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ACVIM Specialty Exam > Metabolic, Nutrition > Flashcards

Metabolic, Nutrition Flashcards

1
Q

Define metabolizable
energy (ME).

A

ME of a nutrient is the amount of energy available to the animal after taking into account losses from digestion (nutrients in foods are not 100% digested),
urine losses, and losses in exhalation of gases.

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2
Q

Average ME for protein vs fat vs CHO in whole food vs commercial dog food?

A

Protein & CHO: 3.5kcal/g (dog food), 4kcal/g (whole food)

Fat : 8.5kcal/g (dog food), 9kcal/g (whole food).

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3
Q

Recommendations for minimum dietary protein intake in working dogs?

A

22-24% ME

(25-28% or higher if maintaining muscle, extreme working envt)

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4
Q

What energy sources do dogs use predominantly during low, moderate & intense exercise?

A

Exercise at </=40% of max aerobic capacity: predominantly fat (aerobic metabolism)

40-70%: CHO (from protein oxidation) & fat

> 70% (e.g. sprinting): glucose (anaerobic metabolism)

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5
Q

Causes of hypercobalaminemia in dogs & cats?

A

Dogs - overall 3% incidence of high B12. DDx chronic GI signs (48%), hypoA (uncommon)
Cats - chronic enteropathy (65%), acute/chronic pancreatitis (24%), cholangiohepatopathy, gastric lymphoma (6%), hyperT (3%).

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6
Q

Short chain fatty acids
- Produced by which bacteria?
- Name the main SCFAs.
- Name 5 key roles.

A

Ruminococcus, Faecalibacterium, Turicibacter - ferment dietary CHO to SCFAs.

Butyrate, acetate, propionate.

Roles:
* Nutrients
* Regulate satiety
* Anti-inflammatory properties
* Regulate intestinal motility
* Downregulate intestinal pH to create an environment that is not suitable for pH-sensitive enteropathogens.

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7
Q

Dietary copper - what forms are available, and which form is recommended?

A

Copper sulfate recommended, more bioavailable vs copper oxide.

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8
Q

Describe copper metabolism.

A

Copper absorption occurs in the upper SI via membrane transporters –> transported to liver in free & protein-bound forms –> uptake by hepatocytes –> added to transcriptional products, bound to metallothionein or cupriproteins for storage, OR shuttled to canaliculi for bile elimination.

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9
Q

Describe roles of copper.

A

Required for function of the following metalloenzymes:
- Lysyl oxidase - essential for molecular cross-linking of collagen & elastin
- Cytochrome c oxidase - essential for electron transport chain that generates ATP –> mitochondrial energy generation
- Copper–superoxide dismutase - role in antioxidation, dismutates superoxide anions that otherwise cause oxidative damage to local protein & lipid cell constituents.

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10
Q

AAFCO recommendation for minimum daily copper intake for maintenance adult dog diet?
How does this compare to prescription copper restricted diets?

A

1.83 mg/1,000 kcal = ~Cu intake of ~0.067 mg/kg/day

(0.9 to 1.1 mg/1,000 kcal, ranging from approx 0.04 to 0.07 mg/kg/d)

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11
Q

What is a disadvantage of feeding a hepatic diet to dogs with copper storage/necroinflammatory liver disease vs dogs with PSS or HE? (Hint: copper & protein content)

A

Most dogs with CSH or NIH don’t have hepatic failure or HE - so protein restriction is not ideal as these patients can be expected to have heightened nitrogen turnover secondary to inflammatory cytokines & catabolism.

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12
Q

Consequences of phosphorus deficiency? (Name 3)

A

Hemolytic anemia
Decreased mobility
Metabolic acidosis

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13
Q

Consequences of phosphorus deficiency? (Name 3)

A

Hemolytic anemia
Decreased mobility
Metabolic acidosis

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14
Q

What dietary factors may affect phosphorus bioavailability?

A

Form of phosphorus (inorganic Na/K phos salts more available than organic e.g. meat, bone meal) - feeding highly available phos with too low Ca can cause renal damage in cats.

Dietary Ca content (Ca:P ratio) - high Ca:P ratio (1.5-2:1) results in less increase in serum P

Dietary Mg content - high dietary Mg content (>0.32g/1000kcal ME) reduces P intestinal absorption by 13%. Unknown mechanism.

