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Medicine II > Protein Losing Enteropathy > Flashcards

Protein Losing Enteropathy Flashcards

1
Q

Obj: Describe pathogenesis of PLE and difference between primary and secondary lymphagiectasia

A
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2
Q

Obj: Explain pathophysiology of common complications in patients w/ PLE and develop a management plan

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3
Q

Obj: Given a scenario, diagnose and recommend treatment for primary lymphangiectasia, including localization of protein loss

A
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4
Q

Obj: Contrast treatment, diagnostic test, and prognosis between primary lymphangiectasia and CE without protein loss

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5
Q

Obj: Given a patient scenario, evaluate risk factors for gastric ulceration and prioritize differentials for melena/hematochezia

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6
Q

Obj: Based on drug mechanisms and evidence of efficacy, develop a treatment plan for patients with GI ulceration

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7
Q

What are the different pathophysiologic causes behind Protein-losing enteropathy?

A
  • Mucosal barrier injury
    • Inflammation/infiltration
    • Increased permeability
    • Plasma protein leakage
  • Mucosal erosions/ulcerations
  • Lymphatic dysfunction
    • Normal: ingestion of dietary fat packaged into chylomicrons → Chylomicrons enter lacteals → submucosal/mesenteric lymphatics → thoracic duct → Cranial vena cava
    • Disruption of chyle flow → extravasation/leakage of protein-rich intestinal lymph
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8
Q

What are the specific etiologies of Protein-losing enteropathy?

A
  • Mucosal Erosions/ulceration
  • Intestinal Crypt Disease
  • Lymphangiectasia
    • Primary:
      • idiopathic dilation of lacteals
        • lymphatic dysfunction → chyle stasis -. lacteal rupture/leakage
      • Breed-associations
        • yorkshire - primary
        • Maltese - primary
        • Soft-coated wheaten terrier - Idiopathic IBD + PLE (primary) + PLN
        • Norwegian lundehund - primary + idiopathic IBD
        • Rottweiler - Primary + idiopathic IBD + crypt lesions
    • Secondary:
      • Infiltrative disease
        • Neoplasia (80% of patients with GI lymphoma)
        • Severe inflammatory bowel disease (10% of patients with IBD)
        • Infectious disease (histoplasmosis, pythium
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9
Q

What are the clinical signs of PLE?

A
  • Diarrhea - 65-90%
  • Effusion/Edema 50-80%
  • Weight loss 80%
  • Vomiting 30%
  • Anorexia 20%
  • Lethargy 20%
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10
Q

What are the consequences of PLE?

A
  • Decreased Albumin (panhypoproteinemia)
  • Decreased oncotic pressure
    • cavitary effusions (Pure transudate)
    • Edema
  • Hypercoagulability
    • loss of anti-coagulant proteins (i.e Antithrombin)
  • Vit & Mineral deficiencies
    • Fat Soluble Vitamins: ADEK
      • Hypovitaminosis D
        • low serum 25-hydroxycholecalciferol associated with more severe clinical signs and worse histopathologic scores
        • Documented in cats w/ chronic diarrhea due to IBD & lymphoma
          • serum concentrations correlate with albumin
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11
Q

How is PLE diagnosed?

A
  • CBC
    • may be normal
    • stress leukogram
    • lymphopenia
    • Anemia of chronic disease
  • Chem
    • Panhypoproteinemia
    • Hypocholesterolemia
    • Electrolyte abnormalities
      • hypocalcemia
        • total - due to ⇣ albumin
        • ionized - due to ⇣ Vit D
      • hypomagnesemia
      • Hyponatremia, hypochloremia, +/- hyperkalemia (effusion-related)
  • UA
    • normal unless concurrent disease
    • Rule out concurrent PLN
  • Tests for GI protein loss:
    • Fecal alpha-proteinase inhibitor
      • Similar size to albumin
      • not degraded in feces → increased in fecal samples of dogs with PLE
      • Helpful to localize low albumin to GI loss in patients w/out diarrhea
    • Fecal occult blood
      • stool based assay that detects heme, resulting in an oxidation reaction and color change
      • Sensitive but non-specific test in dogs and cats (good rule out test)
  • Imaging - abdominal ultrasound
    • Hyperechoic mucosal striations
      • 75% sensitive, >90% specific
    • GI mucosal thickening +/- loss wall layering
  • Biopsies
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12
Q

What is the treatment for PLE?

A
  • Diet
    • different for primary and secondary lymphangiectasia
  • Anti-inflammatory/immunosuppressive therapy
    • many options
  • Vit D supplementation
    • Calcitriol 0.03-0.06 ug/kg/day
  • Calcium Carbonate
    • 0.5-4g elemental calcium/day
    • 1g calcium carb = 400mg elemental calcium
  • Anticoagulant
    • plavix 1-3mg/kg q24hr
  • Cobalamin
    • Dogs 250-1000 ug SQ q7d for 6wks then q30d
    • Cats 2050 ug SQ q7d for 6wks then q30d
    • OR daily oral dosing
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13
Q

What are the different diets for PLE?

A
  • Primary Lymphangiectasia
    • Low to ultra low fat
      • Formulated - Hills, Royal Canin, Purina
      • Home-cooked - Potato & whitefish, low-fat turkey, cottage cheese, cooked egg whites
  • Secondary Lymphangiectasia to sever IBD
    • combination Low fat + novel protein/hydrolyzed
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14
Q

What are the options for Anti-inflammatory/immunosuppressive therapy for PLE treatment?

