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Clin Path > Digestive System Ch 8 D&P > Flashcards

Digestive System Ch 8 D&P Flashcards

1
Q

What are the two categories of dz of the pancreas detected with laboratory evaluation?

A
  • Inflammation and necrosis

- Exocrine pancreatic insufficiency

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2
Q

Are amylase and lipase useful for detecting pancreatitis and are the exclusively produced in the pancreas?

A

They are not exclusively produced by the exocrine pancreas but they can apparently be helpful in dogs but not in cats.

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3
Q

Where does amylase originate and what does it do?

A

Pancreas, liver and small intestine. It digests carbohydrates to maltose and glucose.

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4
Q

What are the causes of BOTH elevated amylase and lipase?

A 
Pancreatitis 
Renal dz (reduced clearance)
Gastrointestinal dz / enteritis
Neoplasia
Hepatic / hepatobiliary dz
Surgical manipulation of pancreas / viscera
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5
Q

What are the conditions that just cause elevations in amylase (not lipase)?

A

Diabetes mellitus

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6
Q

What are the conditions that cause elevations in lipase (not amylase)?

A

Peritonitis
Bowel obstruction
Corticosteroids

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7
Q

What does lipase do and how high does it have to be to start thinking pancreatitis, and where does it come from?

A

In dogs three fold or greater increase suggests acute pancreatitis. Don’t forget to look at BUN/Crea to rule out renal dz as a cause for increase.
It comes from the pancreas and stomach.

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8
Q

What is the most sensitive and specific test for pancreatitis in dogs and cats?

A

PLI, pancreatic lipase immunoreactivity. Measures only lipase that comes from the pancreas. There are species specific tests available for dogs and cats including a SNAP test in dogs.

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9
Q

What else may elevations in PLI be associated with in cats?

A

Some cats with diabetes mellitus have elevated PLI.

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10
Q

What conditions in cats may be associated with pancreatitis?

A

Hepatic lipidosis, diabetes mellitus, cholangitis, cholangiohepatitis, IBD (ie triaditis), interstitial nephritis, vitamin K responsive coagulopathy.

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11
Q

What is the TLI and what does it test?

A

Detects trypsinogen and trypsin in serum.
These originate mostly from the exocrine pancreas in dogs so TLI is highly specific for pancreatic dz.
It has low sensitivity for pancreatitis in dogs and cats.

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12
Q

When will TLI be increased?

A

Pancreatitis in dogs and cats but has low sensitivity.
Renal insufficiency also causes increase
Malnourished dogs may also have increase

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13
Q

What are the CBC findings in pancreatitis?

A
  • relative polycythemia d/t vomiting (dehydration).
  • non regen anemia of chronic dz
  • variable leukogram, stress leukogram, inflammatory leukogram, left shift, toxic neuts all possible.
  • thrombocytopenia d/t DIC
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14
Q

Serum biochem abnormalities with pancreatitis?

A
  • Hypertriglyceridemia (d/t decreased amounts of lipoprotein lipase from pancreas; possible diabetes mellitus d/t pancreatitis may cause lipidemia)
  • prerenal and renal azotemia
  • increased ALT and AST d/t hepatic hypoxia etc
  • increased ALP d/t cholestasis
  • hyperglycemia (glucagon release from alpha cells); catecholamine and cortisol release; diabetes mellitus d/t damage to insulin producing beta cells
  • Hypocalcemia (possilbly d/t saponification of fat) and hypokalemia
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15
Q

Acute phase protein that may be elevated in pancreatitis?

A

C reactive protein, may be elevated before leukocytosis or left shift is detected.

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16
Q

What is the principal cause of maldigestion?

A

Exocrine pancreatic insufficiency / EPI

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17
Q

Which dogs most commonly get EPI?

A

Young dogs, inherited autosomal recessive in GSD’s, rough coated collies and other breeds

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18
Q

What is common cause of EPI in older dogs (3)?

A

pancreatic neoplasia, chronic pancreatitis, immune mediated disease

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19
Q

What is the most common cause of EPI in cats?

A

Chronic pancreatitis

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20
Q

What is the most common test for canine and feline EPI?

A

SERUM Trypsin like immunoreactivity / TLI

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21
Q

How does a decrease in serum TLI occur?

A

Reduction in pancreatic mass that occurs in EPI via panreatic atrophy

22
Q

Under what conditions may you see a false negative TLI for EPI?