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15
Q

What dietary factors may affect phosphorus bioavailability?

A

Form of phosphorus (inorganic salts more available than organic)

Dietary Ca content (Ca:P ratio) - high Ca:P ratio (1.5-2:1) results in less increase in serum P

Dietary Mg content - high dietary Mg content (>0.32g/1000kcal ME) reduces P intestinal absorption by 13%. Unknown mechanism

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16
Q

Apart from neurological signs, what does mucopolysaccharidosis (liposomal storage disease) typically cause?

A

Skeletal & ocular changes.

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17
Q

What IV drug can be used to activate lipoprotein lipase? How does it work?

A

Ettinger

Heparin, used in a liproprotein lipase activity test.

Heparin activates lipoprotein lipase (LPL) by releasing LPL from vascular endothelium where it is normally anchored.
Also activates hepatic lipase (HL). Overall enhances plasma lipolytic activity & elevates FFA levels.

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18
Q

What are the roles of adiponectin? What is the effect on obesity on it?

A

Ettinger Chap 176

Adiponectin = synthesized by mature adipocytes.
Roles vary depending on organ. Increases insulin sensitivity, lowers serum glucose [ ], reduces liver & muscle triglyceride concentrations.
Anti-inflammatory & insulin-sensitising hormone.

Serum concentrations are decreased with obesity (possibly inhibition by inflammatory cytokines)&raquo_space; results in insulin resistance.

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19
Q

What is leptin & its effects? What is its status in obese cats?

A

Adipokine (secreted by fat). Long term regulation (suppressant) of food intake/appetite.
Crosses BBB > binds to leptin receptors in hypothalamus > decreased fat storage –>
- Decreases hypothalamic secretion of appetite stimulants (NPY / ARGP)
- Activates POMC neurons
- Increases production of hypothalamic hormones that decrease appetite
- Increases SNS activity > incr metabolic rate
- Decreases insulin secretion; modulates insulin sensitivity.

Obese cats/dogs are leptin-resistant (high circulating leptin [ ] but less response)

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20
Q

Glycogen storage diseases - types, breeds affected, CSx?

A

Glycogen storage dz – deficient or defective activity of the enzymes responsible for metabolizing glycogen.

  • Type Ia = Maltese (von Gierke dz); deficiency in glucose-6-phosphatase (gene mutation)
  • Type II = Lapland dogs (Pompe dz); deficiency of lysosomal acid a-glucosidase
  • Type III = GSD and Curly-coated retrievers (IIIa) (Cori’s dz) deficiency of glycogen debranching enzyme amylo-1,6-glucosidase&raquo_space; Curly coated affects liver and muscle (AGL gene)
  • Type IV in Norwegian Forest cats (Anderson’s dz), deficiency in glycogen branching enzyme  glycogen accumulation in skeletal m, cardiac m, nervous system
  • Type VII = English springer spaniel (Tauri’s dz) deficiency in PFK&raquo_space; hemolytic anemia, hemoglobinuria
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21
Q

Tryptophan
- Metabolic pathways & roles
- Significance in which diseases

A

Allenspach VCNA 2021 PLE review
- Essential AA in dogs/cats, largely absorbed in SI
- 2 main metabolic pathways in host:
1. Kynurenine pathway (90%) = energy metabolism: precursor for kynurenine
2. Serotonin pathway (5%) (90% in ENS, 10% in brain): metabolized to serotonin
- Melatonin pathway (pineal gland, GIT)&raquo_space; metabolized to melatonin
3. Small % reaches colon&raquo_space; metabolized by luminal bacteria to metabolites (indole, skatole indicant, tryptamine ‘SIT’).
- Microbial metabolites play an essential role in counteracting intestinal inflammation (induce anti-inflammatory cytokines e.g. IL-22).

PLE, canine CIE

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22
Q

What are the major roles of leptin & where are its receptors located? What factors can influence circulating leptin levels?

