Pancreas, Maldigestion and Malabsorption and Electrolytes

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  1. Pancreas
    Gland organ composed of endocrine and exocrine portions.
  2. Endorine pancreas
    Islets of Langerhans, containing Beta cells (Insulin), Alpha Cells (glucagon), Delta cells (Somatostatin) and F cells (Pancreatic polypeptides).
  3. Islets of Langerhans
    • Endocrine pancreas
    • Beta cells (insulin)
    • alpha cells (glucagon)
    • delta cells (somatostatin)
    • F cells (pancreatic polypeptides)
  4. Beta cells
    • From endocrine pancreas, islets of langerhans.
    • Create insulin, which pulls glucose into cells to facilitate metabolism.
  5. Alpha cells
    • From endocrine pancreas, islets of langerhans.
    • Create glucagon, which deals with glucose and metabolism (opposite of insulin)
  6. Delta cells
    • From endocrine pancreas, islets of langerhans.
    • creates somatostatin, which deals with lipid metabolism.
  7. F cells
    • from endocrine pancreas, islets of langerhans.
    • creates pancreatic polypeptides, which deal with protein metabolism.
  8. Exocrine pancreas
    • Largest functional part of pancreas.
    • Acinar cells: secrete digestive enzymes (trypsin, amylase, lipase) and release through ducts into insides of organs.  
    • Leaked into circulation from trauma to pancreas.
  9. Acinar cells
    • secrete digestive enzymes (trypsin, amylase, lipase) through ducts into insides of other organs. 
    • Leak from damage to pancreas into systemic circulation.
  10. Pancreatitis
    • inflammation of pancreas
    • Acute or chronic, causes leakage of digestive enzymes.  
    • Chronic is more common, sometimes a flare-up presents as acute.
  11. Predisposing factors for pancreatitis
    • obesity and high fat diet most common.  
    • Liver disease, infection, recent ab surgery, drugs (azathiopine, furosemide, potassium bromide), duodenal fluid reflux, pancreatic trauma or ischemia, hypercalcemia, infectious agents like FIP, Toxoplam gondii
  12. acute clinical signs of pancreatitis
    • sudden onset
    • fever
    • anorexia
    • V/D (hemorrhagic)
    • weakness
    • cranial abdominal pain
    • shock
    • sudden death
  13. Ways to diagnose pancreatitis
    • radiograph (hazy ground glass)
    • abdominal ultrasound
    • bloodwork (anemia, leukocytosis, hyperamylasemia*, hyperlipasemia*, increased liver enzymes (ALP, ALT), hyperbilirubiemia, prerenal azotemia, hyperglycemia, hyperlipidemia
  14. bloodwork of pancreatitis
    • anemia (chronic inflammation, nonregenerative)
    • variable leukocytosis
    • hyperamylasemia (leaking)**
    • hyperlipidasemia (leaking)**
    • hyperbilirubinemia and increased liver enzymes (ALP, ALT), often cholestasis.  Toxins build up and damage liver.
    • prerenal azotemia (dehydration)
    • hyperglycemia (glucagon)
    • hyperlipidemia
  15. Lab tests for pancreatitis
    • TLI (trypsin-like immunoreactivity) (for EPI)
    • PLI (pancreatic lipase immunoreactivity) (for pancreatitis)
  16. TLI
    • serum trypsin-like immunoreactivity
    • antibodies to detect trypsin and trypsinogen
    • Specific for exocrine pancreatic function in dogs (low sensitivity).  Not specific for pancreatitis.
    • Useful in detecting Exocrine pancreatic insufficiency (EPI) (decreased)
  17. EPI
    • exocrine pancreas insufficiency.  
    • severe maldigestion and malabsorption and atrophied acinar cells.
