Pancreas & Gastrointestinal Tract Flashcards

1
Q

Where are endocrine pancreatic cells found? What are the 4 types of endocrine pancreatic cells? What do they secrete?

A

Islets of Langerhans

  1. α-cells: glucagon
  2. β-cells: insulin
  3. δ-cells: somatostatin
  4. PP cells: pancreatic polypeptide
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2
Q

Where are exocrine pancreatic cells found? What do they produce?

A

acini

enzymes, like lipase, to metabolize proteins, lipid, and carbohydrates in the diet

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3
Q

What are the 4 major stimuli for insulin secretion? What are the 3 major target organs?

A
  1. elevated blood glucose (hyperglycemia)
  2. amino acids
  3. fatty acids
  4. hormones

liver, skeletal muscle, adipose tissue

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4
Q

What are the 2 major disorders associated with abnormalities in the Islets of Langerhans?

A
  1. diabetes mellitus
  2. hyperinsulinemia
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5
Q

What types of diabetes mellitus are most common in dogs and cats? How is it diagnosed?

A
  • DOGS = type 1, insulin deficiency
  • CATS = type 2, increased insulin with peripheral insulin resistance

persistent fasting hyperglycemia and glucosuria upon repeated glucose measurments

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6
Q

What physiologic causes of hyperglycemia may be mistakenly diagnosed at diabetes mellitus?

A
  • stress
  • post-prandial
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7
Q

What are the 3 major findings in the urinalysis in patients with diabetes mellitus?

A
  1. dilute urine (USG in gray zone) due to osmotic diuretic effect of glucose
  2. pyuria, hematuria, proteinuria - prone to UTIs because bacteria can live off of the glucose in the urine
  3. ketonuria upon increased fatty acid metabolism and generation of ketones (ketoacidosis common with DM)
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8
Q

What are the 5 most common findings on the chemistry panel in patients with diabetes mellitus? What may also be seen at very high glucose concentrations?

A
  1. titrational metabolic acidosis caused by ketoacidosis (KLUE!)
  2. hyponatremia, hypochloremia, hypophosphatemia, hypokalemia
  3. increased hepatic and pancreatic enzyme activities
  4. hyperbilirubiemia
  5. hypertriglyceridemia and hypercholesterolemia

hyperosmolarity when glucose concentrations are > 600 mg/dL

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9
Q

How are insulin levels measured? When is this most commonly done?

A

immunoassays

hypoglycemic animals when insulinoma (β-cell neoplasia that secretes excess insulin) is suspected

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10
Q

How should results of immunoassays measuring insulin be interpreted?

A

WITH BLOOD GLUCOSE CONCENTRATIONS

  • hypoglycemic dogs = low insulin levels
  • if hypoglycemic and insulin concentration is WRL or elevated, this is inappropriate and insulinoma is likely
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11
Q

When is fructosamine formed? What is its concentration used to indicate? Why?

A

when glucose is irreversibly linked to amine groups of albumin and other blood proteins

blood glucose levels within previous 2-3 weeks —> provides more reliable information about long-term glucose metabolism than a single BG concentration

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12
Q

What is the most common uses of fructosamine concentrations?

A
  • diagnose diabetes mellitus
  • monitor therapy for diabetic patients

(gives info on long-term glucose metabolism)

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13
Q

What does increased fructosamine indicate? What 2 things can this confirm?

A

persistent hyperglycemia

  1. diabetes mellitus vs. catecholamine-induced hyperglycemia in cats
  2. poor glycemic control in treated diabetic patiens
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14
Q

What does decreased fructosamine indicate? What 3 things can information support?

A

persistent hypoglycemia

  1. insulinoma
  2. hypoproteinemia
  3. hyperthyroidism in cats
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15
Q

What are the 2 major disease processes of the exocrine pancreas?

A
  1. pancreatitis - inflammation and injury to pancreatic parenchyma
  2. exocrine pancreatic insufficiency - loss of pancreatic acinar cells causing a reduction in the production of pancreatic enzymes
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16
Q

What are the 5 major clinical signs of pancreatitis?

