypothyroidism and nephrotic syndrome or protein-losing nephropathy can cause decrease intravascular processing or clearance of lipoproteins and result in ____ cholesterol

A
  • increase

- hypercholesterolemia

21
Q

increase triglyceride production by what 2 things and why

A
  • hepatocytes - equine hyperlipemia or hyperlipidemia

- enterocytes - postprandial hyperlipidemia

22
Q

hypothyroidism, nephrotic syndrome and lipoprotein lipase deficiency can cause decrease intravascular processing or clearance of lipoproteins resulting in ____ triglycerides

A
  • increase

- hypertriglyeridemia

23
Q

what 2 hypothyroidism pathogenesis can cause increase in cholesterol

A
  • T3 and T4

- creates a decrease clearance of LDLs and decrease intravascular processing

24
Q

postprandial pathogenesis resulting in increase triglycerides

A
  • ingest TG-containing meal -> increase formation of chylomicrons -> chylomicrons enter lacteals -> enter blood
25
Q

diabetes mellitus pathogenesis resulting in increase triglycerides

A
  • if insulin deficiency
  • > decrease lipoprotein lipase activity -> decrease intravascular lipolysis
  • > increase mobilization of fuels -> increase production of VLDLs
26
Q

equine hyperlipidemias pathogenesis resulting in increase triglycerides

A
  • negative energy status -> increase glucagon -> increase lipolysis of TG in adipocytes -> increase fatty acids to liver -> increase triglyceride synthesis (may see hepatic lipidosis)
27
Q

portosystemic shunt/liver failure causing decrease cholesterol pathogenesis

A
  • decrease functional hepatic mass -> decrease production of VLDLs -> decrease plasma lipoproteins
28
Q

negative energy balance and fatty acid concentrations (3)

A
  • negative energy balance -> increase glucagon release -> increase HS-lipase in adipocytes -> increase TG to FA
  • diary cow transition period -> excessive increase [FA] -> increase AcCOA (increase ketogenesis and increase TG (hepatic lipidosis)