A

Type of adipokine.
Roles
- Suppress appetite
- Inhibit apoptosis (mitogen)
- Stimulate angiogenesis
- Pro-inflammatory, modulate T cell responses
- Repro - incr during puberty, causes FSH & LH release
- Pro-thrombotic
- Inhibits adiponectin (opp effects)

OB-R in hypothalamus (satiety centre), also hematopoietic SCs

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23
Q
A

Circadian rhythm
Amt of fat mass (linked to BW) - increases leptin expression but causes ‘leptin resistance’
Food (post prandial levels = 2-3x fasting levels)
Breed (Shelties higher)
GCS tx (dex incr, pred no effect, methylpred high dose suppress but low dose incr)

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24
Q

What are the top 2 major endogenous sources of angiotensinogen?

A

1 white adipose tissue (WAT)

#2 Liver

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25
Q

What is SOCS-3 and its effects? What factors induce SOCS-3 expression?

A

Supressor of cytokine signaling 3. Negative regulator of insulin expression –> induces insulin resistance.
Expression induced by leptin, insulin(?), resistin (these are increased in obesity)

26
Q

Where is ghrelin produced and what are its effects? Name a drug that potentiates its effects?

A

Produced by oxyntic glands within the gastric fundus.
Orexigenic (hunger) hormone. Fasting produces acylated active form&raquo_space; crosses BBB & binds to receptor&raquo_space; stimulate appetite & GH synthesis
Capromorelin (ghrelin agonist)

27
Q

What nutrients do cats have higher requirements for?

A

Arachidonic acid
Niacin, B12, pyridoxine, vit A, D
AA - taurine, arginine, methionine, lysine

28
Q

Which part of the GI lymphoid system does oral tolerance to food antigens occur?

A

M (microfold) cells of the Peyers patches

29
Q

What hematologic abnormality & clinical sign may be noted in cats with adverse food reactions and at what %?

A

20-50% peripheral eosinophilia
30% peripheral lymphadenopathy

30
Q

Food elimination diet - how long for GI signs vs dermatologic signs?

A

GI signs only: 2-4 wks
Skin signs: 8-12 wks

31
Q

How are hydrolysed protein diets beneficial for CE?

A

Reduces MW & shape of protein, reduces allergenicity & antigenicity as hydrolysate is too small to cause X-linking of IgE on mast cells, preventing degranulation.

32
Q

What is a common nutritional deficiency noted in unbalanced home-prepared or raw diets? What CSx does this cause?

A

Low Ca-P ratio. Ca +/- vit D deficiencies.
Young animals - long bone abnormalities; adults - bone resorption of mandible & maxilla –> rubber jaw. Nutritional 2’ hyperPTH

33
Q

Melanin (disguised as wheat gluten in diets) - toxic effects?

A

Crystals in renal tubules > AKI

34
Q

What pathogen recognition receptor can dietary fat effect have an effect on? What are the immunological effects?
Which other stimulus similarly binds to this PRR?
What dietary supplementation can inhibit this receptor?

A

TLR-4 (expressed on adipocytes, IELs, Mp, Np)
TLR-4 activation > COX-2 derived cytokines > NFKB > TNF-a > pro-inflammatory.
LPS endotoxin binds to TLR-4 & has similar potency to saturated LCFAs.
O3FA (e.g. DHA)

35
Q

Is dietary fat linked to pancreatitis in cats?

A

Poorly described as risk factor, but anecdotally yes (hyperlipidemia also potential risk factor)
Best to avoid high fat diets in cats with pancreatitis

36
Q

What is the hallmark feature of cancer cachexia? What immune system & biochemical changes are implicated?

A

Weight loss that cannot be reversed by increasing food intake.
Inflammatory cytokines (TNF-a, IL-6) + biochemical changes (glucose intolerance, increased lipolysis, hyperlactatemia (< common))

37
Q

What is the hallmark feature of cancer cachexia? What immune system & biochemical changes are implicated?

A

Weight loss that cannot be reversed by increasing food intake.
Inflammatory cytokines (TNF-a, IL-6) + biochemical changes (glucose intolerance, increased lipolysis, hyperlactatemia (< common))

38
Q

What metabolic complications can occur with parenteral nutrition (highlight those that are most common)?

A

Common - hyperTG, hyperglycemia
Also hyperNH3, hyperBIL, azotemia, incr ALKP, electrolyte derangements. Sepsis (3-12%)

39
Q

What essential AA do crystalline AA solutions (e.g. Travasol) used for parenteral nutrition lack? Is this a major clinical concern?

