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3. Sys Path > C10 Laboratory Evaluation of Lipids & Proteins > Flashcards

C10 Laboratory Evaluation of Lipids & Proteins Flashcards

1
Q

Micelles contain:

A

Long chain fatty acids
Triglycerides
Cholesterol
Vitamins AEDK

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2
Q

Lipid digestion overview

A
  • come in through digestive tract, where lipids are emulsified by bile salts into micelles
    > pancreatic lipase interacts with micelles and tears them apart into different types of fatty acids
    > these products pass into mucosal cells
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3
Q

what causes lipemic samples?

A
  • triglycerides contained into chylomicrons
  • post-prandially, chylomicrons come into the body through the intestine and travel into various tissues
    > the triglycerides in them are stripped out and used for other purposes
    > most commonly a lipemic sample is caused by triglyceride-containing chylomicrons

<><><><>

  • nonpost-pranidal, we can can have hyperlipidemia involving VLDL, which also contain triglycerides
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4
Q

Post-Prandial (Physiologic) Hyperlipidemia
- when does this occur? what does this mean for blood collection?

A
  • when triglycerides in the chylomicrons are high
  • increased chylomicrons starting 1-2h after a meal, peaks at 6 hours, tapers off at 16h
    <><>
  • Lipemia > interferes with many commonly analyzed components of serum
  • Fast 12 h before collecting blood
  • If still lipemic – additional tests > some disease causing pathologic hyperlipidemia
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5
Q

Lipemic Blood Sample = Interference!
- how does it interfere with light and mess up our samples?

A
  • The line on the refractometer – false ↑ TP
  • Biochemical analyzer > spectrophotometric techniques
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6
Q

Lipemic Blood Sample = Interference!
- how does this interfere with cell membranes and mess up our samples?

A
  • RBCs – enhances hemolysis
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7
Q

Clinically Important Lipids in Blood

A
  1. Triglycerides
    * Nonesterified fatty acids (NEFAs, aka free fatty acids, LCFA)
  2. Cholesterol
  3. Ketones (as fat-related compounds)
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8
Q

Hypocholesterolemia:
- seen when, most commonly?

A
  1. Liver failure / portosystemic shunt
    * Often results in hypocholesterolemia
    > not enough liver available to make cholesterol, or nothing is going to the liver so it can’t do anything
    * NB: Animals with concurrent cholestasis
    > no bile or cholesterol is leaving, backs up into blood
  2. Hypoadrenocorticism (Addison’s disease)
    > unknown etiology, perhaps immune mediated
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9
Q

Hypocholesterolemia and hypotriglyceridemia concurrently:
- seen when?

A
  1. Maldigestion / malabsorption
    > maldigestion = no pancreatic lipase to break down micelles. Malabsorption = its just not getting in.
    > steatorrhea
  2. Protein losing enteropathy
    > lymphoma, lymphangectasia…
  3. Cachexia/starvation
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10
Q

Hyperlipidemia - categories

A
  1. Primary hyperlipidemia – inherited
    > schnauzers
  2. Secondary hyperlipidemia – everything else
    > more common
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11
Q

Secondary Hyperlipidemia – Pathologic Altered Clearance or Cellular Uptake
- what is this associated with in cats, dogs, and horses, usually? (very generally)

A
  • some sort of endocrinopathy
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12
Q

Secondary Hyperlipidemia – Pathologic Altered Clearance or Cellular Uptake

  • specific causes in the dog
A

Dog
* Hyperadrenocorticism, hypothyroidism, diabetes mellitus (DM), cholestasis, pancreatitis, obesity
* Protein-losing nephropathy (PLN), glucocorticoids, phenobarbital
* Idiopathic hyperlipidemia of miniature schnauzers with pancreatitis < mechanism not determined

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13
Q

Secondary Hyperlipidemia – Pathologic Altered Clearance or Cellular Uptake

  • specific causes in the cat
A
  • Negative energy balance (NEB), cholestasis, hyperthyroidism, DM
  • Protein-losing nephropathy (PLN), obesity, glucocorticoids
  • pancreatitis < mechanism not determined
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14
Q

Secondary Hyperlipidemia – Pathologic Altered Clearance or Cellular Uptake

  • specific causes in the ruminant, pony, miniature horses, donkeys, sheep, llamas
A
  • Negative energy balance
  • Pituitary Pars Intermedia Dysfunction & Equine Metabolic Syndrome – horses & ponies (obesity)
  • Pregnancy toxemia of sheep
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15
Q

Lipid Metabolism in Ruminants Assessment in the Transition Period
- what do we measure? what do we see?

A

↑NEFAs – pre-calving
* = negative energy balance / stress conditions
* Mobilization of fat from reserves
* ↑ risk:
> LDA, subclinical ketosis, RFM, 1- 1.5 kg/d ↓ milk production, early culling
* If prolonged – fatty liver

<><><><>

Beta-hydroxybutyrate (β-OHB) – post-calving
* NEB
* Ketosis, fatty liver
* Pregnancy toxemia in sheep

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16
Q

Protein Measurement (g/L)
- what and where?