A
  • Coexisting pancreatitis (so you would want to measure another test like fecal proteolytic activity)
  • Renal Failure (results in false negative TLI - ie TLI is high and a low results is what actually means EPI)
  • NOTE TLI requires a 12 hour fast
23
Q

Two other tests besides TLI that can be used to diagnose EPI?

A
  • Fecal proteolytic activity (fecal proteases of pancreatic origin include trypsin, chymotrypsin, carboxypeptidases A, B; these enzymes are secreted as proenzymes and are activated to functional enzymes in the duodenum by trypsin - which itself is converted from trypsinogen by enterokinase).
  • Measurement of cobalamin (vitamin B12) and folate [should measure with TLI cause often low and require supplement].
24
Q

What is the most common lab tests used to diagnose malabsorption?

A

Serum cobalamin / B12 and folate.

Serum concentrations depend on dietary intake, bacterial utilization, production, absorption and body losses.

25
Q

What are some causes of small intestine bacterial overgrowth (SIBO)?

A

Primary / idiopathic also called antibiotic responsive diarrhea (young dogs, often GSDs)
EPI, IBD, obstruction, lymphoma, lymphangiectasia, surgery etc.

26
Q

What is expected with folate, cobalamin and TLI with EPI?

A

Increased folate, decreased cobalamin (B12) and decreased TLI

27
Q

What is expected with folate, cobalamin and TLI with Bacterial overgrowth?

A

Increased folate, decreased cobalamin (B12) and normal TLI

28
Q

What is expected with folate, cobalamin and TLI with proximal SI disease?

A

Decreased folate, normal cobalamin, normal TLI

29
Q

What is expected with folate, cobalamin and TLI with distal SI disease?

A

Normal folate, decreased cobalamin, normal TLI

30
Q

What is expected with folate, cobalamin and TLI with diffuse SI disease?

A

Decreased cobalamin and folate. Normal TLI.

31
Q

Where is cobalamin / B12 come from, how and where is it absorbed and what does it do?

A

Comes from diet.
Liberated from dietary protein in the stomach by acid and pepsin, it binds intrinsic factor and the complex is then absorbed in the ileum by enterocytes.
It plays a role in nucleic acid synthesis.

32
Q

What does cobalamin / B12 deficiency do?

A

Cobalamin deficiency indirectly inhibits nucleic acid synthesis, affecting rapidly dividing cells and so marked hypcobalaminemia can result in crypt atrophy and malabsorbtion.
B12 is necessary to make DNA

33
Q

In what conditions does hypocobalaminemia occur?

A
  • Severe SI disease reduces its absorption
  • SIBO binds up cobalamin decreasing absorption
  • EPI decreased pancreatic enzymes so its not liberated and there is decreased intrinsic factor and you can get secondary SIBO
  • Inherited absorptive defects like in giant schnauzers
  • Common in cats with GI dz
34
Q

Where does folate come from? How is folate absorbed?

A
  • In the diet of dogs
  • Specific carriers for folate only in the proximal SI
  • Must be deconjugated to monoglutamate form before it is absorbed
35
Q

When does decreases in serum folate occur?

A
  • Dz of the proximal SI

- Dec serum conc. attributable to malabsorption indicates severe dz and depletion of body stores

36
Q

In what conditions may you see increased serum folate? (not this does not occur with cobablamin)

A
  • Bacterial overgrowth where bact make folate
  • EPI (with SIBO); also EPI leads to decreased bicarb secretion and decreased intestinal luminal pH which enhances folate absorption.
  • Decreased serum folate usage d/t low Cobalamin may also occur and so serum folate would be high
37
Q

So increased folate and decreased cobalamin tells you what? How does this occur?

A

EPI and bacterial overgrowth. Bact overgrowth increases folate production and absorption in the proximal intestine and there is increased binding and utilization of cobalamin and its prevented from being absorbed in the distal SI so it goes down.
(Note B12 and cobalamin are not sensitive for SIBO and may be normal when SIBO present).

38
Q

IN what conditions would you have decrease in both serum folate and cobalamin?

A

Severe diffuse SI disease and sometimes EPI

39
Q

What is lymphangiectasia?

A

Obstruction and dysfunction of the intestinal lymphatic system resulting in PLE and malabsorption.

40
Q

What are some potential causes of lymphangiectasia?