A
  • Corticosteroids
  • Chlorambucil
  • Cyclosporine
  • Mycophenolate
  • Azathioprine - NEVER use in cats
  • Octreotide (somatostatin analog)
    • Mechanisms:
      • ⇣ GI blood flow and fluid secretion
      • ⇣ Triglyceride absorption
      • ⇣ lymphatic flow
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15
Q

What is the distribution of Protein-losing disease in Soft-coated Wheaten Terriers?

A
  • PLE in 34%
  • PLN in 40%
  • Combined PLE + PLN 30%
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16
Q

What is the case of Protein-losing disease in Soft-coated Wheaten Terriers?

A
  • Genetic mutation → immune dysregulation
    • Complex mode of inheritance
17
Q

What clinical signs of Protein-losing diseases are seen in Soft-coated Wheaten Terriers?

A
  • Diarrhea (90%)
  • Vomiting (65%)
  • weight loss (55%)
  • effusion (40%)
  • thromboembolism (up to 20%)
18
Q

What complications of Protein-losing disease are seen in Soft-coated Wheaten Terriers?

A
  • PLE: Non-responsive effsion, thromboembolic disease
  • PLN: Renal failure, systemic hypertension, thromboembolic disease
19
Q

What is the prognosis of PLE in Yorkshire terriers?

A
  • MST - 44 months in responsive animals, 12 months in non-responsive
    • 40% - Complete response
    • <15% - Partial response
    • 50% - no response w/ diet and prednisone
20
Q

What are the negative prognostic indicators for PLE in Yorkshire terriers?

A
  • Clinical - vomiting
  • Laboratory:
    • monocytosis
    • severe decrease in albumin
    • Low BUN
    • Villus blunting (survival <4mo)
21
Q

What is the prognosis for protein-losing diseases in Soft-coated Wheaten terriers?

A
  • PLE: 5mo MST
  • PLN: 3mo MST
  • PLE + PLN: 2mo MST
22
Q

What is the prognosis for PLE? (overall not breed specific)

A
  • >50% mortality in 3mo
23
Q

What causes death in PLE cases?

A
  • Thromboembolic disease
    • (e.g. pulmonary thromboembolism)
  • Non-responsive effusion
  • Malnutrition
24
Q

How can response to treatment for PLE be monitored?

A
  • Responders:
    • takes 14days (up to 80days) for Albumin to increase >2g/dL
25
Q

What are the negative prognostic indictors for PLE? (overall not breed specific)

A
  • Clinical:
    • Ascites
    • Chronic enteropathy activity index >12
    • lack of clinical response at 4-8wks
  • Laboratory:
    • Albumin <½g/dL
    • Hypocobalaminemia
    • ⇡/⇣ BUN
  • Histo: Crypt abscesses
26
Q

What are the positive prognostic indicators for PLE?

A
  • Normalization of canine inflammatory bowel disease activity index score and serum albumin with first 50 days of treatment
  • Response to a diet trial
27
Q

What are the clinical signs of GI Ulceration?

A
  • Vomiting (90%)
  • Hematemesis (30%) or Melena (30%)
    • not observed in all patients
  • Abdominal pain
  • Hypersalivation
  • Anemia-related if chronic or severe
28
Q

What is melena?

A
  • Black, tarry stool de to hemoglobin breakdown
29
Q

What lab abnormalities are common with GI ulceration?

A
  • Anemia: regenerative or non-regenerative depending on chronicity
  • Microcytosis with chronicity and development of iron deficiency
  • Elevated BUN:Creatinine
  • Panhypoproteinemia
30
Q

How are GI Ulcerations diagnosed?

A
  • Rule-out toxins and systemic disease
    • Other causes of melena:
      • Hemoptysis, oral hemorrhage, epistaxis, congenital/acquired coagulopathies
      • False-positive w/ bismuth and salicylate anti-diarrheal medications
  • Abdominal imaging
    • Rads: Normal unless GI perforation
    • US: GI mural lesion, GI mucosal defect
    • Both may be normal
  • Endoscopy and biopsies
  • Capsule endoscopy (pill camera)
31
Q

What are the causes of Gastric (or gastroduodenal) ulcerations?

A
  • Drugs
    • NSAID + steroid therapy **
    • NSAIDS
    • Steroids - usually w/ another high-risk disease process
      • may produce sub-clinical gastric ulcerations
  • Increased Gastric acid secretion
    • Mast cell disease
    • Gastrinoma
    • Liver failure - associated with portal hypertension with cirrhosis and patients with intrahepatic portosystemic shunts
  • Local disease
    • Gastric neoplasia
    • Chronic, severe gastritis
    • Pyloric outflow obstruction
  • Hypoperfusion/”Stress”-related conditions
    • Hypotension or hypovolemia (pancreatitis, anesthesia)
    • Sepsis
    • Spinal cord disease (intervertebral disc disease)
    • Hypoadrenocorticism
    • Exercise-induced (sled dogs)
32
Q

What causes GI ulceration in cats?

A
  • Neoplasia - gastric lymphoma*, mast cell tumors, gastrinoma
  • Benign disease - IBD
  • NSAIDS
  • Liver Failure
33
Q

What is the treatment for PLE?

A
  • Treatment of underlying disease
  • Gastroprotection
    • Proton pump inhibitors
      • omeprazole 1mg/kg q12h
    • Mucosal barrier coating agents
      • Sucralfate, barium
    • Prostaglandin analogs if NSAID induced - Misoprostol
  • Surgery if non-responsive to medical management or resectable neoplasiae

Medicine II (46 decks)

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