    • Loss of 85%-90% of exocrine pancreatic mass
    • decreased TLI good test for it
    • can be congenital (dogs) or acquired (cats)
  18. PLI
    • serum pancreatic lipase immunoreactivity (cPLI or fPLI)
    • measures mass of pancreatic lipase in serum rather than enzymatic activity
    • sensitive for canine and feline pancreatitis
    • Also IDEXX SNAP test, using elisa technology (looks for lipase)
  19. ELISA
    enzyme-linked immunosorbant assay
  20. Treatment for pancreatitis
    • get eating right away, low fat diet.  Feeding tube if anorexic.
    • control pain
    • correct fluid/electrolyte, etc disturbances
    • If necessary, give plasma (if albumin too low. DIC)
    • antiemetics (to avoid loss of fluid/nutrients/electrolytes)
    • H2 blockers
    • +/- antibiotics (peritonitis)
  21. Acute pancreatitis
    • Occurs in d/c, most common form in dogs, rare in cats
    • can be severe and result in death, or reversible.
  22. Chronic pancreatitis
    • Occurs in d/c, rare in dogs, most common in cats (triaditis).  
    • Significant scarring and atrophy of pancreas.  
    • Waxing and waning signs, irreversible changes.
    • Rarely fatal.
  23. Triaditis
    Pancreatitis with hepatitis and IBD, common in cats, who get chronic pancreatitis with GI involvement.
  24. Clinical signs of chronic pancreatitis
    • VDA
    • weight loss
    • weakness
    • abdominal pain
    • dehydration
    • if Islet cell destruction, EPI and diabetes mellitus
  25. cat EPI
    • not too common, generally chronic pancreatitis.  
    • Usually older, GI trouble entire life, IBD
  26. dog EPI
    • acinar atrophy most commonly
    • Chronic pancreatitis less common, pancreatic hypoplasia very rare (G. Shep, congenital)
  27. Maldigestion
    • EPI
    • Insufficient synthesis and secretion of digestive enzymes by exocrine portion of pancreas.  
    • Weight loss, ravenous appetite, voluminous loose greasy stool, poor hair coat
  28. Clinical signs of maldigestion
    • weight loss with ravenous appetite
    • voluminous pale loose greasy stools
    • poor hair coat
  29. Steatorrhea
    voluminous pale greasy loose stools
  30. Diagnosis and treatment of EPI
    • decreased TLI (dogs < 2.5, cats < 8.0)
    • treat with pancreatic enzymes for life
  31. Juvenile Pancreatic Atrophy
    • Congential EPI caused by lack of pancreatic enzymes
    • common in young adult G. Shep
    • Recognize, diagnose and treat like EPI
  32. Malabsorption disease
    • Failure of digestive tract to absorb, but nutrients get digested.  Variety of small intestinal causes
    • chronic parasitism (hookworms)
    • chronic IBD
    • intestinal lymphoma
    • severe dietary sensitivities
    • lymphangietasia (obstruction and dysfunction of intestinal lymphatic system)
  33. Clinical signs of malabsorption disease
    • +/- chronic diarrhea
    • vomiting
    • dehydration
    • anemia
    • ascites or edema
    • altered appetite (anorexia or polyphagia, more common)
    • weight loss despite ravenous appetite (coprophagia or pica)
    • steatorrhea (pale, greasy loose stools) (sometimes)
    • thickened bowl loops
    • enlarged mesenteric lymph nodes
  34. pica
    will eat ANYTHING, doesn't have to be food
  35. tests to diagnose malabsorption disease
    • fecal sedimentation and culture (parasites and pathogenic bacteria)
    • history (dietary indiscretion or sensitivity)
    • lab work (CBC, chemistry and UA for systemic diseases, TLI, PLI, Cobalamin, Folate)
    • Imaging (radiograph, ultrasound)
  36. Cobalamin
    • B12 vitamin.  
    • Mostly absorbed in ileum so B12 deficiency if not absorbing in ileum.  
    • rapidly dividing cells need B12.  Can be used up by bacteria
  37. Folate
    • Test for malabsorption.  Increased in IBD, decreased in PROFUSE small intestinal disease.  
