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Small Animal Nutrition > Lymphangiectasia, Pancreatic exocrine insufficiency, Hepatic lipidosis > Flashcards

Lymphangiectasia, Pancreatic exocrine insufficiency, Hepatic lipidosis Flashcards

1
Q

What is lymphangiectasia

A

dilation and dysfunction of intestinal lymphatics

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2
Q

Primary LGE

A

limited to intestine +/- chylothorax

pretty uncommon

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3
Q

Secondary LGE

A

severe intestinal infilrative disease
e.g. IBD, lymphosarcoma, enteritis (severe inflammation)
intestinal lymph obstruction

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4
Q

Etiopathogenesis of LGE

A

GI disorders disturb protein balance along with mucosal barrier and lymph
drainage -> overdistended lacteals rupture and release (reflux) intestinal
lymph into gut lumen -> diarrhea and protein losses

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5
Q

Clinical picture of LGE

A
  • weight loss and poor BCS
  • pitting edema, ascites, pleural effusion from protein loss
  • chronic diarrhea, steatorrhea, increased stool production
  • panhypoproteinemia (loss of globulin), hypocholesterolemia, lymphopenia, hypocalcemia
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6
Q

Intestina biopsy of LGE

A

dilated, chyle-engorged lacteals and submucosal lymphatics, edema, lipogranulomas

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7
Q

Breed predilection for LGE

A

yorkies, maltese, dachshund

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8
Q

Goals of dietary management of LGE

A
  • minimize lymph flow
  • reduce lacteal and lymphatic distention
  • limit fat intake (esp LCFA)
  • minimize protein loss (occurs with decreasing lymph flow)
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9
Q

Key nutritional factors for LGE

A
  • low fat diet (25% for dogs, >35% for cats), novel/hydrolized source (IBD), protein supplement (e.g. cooked egg whites); decrease lymphatic flow to allow for healing of lymph vessels
  • fiber: low to high depending on BCS, avoid high fiber in low BCS patients; insoluble fiber -> decreased intraluminal fat digestion and micelle formation -> decreased LCFA absorption
  • digestibility: 87% for protein, soluble CHO, fat; low residue foods -> reduced diarrhea from fat/CHO maldigestion -> reduced intestinal gas production
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10
Q

Vitamin and mineral nutritional factors for LGE

A
  • vitamins: vitamin A, D, E product, 1 ml divided into 2 sites, IM q 3 m
  • minerals: consider IV Ca; Mg, Zn, Cu may also become deplete if disease is severe/chronic
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11
Q

Pancreatic exocrine insufficiency (PEI or EPI), General Info

A
  • maldigestion
  • partial or complete deficiency of pancreatic enzymes -> poorly digested food
  • chronic small bowel diarrhea
  • frequent defecation of greasy, foul smelling, pale (gray/brown), voluminous stools
  • weight loss/failure to thrive (low BCS, polyphagia [eat anything and everything], pica coprophagia)
  • hemorrhages (vit K deficiency)
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12
Q

Breed predilection for PEI/EPI

A

German shepherds, rough coated collies, Siamese cats

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13
Q

Etiopathogeneis of Juvenile PEI

A
  • atrophy of pancreatic acinar tissue
  • clinical signs develop at 6-18 m of age
  • animals are NOT dibetic
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14
Q

Etiopathogenesis of Acquired PEI

A
  • inflammation and fibrosis associated with end-stage chronic pacreatitis
    +/- diabetes mellitus
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15
Q

Mechanisms of PEI

A
  • failure of intraluminal digestion and ineffective nutrient utilization
  • impaired mucosal enzyme activity (lack of trophic pancreatic secretions, osmotic or secretory diarrhea)
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16
Q