A
  1. vomiting/diarrhea
  2. fever
  3. inappetence
  4. weight loss
  5. abdominal pain
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17
Q

What are 5 possible sequelae to pancreatitis?

A
  1. shock
  2. DIC
  3. diabetes mellitus
  4. peritonitis
  5. obstructive hepatic disease
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18
Q

What is the gold standard for diagnosing pancreatitis? What is most commonly seen in biochemistry profiles in dogs?

A

histopathology

elevated lipase and amylase (hyperlipasemia, hyperamylasemia), which are enzymes produced and stored in acinar cells and leaked into plasma during pancreatic cellular injury

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19
Q

Does a normal lipase value rule out pancreatitis?

A

NO —> lipase values are not specific to the pancreas - also synthesized in the stomach and liver

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20
Q

Hyperlipasemia is not specific to pancreatitis. What value is most likely seen in pancreatitis? What else can high levels indicate?

A

> 3x above the RI with no evidence of azotemia

  • dehydration and renal disease (decreased GFR)
  • hepatic disease
  • pancreatic and hepatic carcinomas
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21
Q

Does a normal amylase value rule out pancreatitis?

A

NO —> amylase values are not specific to the pancreas - also synthesized in the liver and small intestine

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22
Q

Hyperlipasemia is not specific to pancreatitis. What value is most likely seen in pancreatitis? What else can high levels indicate?

A

> 3-4x about RI with no evidence of azotemia

  • dehydration and renal disease (decreased GFR)
  • hepatic disease
  • pancreatic and hepatic carcinomas
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23
Q

What is pancreatic lipase immunoreactivity (PLI) used for? How are results interpreted?

A

most sensitive and specific test for diagnosing pancreatitis in dogs and cats by measuring lipase originating specifically from the pancreas

  • INCREASED with pancreatitis or decreased GFR
  • DECREASED with chronic pancreatitis or acinar atrophy/EPI
24
Q

What is trypsin-like immunoreactivity (TLI)? How are results interpreted?

A

measures trypsinogen that enters the bloodstream from the pancreas (short half-life = high degradation and elevation during acute pancreatitis)

  • INCREASED with acute pancreatitis or decreased GFR
  • DECREASED with chronic pancreatitis or acinar atrophy/EPI
25
Q

Why is PLI preferred over TLI for diagnosing pancreatitis?

A
  • TLI has a low sensitivity
  • trypsin has a very short half-life and will be rapidly degraded
26
Q

What leukogram and erythrogram findings are supportive of pancreatitis?

A

inflammatory leukogram +/- concurrent stress

  • anemia of inflammatory disease (non-regenerative, normocytic, normochromic) OR
  • hemoconcentration secondary to vomiting and/or diarrhea - erythrocytosis, hyperproteinemia, pre-renal azotemia
27
Q

What electrolyte and acid-base abnormalities are supportive of pancreatitis?

A
  • hypokalemia
  • hypocalcemia: ionized calcium bound to free fatty acids in necrotic fat
  • metabolic alkalosis from vomiting (loss of HCl)
  • metabolic acidosis from diarrhea (loss of HCO3)
28
Q

What blood glucose and lipid findings are supportive of pancreatitis?

A

hyperglycemia due to decreased insulin production

hypertriglyceridemia and hypercholesterolemia due to decreased insulin, which inhibits lipoprotein lipase

29
Q

What liver values are supportive of pancreatitis? What inflammatory response is commonly observed?

A

elevated ALP, GGT, and bilirubin due to bile duct obstruction secondary to pancreatic/duodenal swelling

peritoneal effusion with high cell and protein counts

30
Q

What animals are predisposed to exocrine pancreatic insufficiency (EPI)? What is the most common cause? What does it result in?

A

German Shepherd and rough-coated Collies

chronic or recurrent episodes of pancreatitis causes destruction of pancreatic tissue

maldigestion and malabsorption leading to reduced electrolytes (decreased pancreatic enzymes, like lipase, amylase, trypsin, and chymotrypsin that would break down nutrients in the GIT)

31
Q

What is the diagnostic test of choice to confirm exocrine pancreatic insufficiency? What confirms the diagnosis?