A
  1. Plasma protein =
    a. Albumin
    b. Globulins
    c. Fibrinogen – inflammation – LA
  2. Serum total protein (TP)
    a. Albumin
    b. Total Protein - albumin = globulins

<><><><>

  1. Serum protein electrophoresis quantitates & separates
    * Albumin and the 5 fractions of globulins in serum
17
Q

Hyperfibrinogenemia causes

A
  • Inflammation in LA
  • Dehydration (hemoconcentration)
18
Q

Hypofibrinogenemia causes

A
  • Consumptive coagulopathies – DIC
  • Decreased production
    > Liver failure; liver is what produces fibrinogen
19
Q

Hyperproteinemia – The Patterns
- what might we see?

A

↑ albumin ± ↑ globulins
* Dehydration (hemoconcentration)
>Skin tent / PCV / urea / creatinine / USG…

<><><><>

↑ globulins and ↓ albumin
* Increased protein synthesis
> Infectious & non-infectious inflammatory disease
> B-cell neoplasia (lymphoma / multiple myeloma)
> in this case alnbumin decreases to make sure plasma oncotic pressure is balanced

20
Q

how can we tell normal values in an electrophoresis measurement from a chronic inflammatory response from a monoclonal gammopathy

A

NORMAL:
-tons of albumin, everything else pretty low

CHRONIC INFLAMMATORY:
- lower albumin
- increased alpha-1 and -2 peaks (pro-inflammatory cytokines)
- decrease in beta region (negative acute phase reactant here)
- broad-based increase in gamma globulins due to stimulation of B cells and plasma cells

MONOCLONAL GAMMOPATHY
- spike in gamma region
> One clone of a single type of neoplastic plasma cell, making a single type of immunoglobulin
- As tall or taller & as narrow or narrower than the albumin spike

21
Q

Monoclonal Gammopathy – Multiple Myeloma
- required findings to diagnose?

A

Need 2 of the following 4:
1. Monoclonal gammopathy
2. Increased plasma cells in bone marrow
* >20%
* unusual to see plasma cells in peripheral blood
3. Bence-Jones proteinuria (light chains)
4. Lytic lesions in bones (rare in cats)

22
Q

Common Causes of Hypoproteinemia

A
  1. Increased loss
  2. Dilution
  3. Inadequate production
  4. Inadequate intake
23
Q

Hypoproteinemia – The Patterns of Loss
↓ albumin and ↓ globulins
- why?

A

↓ albumin and ↓ globulins
* Hemorrhage / blood suckers
* Protein Losing Enteropathy > gut becomes ‘holey’ and we lose very large globulins and smaller albumin out the back end (lymphangectasia, lymphoma… can cause)
* Malabsorption/maldigestion
* Cachectic states
> inadequate plane of nutrition
* Exudative skin disease (burns / large wounds - plasma oozes out, can’t be recaptured)

“Panhypoproteinemia”

<><><><>

– Dilution
* Hemodilution (eg. LRS)
* Repeated effusion draining

24
Q

what does panhypoproteinemia look like on the electophorogram?

A
  • decreased albumins
  • decreased gamma globulins
  • decreased beta and alpha-2 region
25
Q

when do we see hypoalbuminemia

A

↓ albumin
* PLN > only place we will see decreased albumin but not globulins is through the kidney
* Hallmarks are low albumin and high cholesterol
* Hypercoagulable

26
Q

Hypoproteinemia – Inadequate Production
- what will we see?

A

↓ albumin and ↑ globulins

  • Advanced liver disease <20% functional tissue - not filtering antigens, they end up in lymph nodes, antigenic stimulation of B / plasma cells
    > not enough liver to make albumin
  • Cirrhosis, neoplasia, necrosis, inflammation
  • PSS leading to hepatic atrophy
    > no materials to make albumin
27
Q

Hypoproteinemia
- when do we see just ↓ globulins

A
  • Failure of passive transfer (FPT)
28
Q

Which of the following causes a falsely increased reading in total solids protein (i.e., plasma protein measurement estimate using the refractometer)?

  1. Hyperbilirubinemia (icteric plasma)
  2. Lipemia
  3. Hemolysis
A
  1. Lipemia
    - yes
  2. Hemolysis
    - moderate to severe hymolysis is associated with a false increase as well
29
Q

Which of the following are causes of hypolipidemia? Select all that apply.

A. Hyperadrenocorticism
B. Malabsorption/maldigestion
C. Hypothyroidism
D.Protein losing enteropathy

A

B. Malabsorption/maldigestion

D.Protein losing enteropathy

30
Q

Which of the following are causes of hyperlipidemia? Select all that apply.

A. Hypoadrenocorticism
B. Hyperadrenocorticism
C. Hypothyroidism
D. Hyperthyroidism
E. Protein losing Nephropathy
F. Negative energy balance

A

B. Hyperadrenocorticism

C. Hypothyroidism
- Yes, in dogs

D. Hyperthyroidism
- Yes, in cats

E. Protein losing Nephropathy

F. Negative energy balance
- Yes, often in overconditioned animals that experience a sudden decrease in food intake – decreased beta-oxidation of fats

31
Q

While species differences exist at the fine detail level, what is the general sequence of events in the development of fatty liver?

A. Overconditioning > acutely off food > lipid mobilization > hepatocellular lipid accumulation
B. Acutely off food > lipid mobilization > overconditioning > hepatocellular lipid accumulation
C. Lipid mobilization > hepatocellular lipid accumulation > acutely off food > overconditioning
D. Hepatocellular lipid accumulation > lipid mobilization > overconditioning > acutely off food

A

A. Overconditioning > acutely off food > lipid mobilization > hepatocellular lipid accumulation

3. Sys Path (28 decks)

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