    • absorbed in jejunum (proximal)
    • Body needs folate to make DNA.  Overgrown bacteria can use it all up.
  38. Folate and Cobalamine in EPI
    increased or normal folate, decreased cobalamine
  39. Folate and cobalamine in bacterial overgrowth
    increased folate decreased cobalamine
  40. folate and cobalamine in proximal small intestinal disease
    decreased folate and normal cobalamine
  41. folate and cobalamine in distal small intestinal disease
    normal folate and decreased cobalamine
  42. folate and cobalamine in diffuse small intestinal disease
    both decreased
  43. diagnosis of malabsorptive disease
    • TLI (to differentiate from EPI)
    • Theraputic trials (deworming, antiprotozoals, antibiotics, pancreatic enzymes, food trial)
    • Intestinal biopsy (definitive diagnosis)
  44. Therapeutic food trial
    • Way to help diagnose malabsorptive disease.  
    • Consists of a novel, single-source protein (scrip to prevent cross-contamination) and hydrolyzed protein diet (smaller sized molecules can't set off a reaction)
  45. Intestinal biopsy to diagnose malabsorptive disease
    • open laparotomy: full-thickness sample but invasive surgery.  Can get multiple samples
    • laparoscopic: less invasive, still can get full-thickness biopsy
    • Endoscopy: less invasive, can do both ends, but tunnel vision, can't see outside, can't get full thickness.  Easier on animal, may not give diagnosis
  46. Fecal starch
    • Undigested starch in feces detected by staining feces with Lugol solution
    • Fecal starch + suggests EPI
    • test is insensitive and nonspecific.
    • Meant to test malabsorptive vs maldigestive
  47. fecal fat
    • undigested and digested fat in feces (stain is sudan III or IV)
    • + direct fecal fat very specific for EPI.  
    • Insensitive
  48. Muscle fiber test
    • undigested striated muscle fibers, stain with Lugol.  
    • Not senstive
  49. microscopic stained fecal fat, starch and muscle
    suggests maldigestion, but not terribly accurate.
  50. Tests for maldigestion vs malabsorption
    • fecal fat/starch/muscle fiber
    • fecal proteolytic activity
    • TLI, PLI
  51. Fecal proteolytic activity
    • measures protease activity in stool (trypsin, chymotrypsin, and carboxypeptidase)
    • Historically was the test for EPI in small animals, but TLI is better and easier.
  52. Electrolytes
    • chemical substances that separate in solution to form electrically charged ions.  
    • anions: Cl-, HCO3-, HPO42-
    • cations: Na+, K+, Ca2+
    • Function in energy production, enzyme reactions, acid base balance, osmosis and diffusion, and muscle contractions
  53. Renin Angiotensin system
    • response of body to falling BP.  
    • Kidney notices decrease in BP
    • kidney releases Renin
    • Renin activates circulating angiotensinogen, made in liver, into angiotensin I
    • Angiotensin converting enzyme (found in epithelium, esp lungs) turns angiotensin I into angiotensin II.  
    • Angiotensin II causes increased thirst, vasoconstriction, and stimulates the adrenal to make aldosterone
    • Aldosterone stimulates kidney to retain Na and therefore water.
  54. Angiotensin-converting enzyme (ACE)
    • found in endothelium, especially in the lungs but all over the body.
    • Converts angiotensin I to angiotensin II in renin-angoitensin response to falling BP
  55. Hyperadrenocorticism and electrolytes
    • Hypernatremia
    • increase in aldosterone causes Na retention.
    • Cushings.
  56. Hypoadrenocorticism and electrolytes
    • decrease in aldosterone causes Na eliminationa and K retention.  
    • Hyponatremia, Hyperkalemia.  
    • Addison's.