A

serum trypsin-like immunoreactivity

TLI (and PLI) are typically decreased, since the number of active exocrine pancreatic acinar cells are decreased

32
Q

How can the cause of exocrine pancreatic insufficiency be differentiated? How must this test be done?

A

dogs with EPI due to immune-mediated destruction typically have a much more decreased TLI than dog with EPI due to chronic pancreatitis

12 hour fast before drawing blood, since TLI will be mildly increased after a meal

33
Q

What are the most common clinical signs of intestinal malabsorption?

A
  • diarrhea
  • weight loss
  • steatorrhea

(similar to maldigestion, or pancreatic disorders)

34
Q

Where are cobalamin and folate absorbed? What are they used to diagnose?

A

proximal small intestine

measurements of both can help further classify GI disorders

35
Q

What are the 3 major intestinal malabsorptive disorders?

A
  1. protein-losing enteropathy (PLE)
  2. small intestinal bacterial overgrowth (SIBO)
  3. exocrine pancreatic insufficiency (EPI)
36
Q

What is protein-losing enteropathy (PLE)? What are the 2 major mechanisms?

A

excess protein is being lost through the intestine and not reabsorbed

  1. mucosal ulceration
  2. lymphangiectasia from inflammation, neoplasia, or CHF
37
Q

What is the major way that protein-losing enteropathy (PLE) is diagnosed from the lab findings? What happens upon concurrent inflammation?

A

panhypoproteinemia - hypoalbuminemia, hypoglobulinemia

globulins may be WRI or slightly increased

38
Q

What 3 other laboratory diagnoses are supportive of protein-losing enteropathy?

A
  1. lymphopenia - lymph lost into intestinal lumen
  2. hypocholesterolemia
  3. peritoneal effusion - albumin < 1.0-1.5 g/dL reduced oncotic pressure
39
Q

What GI values are altered in protein-losing enteropathy?

A

hypocobalaminemia and decreased folate ocncentration due to decreased GI absorption

40
Q

What fecal sample test can be done to diagnose protein-losing enteropathy? What may cause false increases in this test?

A

fecal α1-proteinase inhibitor concentration

  • in health, it is not present in the GI lumen
  • increased amounts are recorded in cases of transmural plasma or lymph loss seen in PLE

disorders causing blood loss into the alimentary tract, like thrombocytopenia and coagulopathies

41
Q

What is small intestinal bacterial overgrowth (SIBO)? What animals are predisposed? What are some secondary causes?

A

overgrowth of bacteria in the duodenum and jejunum leading to malabsorption

German Shepherds

  • IBD
  • intestinal stagnation (ileus)
  • intestinal obstruction
  • lymphoma
42
Q

How is small intestinal bacterial overgrowth (SIBO) diagnosed?

A

serum cobalamin (vit B12) and folate concentrations

  • decreased cobalamin
  • increased folate

(Bacteria consume cobalamine and fart folate)

43
Q

How are GI values used to diagnose exocrine pancreatic insufficiency (EPI)?

A
  • hypocobalaminemia due to secondary SIBO
  • increased folate due to impaired bicarbonate secretion from pancreas, which causes the pH of the intestinal lumen to decrease —> enhanced absorption
44
Q

What are the 2 major causes of hypercobalaminemia?

A
  1. vitamin supplementation (oral or parenteral)
  2. release from damaged hepatocytes that usually store cobalamin
45
Q

CASE: 15 y/o male Yorkshire Terrier has PU/PD for several weeks with progressive weakness and lethargy.