Secondary concerns of PEI

A
  • SIBOG (small intestinal bacterial overgrowth): lack of antibacterial factors from pancreatic secretions
  • intestinal IgA deficiency (may be genetic component in German shepherds)
17
Q 
Key nutritional factors of PEI
Digestibility
Fat
Fiber
Fat soluble vitamins
Water soluble vitamins
A
  • high; >/= 87% protein, >/= 90% fat and soluble CHO
  • moderate; dogs- 10-15% DMB, cats- 15-25% DMB; consider MCT as supplement or in diet (for extra cal)
  • low fiber diet! (<5%)
  • A, D, E (1 ml IM q 3 m); K1 (5-20mg q 12 hrs parenteral) if coaguopathies are detected
  • cobalamin (B vit) [100-250 mg IM or SQ q 7 days for 2 wks]
18
Q

Feeding management for PEI

A
  • parenteral feeding may be your initial approach (but not always needed)
  • reduce osmotic load by BID-TID feedings
  • feed underweight patients at DER for optimal BW + 20% (this increases the likelihood of utilizing/gaining more cals)
  • pancreatic enzymes (essential in successful mgt of PEI, dried powder extracts of bovine/porcine pancreas or fresh)
19
Q

Pancreatic enzymes/RX for PEI

A
  • though it is possible to feed fresh pancreas it is not recommended b/c of the associated health risks; powdered extracts are safer
  • give powder with food or it won’t be useful
  • antacids or H2 blockers are used to reduce gastric acid induced destruction of enzymes
  • use abx like metronidazole when SIBOG
  • use insulin with concurrent diabetes mellitus
20
Q

What can be fed to PEI animals in addition to specially formulated Rx diets?

A

high quality adult maintenance diet

21
Q

Mechanism of hepatic lipidosis

A
  • excessive peripheral lipolysis
  • increased TG synthesis in hepatocyte
  • decreased fatty acid oxidation in hepatocyte
  • decreased VLDL transport from hepatocyte
  • protein deficiency
22
Q

Clinical signs/diagnosis of hepatic lipidosis

A
  • obese (but not always)
  • anorexia, jaundice, weight loss, +/- hepatic encephalopathy,hematomegaly
  • hyperbilirubinemia, elevated ALP (assoc with cholestasis)
  • hypoalbuminemia, anemia, muscle wasting (b/c in catabolic state)
  • fatty liver on histo
23
Q

Dietary management of hepatic lipidosis

A
  • nutritional support is essential or life threatening prognosis (prevent catabolism, inhibit peripheral lipolysis)
  • avoid excess energy consumption- hepatic TG accumulation
  • assisted feeding is necessary: NE tube (when can’t be anesthetized, E tube, PEG tube, parenteral, needed for 2-6 wks
  • force feeding is inappropriate
24
Q

Energy nutritional factors for hepatic lipidosis

A
  • adequate daily energy intake
  • increase daily fat at 25-40% DMB
  • increase energy density >/= 4.4 kcal/g DMB
  • feed at RER (IBW) in hospital- avoid refeeding syndrome
  • increase to RER(IBW) x 1.1-1.2 at home
  • hospitalized based on recovery progress
25
Q

Protein and potassium nutritional factors of hepatic lipidosis

A
  • increase protein to >30% DMB, but lower range if hepatic encephalopathy (b/c ammonia makes it worse)
  • increase potassium; decreased via vomiting, pu/pd, anorexia, CRF; dietary goal of 0.8-1% DMB; hypokalemia: supplement 2-6 mEq potassium gluconate every day
26
Q

L-carnitine for hepatic lipidosis

A
  • can help drive beta-oxidation in mitochondria of liver
  • synthesized in liver from lys and met
  • some controversy as to value in hepatic lipidosis
  • shown to protect obese cat from hepatic lipid accumulation
  • during cal restriction: 250-500 mg/cat/day
27
Q

Fat soluble vitamins, water soluble vitamins, SAMe, water for hepatic lipidosis

A
  • vitmains K1 and E
  • vitamin B complex
  • SAMe: 20-40 mg/kg/d, given to protect liver cells from oxidative damage
  • maintain hydration status, suspected lactate intolerance (so no LRS)

Small Animal Nutrition (10 decks)

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