    • Plasma Na:K < 27:1 (normal 27:1- ~40:1)
  57. HCO3-
    generated in body (lungs, gastric mucosa, kidneys and erythrocytes), altered by other electrolytes and acid-base balance
  58. Ways electrolyte concentration can be changed
    • increase or decrease intake
    • shift to/from ICF (out of gen. circ.)
    • increased renal retention
    • increased loss via kidneys, alimentary tract, skin, or airways or (HCO3) indirectly
  59. Sodium
    • Principle cation in ECF
    • Co-factor in metabolic reactions
    • Driver of fluid movement
    • Controlled by blood volume regulation or plasma osmolarity regulation.  
    • Enters body from food/drink intake
  60. Blood volume regulation of Na
    • decreased blood volume, renin system, aldosterone increases Na retention. 
    • increased blood volume, decreased Na absorption due to atrial natriuretic peptide (amino acid found in myocytes of atria, released when stretched).
  61. Atrial natriuretic peptide
    • amino acid found in atria of heart, released when atria are stressed by too much blood volume.  Causes decreased Na absorption in distal nephron.  
    • Seen in congestive heart failure.  
    • New blood test that can look for it, detect heart problems in asymptomatic cats.
  62. Plasma Osmolarity regulation of H2O
    • Hyperosmolarity causes more drinking and release of ADH, causing water resorption from collecting duct.
    • hypoosmolarity causes decreased thirst and no ADH, so no water retention.
    • Osmolarity of plasma usu ~300
  63. Self regulation of plasma Na
    • hypernatremia causes decreased aldosterone, and therefore less resorption
    • hyponatremia causes increased aldosterone and sodium retention
    • Affected by plasma K+ levels and effective blood volume
  64. Major Na/K regulator
  65. Simple: Na levels are controlled by
    • dietary/fluid intake
    • renal H2O/Na resorption and secretion
    • aldosterone
  66. Causes of hyponatremia
    • V/D
    • CRF (kidneys not responding to aldosterone)
    • Addisons (less Aldosterone)
    • diuretics (medullary washout, no gradient at Henle)
    • CHF (blood volume)
    • Hepatic cirrhosis (no angiotensinogen leads to no aldosterone)
    • Over-hydrating with half saline
  67. Clinical signs of hyponatremia
    • lethargy
    • muscle weakness
    • confusion
    • seizures
    • dullness
    • coma
    • nausea, vomiting
    • DECREASED blood pressure
    • increased aldosterone
  68. Hypernatremia causes
    • Dehydration: H2O deprivation, defective thirst response, insensible loss (fever, panting, hyperventilation), diabetes insipidus, renal osmotic diuresis, diarrhea/vomiting
    • Increase in body Na: salt poisoning, hypertonic saline, hyperaldosteronism.
  69. diabetes insipidus
    decreased aldosterone production or nonfunctioning receptors in kidney for aldosterone.
  70. Renal osmotic diuresis
    Washout of osmotic gradient in loop of Henle, washed out by too many diuretics.
  71. Clinical signs of hypernatremia
    • lethargy
    • weakness
    • disorientation
    • behavior changes
    • ataxia
    • seizures
    • stupor
    • coma
    • fluid retention (third-spacing)
    • INCREASE in blood pressure.
  72. Potassium
    • Principal cation of ICF (not shown in BW usu).
    • Functions in resting membrane potential, repolarization, cardia rhythms and rate, Na in renal, acid-base metabolism (exchange for H+ in/out of cell)
    • Regulated by renal excretion and distribution between ICF and ECF (dietary, feces and sweat a little).
  73. Aldosterone and K+
    • Hyperkalemia and angiotensin II stimulate aldosterone, trade Na for K, so K goes into urine.  
    • Hypokalemia lowers aldosterone secretion.