  • List 2 differentials for glucose change.
  • Explain the change in urea.
  • Can something in the sample interfere with spectrophotometry? What analytes will be affected?
  • Interpret the albumin levels.
  • Evaluate the lipids.
  • Interpret liver enzymes.
A
  • marked hyperglycemia: DM, stress-related (magnitude and species makes it unlikely stress)
  • liver insufficiency or portosystemic shunts causes increased BUN
  • lipemic plasma = hyperphosphatemia, increased TP and globulin
  • hyperalbuminema: hypovolemia, signs of dehydration should be evaluated
  • moderate hypertriglyceridemia and hypercholesterolemia: DM due to accelerated synthesis of lipids —> Ddx: hyperadrenocorticism
  • elevated ALT = hepatocellular damage likely due to metabolic disorder like lipidosis frequently associated with DM
  • elevated ALP = intra- or post-hepatic cholestasis resulting from metabolic disease (DM, lipidosis, hyperadrenocorticism)
46
Q

CASE: 15 y/o male Yorkshire Terrier has PU/PD for several weeks with progressive weakness and lethargy.

  • What are the most remarkable changes in the urinalysis?
  • Interpret the glucose in the urine. How can it be compared to the biochemistry profile?
  • Based on the history and lab results, what is the most likely diagnosis?
  • What further tests would you recomend?
A
  • glucosuria, proteinuria
  • glucosuria in the face of hypertrygliceridemia indicates the reabsorption capacity of the renal PT for glucose has been exceeded
  • DM with subsequent hepatocellular disease, most likely hepatic lipidosis

~ US and pancreatic enzymes to rule out pancreatitis or hepatic lipidosis as the cause of DM
~ FNA of liver to confirm hepatic lipidosis and cholestasis
~ urine culture - glucosuria commonly leads to UTIs and may cause pyuria
~ phosphate and protein concentrations repeated with a non-lipemic sample; or ultracentrifugation to clear lipids; freeze to separate lipids from serum
~ ACTH stimulation test - hyperadrenocorticism may contribute to unstable DM

47
Q

CASE: 13 y/o male neutered DSH was found hung in a partially opened window and thought to have been there for 4 hours. The cat is panting severely and has hemorrhages on the tongue. Moderate lethargy is noted.

  • What is the main interpretation of hematology findings?
A

LYMPHOPENIA - in the absence of other abnormalities, this is likely due to stress (endogenous or exogenous GCs) response

48
Q

CASE: 13 y/o male neutered DSH was found hung in a partially opened window and thought to have been there for 4 hours. The cat is panting severely and has hemorrhages on the tongue. Moderate lethargy is noted.

  • Interpret the biochemical profile.
A
  • CK: severely increased = excessive muscle damage after hypoxa and squeezing while the cat was in the window
  • ALT: mild increased due to muscle damage or hepatocellular damage
  • creatinine: moderate azotemia consistent with a reduced GFR, likely pre-renal due to hypoxia or dehydration, or renal disease
  • glucose: slightly elevated likely due to stress, DM cannot be exluded, but history makes this less likely
49
Q

CASE: 13 y/o male neutered DSH was found hung in a partially opened window and thought to have been there for 4 hours. The cat is panting severely and has hemorrhages on the tongue. Moderate lethargy is noted.

  • Would you like to order further analyses?
  • What is the likely diagnosis?
A
  • URINALYSIS to differentiate pre-renal from renal causes for azotemia and evaluate renal function
  • REPEATED GLUCOSE MEASUREMENTS (+ fructosamine assay) to exclude DM

changes due to hypoxia

50
Q

CASE: 3 y/o Holstein cow presented approximately 4 mos following breeding with decreased milk production and partial anorexia for 3 weeks. A distended abdomen was observed with a “ping” following percussion. Auscultation of the left abdomen is consistent with abomasal displacement. 35 L of abomasal reflux were removed by orogastric tube.

  • What information from CBC and/or biochemistry can evaluate/identify hydration?
  • Is there evidence of dehydration?
A
  • increased RBC, HCT, TP, and albumin support dehydration
  • likely due to partial anorexia and abomasal reflux

YES —> neutrophilia and increased fibrinogen

51
Q

CASE: 3 y/o Holstein cow presented approximately 4 mos following breeding with decreased milk production and partial anorexia for 3 weeks. A distended abdomen was observed with a “ping” following percussion. Auscultation of the left abdomen is consistent with abomasal displacement. 35 L of abomasal reflux were removed by orogastric tube.