A 
Inflammatory or neoplastic infiltration
Fibrosis
Inadequate or obstructed flow of the thoracic duct
Congestive heart failure
Pericarditis
Congenital lymphatic malformation
Inflammatory dz is the most common cause
41
Q

What are the clin path changes in lymphangiectasia?

A

Panhypoproteinemia
Lymphopenia
Hypocholesterolemia
Hypocalcemia

42
Q

What causes lymphopenia in lymphangiectasia?

A

Loss of lymphocytes in lymphatic fluid.

43
Q

What are the list of causes of megaesophagus (7)?

A
  • Idiopathic is number one
  • Neuromuscular dz (myasthenia gravis, brainstem injury, neoplasia)
  • Endocrinopathies (hypothyroid, hypoadrenocorticism/Addisons - NOTICE ITS HYPO FOR BOTH ENDOCRINOPATHIES)
  • Inflammatory dz
  • Immune mediated dz (lupus, polymyositis)
  • Toxins (lead, organophosphates)
  • Infection (C. botulinum)
    Remember: IIIITEN
44
Q

What are the causes of Myasthenia gravis and how does it occur, breeds most effected and how do you test for it?

A

Congenital or acquired

  • Reduced number of ACh Receptors on the post synaptic sarcolemmal membrane
  • If acquired its due to autoantibodies on the AChR
  • Golden retrievers and GSDs most affected
  • Definitive test via Measurement of AChR antibody titers
45
Q

Dogs with megaesophagus should be tested for what disease? How should the testing be done and why?

A

Hypothyroidism (20% of dogs with MG also are hypoT4).(measure TT4, free T4 and TSH ideally, not just TT4).

  • Megaesophagus may cause pneumonia and “euthyroid sick” state where TT4 is low but fT4 is normal and thyroid function is normal).
  • NOTE megaesophagus in dogs with hypothyroidsim rarely resolves with thyroid txment
46
Q

Whats the other endocrine dz in dogs associated with megaesophagus? Why does it occur and how do you test for it?

A
  • Addisons / Hypoadrenocorticism.
  • Muscle weakness from inadequate cortisol and/or effects of electrolyte abnormalities on neuromusc fxn (HYPERKALEMIA, HYPONATREMIA)
  • ACTH stim testing
  • Typically resolves with adequate adrenal hormone supplementation (in contrast to hypothyroid)
47
Q

What are the 4 most common causes of PLE in adult dogs and then 4 other less common miscellaneous causes?

A

Most common: IBD (LP enteritis), GI lymphoma, Lymphangiectasia, Chronic parasitism (ie Giardia).
Four others: Hookworms, Chronic intussusception (young dogs), Histoplasmosis, Pythiosis

48
Q

What are the two most common causes of PLE in cats?

A

Intestinal lymphoma

Severe IBD

49
Q

What are two of the main ddx for PLE and associated hypoproteinemia?

A
  • PLN with decreased serum albumin and increased urine protein:creatinine ration; globulin unchanged
  • Liver insufficiency / failure (decreased albumin, increased bile acids)
50
Q

What is another way to test for PLE, whats it test and how do you interpret it?

A

Fecal alpha 1 protease inhibitor

  • Protein about the size of albumin not normally present in GI tract but may enter intestinal lumen in GI dz (inflammation etc.).
  • Its not degraded so its a better marker of early PLE than panhypoproteinemia is and it will be ELEVATED in the feces prior to development of serum hypoproteinemia
51
Q

Why would you see hypocalcemia with PLE?

A
  • Associated with hypoalbuminemia
  • iCa++ may be low if there is compromised vitamin D absorption and secondary hypothyroidism
  • Lymphangiectasia may be more commonly associated with low iCa++ than other causes of PLE
52
Q

In horses when may you see hyperammonemia without liver dysfunction?

A

Horses with colic.
Increased absorption of ammonia across inflamed intestinal mucosa, and/or overproduction of ammonia by urease producing bacterial (Gm- bacilli like E. Coli, Proteus, Klebsiella etc and Gm+ bacilli like Clostridium)- - BLUF is that the urea cycle in hepatocytes is overwhelmed by the amount of ammonia delivered via enterohepatic circulation via portal blood.
- You would want to rule out hepatic dysfxn, abnormal portal circulation or urea/ammonia intoxication to dx this.
- You can measure ammonia via CSF or intraocular humor ante or post mortem

Clin Path (14 decks)

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