  74. Causes of hypokalemia
    • shift from ECF to ICF
    • decreased intake--anorexic
    • increased loss: increased insulin activity, diuretics, VDA, sweating in horses, hyperaldosteronism
    • alkalosis
  75. How alkalosis causes hypokalemia
    increased pH causes ECF to want to lose H+, swaps with K+ so less K+ in ECF
  76. Clinical signs of hypokalemia
    • Profound muscle weakness
    • In cats: ventroflexion of neck, forelimb hypermetria (goose-step), broad based hind limb stance
  77. Causes of hyperkalemia
    • tissue necrosis (released from dying cells)
    • renal failure (not excreted)
    • UT obstruction or ruptured bladder (not excreted)
    • hypoaldosteronism (often hypoadrenocorticism)
    • administration of K+
    • acidosis (too much H in ECF, switch with K)
    • insulin deficiency (diabetes mellitus)
    • inherited periodic hyperkalemia (horses)
    • Oleander toxicity
    • Pseudohyperkalemia (sampling error)
  78. Clinical signs of hyperkalemia
    Cardiac effects.  Life-threatening bradycardia can lead to arrest.  Addisons often presents with bradycardia.
  79. Treatment of hyperkalemia
    • Attempt to determine cause (oleanders, addisons) and treat
    • decrease K+ intake, increase uptake into cells, increase excretion.  
    • Calcium supplementation decreases signs of cardiac toxicity.
    • fluid therapy with 0.9% saline (exchange)
    • Give insulin with dextrose, send K into cell
    • sodium bicarb supplementation, gets K into cell and treats acidosis
  80. Chloride
    • follows Na passively.  
    • Principle anion in ECF
    • Maintains neutrality/balance
  81. Hypochloremia
    • Loss of HCl or KCl (V/D)
    • Upper GI obstruction
    • drugs that block Cl transport
    • Hyperalbuminemia (albumin is an anion, so Cl balances)
    • decreased Na, so: 
    • CRF (kidneys not responding to aldosterone)
    • Addisons (less Aldosterone)
    • diuretics (medullary washout, no gradient at Henle)
    • CHF (blood volume)
    • Hepatic cirrhosis (no angiotensinogen leads to no aldosterone)
    • Over-hydrating with half saline
  82. Hyperchloremia
    • Drugs that block Cl transport
    • hypoalbuminemia (Cl balances)
    • Same as Na: 
    • Dehydration: H2O deprivation, defective thirst response, insensible loss (fever, panting, hyperventilation), diabetes insipidus, renal osmotic diuresis, diarrhea/vomiting
    • Increase in body Na: salt poisoning, hypertonic saline, hyperaldosteronism.
  83. Three forms of Calcium
    • ionized (50%)
    • protein bound-bound primarily to albumin to minimize changes in body (40%)
    • chelated-complex with phosphate, citrate, bicarb, sulfate or acetate (10%)
  84. PTH on Calcium and Phosporus
    • Net effect, increase blood calcium, lower blood phosphate
    • Low concentration of calcium in blood
    • release of PTH
    • pull Ca and P out of bone, decrease loss of Ca in urine by switching for P, tell kidneys to release calcitriol to absorb more Ca and P from intestines.
  85. Calcitonin on Ca and P
    • Net effect, decrease blood Ca, increase in blood P
    • Rising Ca in blood stimulates thyroid to release calcitonin.  
    • stimulates deposition of Ca in bone
    • inhibits renal resorption of Ca, so no switch for P
  86. Calcitonin
    released by thyroid in response to rising blood Ca levels.  Lowers levels by sending to bone and stopping kidney resorption.
  87. Calcitriol on Ca and P
    • Net effect, increase blood Ca and P
    • low Ca in blood, PTH tells kidney to release/activate calcitriol.  
    • More Ca and P absorbed in intestine.