A

Taurine.
Usually not a concern as used for short term (up to 10d) only)

40
Q

Name 1 proposed adverse effect & 1 relative contraindication of IV lipid infusions.

A

AE - immunosuppression (impairs reticuloendothelial system; suppress Np & Lc function). But studies have not correlated lipid use & increased rates of infections.
Relative contraindication - hyperTG. Lipid infusions have not been shown to worsen pancreatitis or increase pancreatic secretion (so safe to give in these patients), BUT acc to human guidelines, markedly reduce or eliminate lipid component if TG >400mg/dL (4.2mmol/L)&raquo_space; aim to maintain normal serum TG.

41
Q

What are the different forms of vitamin K & where are they absorbed?
What is the main source of vitamin K in cats & dogs?

A

Vitamin K1 - diet. Absorbed in the proximal SI & requires bile for absorption (being fat soluble).

Vitamin K2 - bacterial synthesis in the intestinal tract. Absorbed in the ileum and colon. Main source of vit K.

42
Q

Why is atherosclerosis rare in dogs & cats compared to people?

A

High [HDL] cholesterol but lack cholesterol ester transfer protein (CETP) enzyme responsibel for reverse cholesterol transport.

43
Q

What cardiac changes may be observed in obese dogs? Is this reversible?

A

LV hypertrophy. Reversible with weight loss.

44
Q

What are the potential effects of obesity on glomerular health? Reduction in which urinary biomarkers were observed following weight loss in obese dogs?

A

Increased renal blood flow, filtration fraction & GFR; increased renal mass & glomeruli diameter w/o concurrent expansion of podocytes > could form gaps & lead to loss in protein filtration selectivity.
Obesity also stimulates RAAS > glomerular hypertension.

Markers - UPC, urine albumin, USG, homocysteine, cystatin C, clusterin (tubular marker).

45
Q

What effects does obesity have on RAAS & cardiac disease in dogs & cats?

A

Increased fat mass > increased adipose-derived angiotensinogen increases plasma angiotensinogen > increased AT-II > incr aldosterone.
High fat diets may also cause Na retention.

46
Q

What effects does obesity have on RAAS & cardiac disease in dogs & cats?

A

Increased fat mass > increased adipose-derived angiotensinogen increases plasma angiotensinogen > increased AT-II > incr aldosterone (cardiac remodelling)
High fat diets may also cause Na retention.

47
Q

How does EPA (O3FA) help to preserve lean muscle?

A

Interferes with ubiquitin-dependent protein degradation pathway

48
Q

How do acid-base derangements contribute to protein imbalance & muscle wasting?

A

Acidosis perpetuates insulin resistance > influences signaling pathways that trigger reduction of phosphoinositide 3-kinase (PI3K) activity > up-regulates the ubiquitin proteasome pathway (key pathway for protein degradation).
(Common animal proteins are metabolised to acid residues)

49
Q

What clinical manifestations does taurine deficiency cause in cats?

A

DCM (not all cats develop)
Central retinal degeneration
Hepatic lipidosis (taurine def limits lipoprotein synthesis needed for lipid metabolism and transport in the liver)

50
Q

Where are apolipoproteins found and what types are there?
Which ones activate a) lipoprotein lipase, b) lecithin cholesterol actyltransferase and c) chylomicrons?

A

Found in amphophilic membrane (with phosphlipids & free cholesterol) as part of lipoprotein molecule. Types A, B, C, E
Apolipoprotein C II - LPL co-factor (found on surface of CMs)
Apolipoprotein A1 - LCAT
Apolipoprotein B48 - chylomicrons

51
Q

Describe the roles of the following enzymes:
1 Lipoprotein lipase
2. Hepatic lipase
3. Lecithin cholesterol acyltransferase (LCAT)
4. Diacylglycerol acyl transferase 2

A
  1. LPL
    - On vascular endothelium. Hydrolysis of TG to FFA + glycerol in circulation - for CM & VLDLs.
    - Needs apolipoprotein C-II (on cell surface of CMs & VLDL) for activation.
    - For VLDLs > forms CM remnants, LDL.
  2. Hepatic lipase
    - Hydrolysis of TG & phospholipids
    - Facilitates liver uptake of TG & phospholipids from CM & VLDL remnants
    - On endothelium of hepatic sinusoids, some extra-hepatic tissues.
    - Converts VLDL to LDL (tgt with LPL)
    - Converts HDL2 to HDL3
  3. LCAT
    - Role in reverse cholesterol transport
    - Activated by Apo A1
    - Circulates in blood mainly bound to HDL > acts on HDL to convert cholesterol from tissues into cholesterol esters for incorporation into HDL molecules.
    - Esterifies and sequesters cholesterol in HDL > returns cholesterol is returned to liver.
  4. Diacylglycerol acyl transferase 2 = enzyme that catalyses conversion of diglycerides to TG
52
Q

What is the normal role of hormone sensitive lipase and where is it located? What physiologic/pathologic factors activate or decrease its activity?

