SA Lipid Disorders

Question 1

describe primary lipid disorders

Answer 1

1. more common in dogs than cats
2. main causes:
   -postprandial: hypertriglyceridemia; increases are mild and typically last <15 hours, most common cause of hyperlipidemia

-high fat diets: HTG and/or HCH
–fat content must be very high (typically >50%) to cause fasting hyperlipidemia

Question 2

describe secondary hyperlipidemias

Answer 2

1. most common form in dogs
2. usually result of endocrinopathy:
   -hypothyroid
   -DM
   -cushing’s
3. pancreatitis?
   -infrequent in experimentally induced
   -pancreatitis + severe fasted hyeprlipidemia: investigate causes of hyperlipidemia

Question 3

what are ddx for high triglycerides (HTG) and high cholesterol (HCH)?

Answer 3

1. DM
2. hypothyroid
3. hyperadrenocorticism
4. pancreatitis
5. obesity
6. PLN
7. cholestasis
8. hepatic insufficiency
9. lymphoma
10. glucocorticoids
11. phenobarbital

Question 4

describe primary hyperlipidemias

Answer 4

1. MINI SCHNAUZERS
   >30% of the breed in USA is affected
   -get the most severe elevations
2. HTG resulting from abnormal accumulation of VLDLs or VLDLs + chylomicrons
3. HCH not always present
4. pathogenesis unknown, but increasing age increases severity and prevalence
5. also seen in:
   -beagles
   -shelties
   -dobies
   -rotties
   -rough coated collies
   -pyrenees
   -cats (idiopathic)

Question 5

what are the consequences of elevated HTG in dogs?

Answer 5

1. moderate to severe HTG (500-900)
   -abdominal: anorexia, V/D, acute necrotizing pancreatitis, hepatobiliary disease

-ocular: lipid keratopathy, arcus lipoides, lipid in aqueous humor, uveitis, blindness, lipemia retinalis

-derm: cutaneous xanthomata, pruritis, alopecia, xanthomas of liver, spleen, kidney, heart, skeletal muscle, intestine

2. severe (>1000)
   -CNS disturbances: seizures, changed behavior, neuropathy, cerebral artherosclerosis

Question 6

describe consequences of LPL deficiency resulting in HTG and HTG/HCH in cats

Answer 6

HTG: xanthomata

HTG/HCH: ocular disease

clinical signs: after 6-9 months old
-peripheral neuropathies, cutaneous xanthomas, formation of lipid granulomas in abdominal organs
-most affected kittens will not show clinical signs other than lipemia retinalis

Question 7

describe lipoprotein lipase deficiency in cats

Answer 7

1. located on capillary epithelium of many tissues
   -hydrolyzes TAGs in circulating lipoproteins when activated by insulin resulting in fatty acid oxidation (catabolic phase)
   -also facilitates TAG reassembly and storage in adipose tissue (anabolic phase)
2. naturally occurring mutation results in HTG and HHC

Question 8

describe diagnostic approach to lipidemias

Answer 8

1. ## get increased serum triglyceride and/or cholesterol concentrations
2. confirm animal is fasted
   -if not, possibly postprandial so consider fasting and retesting
3. if fasted, get a complete history and PE
   -ID findings that might suggest secondary hyperlipidemia
   -run CBC, chem, UA
   -then diagnostics as needed to ID cause
4. if predisposed breed to primary, search for underlying cause but be prepared to treat without finding one

Question 9

describe treatment goals of hyperlipidemias (primary and secondary)

Answer 9

treat both conditions using same principles

1. consider starting treatment when severity of HTG is low to decrease risk of complications
   -NO universally accepted parameters for when to start treatment though
2. initial treatment goal for severe HTG:
   -fasting serum TG <500mg/dL
   -start with dietary management (ultra-low fat diets)
   -drug therapy and/or supplements if necessary
3. once serum TG <500mg/dL, further reduction towards normalized serum TG (using lipid lowering drug) is decided on risk-to-benefit
4. continue to monitor serum TGs and cholesterol
   -every 3-6 weeks initially
5. for secondary hyperlipidemia specifically:
   -treat primary disease (endocrinopathy)
   -confirm with laboratory testing 4-6 weeks post initiation of treatment