  • Interpret creatinine.
  • What test can help interpret creatinine levels?
A

increased likley due to pre-renal (dehydration) or post-renal conditions

urinalysis and USG to determine if conditions other than dehydration may be contributing

52
Q

CASE: 3 y/o Holstein cow presented approximately 4 mos following breeding with decreased milk production and partial anorexia for 3 weeks. A distended abdomen was observed with a “ping” following percussion. Auscultation of the left abdomen is consistent with abomasal displacement. 35 L of abomasal reflux were removed by orogastric tube.

  • Interpret electrolytes and acid-base status.
  • What is the mechanism for the TCO2 results?
  • What is the likely diagnosis?
A

paradoxical aciduria expected due to increased aldosterone secretion that stimulates Na+ resorption and water retention in the kidney —> hypochloremia = HCO3- is absorbed to maintain electroneutrality; H+ is exchanged with K+

  • urine chloride concentrations should be low
53
Q

CASE: 10 y/o female Siamese cat had been lethargic for several weeks and has a decreased appetite. Owners noted mild weight loss. Mild discomfort in cranial abdominal region was noted upon PE. Parasitological fecal was unremarkable.

  • What is the most striking find in the biochemistry profile? What is it consistent with?
  • What else is abnormal? Give Ddx.
A
  • increased fPLI = pancreatitis, which matches the non-specific clinical signs
  • mild hyperbilirubinemia = pre-hepatic (hemolysis), hepatic, or post-hepatic disease —> no erythrogram findings rules out hemolysis; pancreatitis can block the common bile duct (post-hepatic); common to have concurrent liver disease, like lipidosis, inflammation, or neoplasia (renal)
  • increased ALP and ALT activity = cholestasis due to impaired bile flow, hepatic lipidosis, bilirubinemia —> leads to hepatocellular damage
54
Q

CASE: 10 y/o female Siamese cat had been lethargic for several weeks and has a decreased appetite. Owners noted mild weight loss. Mild discomfort in cranial abdominal region was noted upon PE. Parasitological fecal was unremarkable.

  • What do the urea, creatinine, and phosphorus suggest?
  • What test is necessary to interpret/classify urea and creatinine?
  • Interpret proteins.
A
  • increased CREA and BUN + hyperphosphatemia = azotemia consistent with decreased GFR —> decreased appetite, diminished fluid intake —> dehydration OR pancreatitis causes vascular leakage of enzymes (pre-renal)
  • urinalysis = differentials renal causes of azotemia using USG
  • hypoproteinemia with mild hypoalbumimemia = vascular leakage, malnutrition, impaired intestinal absorption of protein, diminished hepatic albumin synthesis —> cause cannot be determined based on present results
55
Q

CASE: 10 y/o female Siamese cat had been lethargic for several weeks and has a decreased appetite. Owners noted mild weight loss. Mild discomfort in cranial abdominal region was noted upon PE. Parasitological fecal was unremarkable.

  • Interpret glucose.
  • Would a feline trypsin-like immunoreactivity (fTLI) help assess the case?
A
  • mild hyperglycemia = stress-induced due to chronic illness, inflamed pancreas releases glucagon in higher concentrations than insulin (increased gluconeogenesis and glycogenolysis
  • it may: sensitivity and specificity is not as good as fPLR, so negative results DO NOT rule out pancreatitis
56
Q

CASE: 10 y/o female Siamese cat had been lethargic for several weeks and has a decreased appetite. Owners noted mild weight loss. Mild discomfort in cranial abdominal region was noted upon PE. Parasitological fecal was unremarkable.

  • What further tests are recommended?
A
  • URINALYSIS: determines if there is renal cause of azotemia
  • REPEATED GLUCOSE MONITORING: include/excludes DM
  • FNA OF LIVER: may rule in/out hepatic lipidosis (common in cats with anorexia or decreased appetite) due to the slightly increased hepatic enzyme activity
  • BIOPSY: gold standard for pancreatitis (multifocal, multiple samples or else false negative)