  88. Functions of Ca
    • skeletal structure and function
    • muscle contraction
    • blood coagulation (clotting cascade)
    • nerve impulses
  89. Functions of Phosphorus
    • Skeletal structure and function
    • energy reactions (ADP, ATP)
  90. Hypercalcemia Causes
    • Granolomatous
    • Osteolytic
    • Spurious
    • Hyperparathyroidism
    • D hypervitaminosis
    • Addisons
    • Renal failure
    • Neoplasia (LYMPHOMA)
    • Idiopathic
    • Temperature
  91. Hypercalcemia clinical signs
    • PU/PD
    • lethargy
    • anorexia
    • vomiting
    • constipation
    • weakness
    • renal failure (mineralizing)
  92. Hypocalcemia causes
    • Hypoproteinemia (hypoalbuminemia)
    • hypoparathyroidism
    • Hypovitaminosis D (renal, causes less absorption in intestine)
    • antifreeze (ethylene glycol toxicity) (excretion)
    • blister beetle toxicosis (excretion)
    • fracture healing
    • acute pancreatitis (not sure why)
    • Eclampsia (pregnancy, mom's Ca fatally low)
    • Milk fever (dairy cows after birth can't keep up)
    • Alkalosis (protein ionizes, binds with more Ca)
    • Ca binds with diffuseable anion
  93. Calculate hypocalcemia correcting for albumin
    3.5 - albumin + calcium
  94. Clinical signs of hypocalcemia
    • nervousness
    • behavioral changes
    • focal muscle twitching
    • tetany
    • seizures
    • cardiac arrhythmias
  95. hyperphosphatemia causes
    • decreased GFR, leading to decreased secretion (prerenal, renal or postrenal)
    • increased absorption in intestine with calcitriol or phosphate enema
    • shift into ECF from ICF in myopathies (endurance races)
    • hyperthyroid in cats
    • hyperadrenocorticism in dogs
    • Increased in young, growing animals (like ALP and lymphocytosis)
  96. Causes of hypophosphatemia
    • primary hyperparathyroidism (increased excretion)
    • pseudohyperparathyroidism (lymphoma or anal gland tumors cause PTHrp, like PTH)
    • less absorption due to anorexia or less calcitriol
    • hyperinsulinism (OD causes shift from ECF to ICF)
    • eclampsia (pregnancy, not enough from bone)
    • equine renal disease
  97. 2 major pumps in acid-base balance
    • Cl-/HCO3- (resorbed/excreted in direct opposition)
    • Na+/H+ (energy from Na+ gradient moves H+ out of cell in exchange for K+)
  98. Method to fix Acidosis
    • decreased pH = increased H+ in cell.  Na/H+ pump pumps H+ out of renal cells into tubules to be excreted
    • Cl-/HCO3- pump inhibited to increase HCO3 inside cell.  
    • Intracellular H+ decreases, HCO3 increases, Cl decreases, pH becomes higher/more alkalotic/normal.
  99. Method to fix alkalosis
    • increased pH = decreased H+ in cell.  Na/H pump inhibited, keeping H in cell. 
    • Cl/HCO3 pump sends HCO3 out of cell to be excreted.  
    • As H+ increases and HCO3 decreases, cell moves toward normal pH.
  100. Respiratory acidosis
    • increase in partial pressure of CO2
    • hypoventilating.  Anesthesia.
  101. Respiratory alkylosis
    • decrease in partial pressure of CO2
    • hyperventilating
  102. Metabolic acidosis
    • decrease in HCO3
    • Can be caused by chronic renal failure
  103. Metabolic alkylosis
    increase in HCO3
  104. Blood gas, order to read and what it means.
    • pH, then bicarb, then PCO2.
    • pH tells you alkalosis or acidosis.  If matches bicarb (both increased = metabolic alkalosis, both decreased = metabolic acidosis), metabolic.
    • Look at PCO2.  If same, trying to compensate.  If dif, adding to problem (mixed disturbance).  
    • If PCO2 opposite pH and HCO3 opposite pH, respiratory with metabolic compensation.  
    • If normal, no compensation.
Card Set:
Pancreas, Maldigestion and Malabsorption and Electrolytes
2013-10-29 00:01:03
Clin Path

Pancreas, Maldigestion, Malabsorption and Electrolytes in Clinical Pathology Quiz 2
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