A

I/C enzymes (within adipocytes). Cleaves FAs from intracellular TG. Activated by phosphorylation.
Essentially a physiologic response to provide energy from FA during fasting.
Factors - activated by insulin deficiency, ACTH, GCS, GH, thyroid hormone, catecholamines (NAd, Epi). Bolded = impt hormones.

53
Q

What factors increase vs decrease LPL activity?

A

Increase - heparin, insulin & thyroid hormone
(NB Insulin has opp effects on HSL - decreases HSL activity)

Decrease - GCS, inflammmatory cytokines (e.g. acute panc)

Heparin release test can be used to assess LPL activity (give IV heparin, check TG at baseline & 15min, LPL defect > no rise in TG)

54
Q

List some breeds that are prediposed to:
- Primary hyperTG
- Primary hyperchol

A

HyperTG - Mini Schnauzers, Beagles
Hyperchol - Briards, Dobermans, Rotties

55
Q

What bloodwork values may be affected by lipemia?

A

Increased - bile acids, TBIL, TP
Decreased, Na, K, Cl, crea
Increased/decreased LE, glucose

56
Q

What are treatment recommendations & goals for hyperTG in dogs/cats?

A
  1. 1st line low fat diet: dietary fat <12% DM (20% ME basis) OR <20g fat/1000kcal ME; lower if already on lower-fat diet. NB cats <24% fat
  2. Omega3 FAs (DHA, EPA) - GI
  3. Fibrates - PPARa agonist, LP activation, inhibits diacylglycerol acyl transferase 2, stim FA oxidation. AE: cholelithiasis, panc, GI, LE incr, azotemia > myalgia.
  4. Niacin (B3) - AE: LE incr, myotox, hepatotox, increase BG, erythema, puritus
  5. Soluble fibre - interferes with enterohepatic reabsorption of BAs
    Aim TG <400-500mg/dL
57
Q

What are treatment recommendations & goals for hyperCHOL in dogs/cats?

A

Tx overlaps with that for hyperTG
PLUS
1. Statins - reversible inhibitors of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase – enzyme catalyzing rate-limiting step for cholesterol synthesis. AE: GI (V+, D+, hyporexia), myopathy, rhabdomyolysis, hepatotox. NOT to be given with fibrates
2. Cholestyramine

58
Q

What is a potential negative sequelae of feeding dogs a diet with a very low n6: long chain n3 OFA ratio?

A

Coagulopathy (2’ vitamin K deficiency)

59
Q

GI dysbiosis can result in alterations of which 3 major pathways that can trigger intestinal inflammation?

A
  • Bile acid dysmetabolism (reduced conversion of 1’ > 2’ BAs due to reduced C hiranois) - normally regulates intestinal inflmamation
  • Indole pathway (AI effects)
  • Reduced pdtn of SCFAs - esp butyrate from fibre (AI effects) - Faecalibacterium, Bacteroides, Prevotella, Firmicutes
    (NB C perfingens & fusobacterium can produce butyrate from protein in carnivores)
60
Q

Which intestinal bacterial metabolites have interplay with the nervous system?

A

Neurotransmitters - serotonin, GABA (gamma-aminobutyric acid)

61
Q

What are orthopedic consequences of feeding an all-meat diet without vit D supplementation?

A

Rickets = metabolic bone disease, involves widening of the physeal growth plates of fast-growing bones (e.g. radius & ulna); histo - hypertrophic chondrocytes accumulate > thickened, irregular growth plates.

(NB: these dogs/cats are more likely to develop fibrous osteodystrophy rather than rickets due to dvpt of nutritional hyperPTH)

ACVIM Specialty Exam (20 decks)

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