Pancreas, Maldigestion and Malabsorption and Electrolytes

Gland organ composed of endocrine and exocrine portions.

Islets of Langerhans, containing Beta cells (Insulin), Alpha Cells (glucagon), Delta cells (Somatostatin) and F cells (Pancreatic polypeptides).

• Endocrine pancreas
• Beta cells (insulin)
• alpha cells (glucagon)
• delta cells (somatostatin)
• F cells (pancreatic polypeptides)

• From endocrine pancreas, islets of langerhans.
• Create insulin, which pulls glucose into cells to facilitate metabolism.

• From endocrine pancreas, islets of langerhans.
• Create glucagon, which deals with glucose and metabolism (opposite of insulin)

• From endocrine pancreas, islets of langerhans.
• creates somatostatin, which deals with lipid metabolism.

• from endocrine pancreas, islets of langerhans.
• creates pancreatic polypeptides, which deal with protein metabolism.

• 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.

• secrete digestive enzymes (trypsin, amylase, lipase) through ducts into insides of other organs. 
• Leak from damage to pancreas into systemic circulation.

• inflammation of pancreas
• Acute or chronic, causes leakage of digestive enzymes.  
• Chronic is more common, sometimes a flare-up presents as acute.

• 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

• sudden onset
• fever
• anorexia
• V/D (hemorrhagic)
• weakness
• cranial abdominal pain
• shock
• sudden death

• radiograph (hazy ground glass)
• abdominal ultrasound
• bloodwork (anemia, leukocytosis, hyperamylasemia*, hyperlipasemia*, increased liver enzymes (ALP, ALT), hyperbilirubiemia, prerenal azotemia, hyperglycemia, hyperlipidemia

• 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

• TLI (trypsin-like immunoreactivity) (for EPI)
• PLI (pancreatic lipase immunoreactivity) (for pancreatitis)

• 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)

• 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)

• 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)

enzyme-linked immunosorbant assay

• 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)

• Occurs in d/c, most common form in dogs, rare in cats
• can be severe and result in death, or reversible.

• 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.

Pancreatitis with hepatitis and IBD, common in cats, who get chronic pancreatitis with GI involvement.

• VDA
• weight loss
• weakness
• abdominal pain
• dehydration
• if Islet cell destruction, EPI and diabetes mellitus

• not too common, generally chronic pancreatitis.  
• Usually older, GI trouble entire life, IBD

• acinar atrophy most commonly
• Chronic pancreatitis less common, pancreatic hypoplasia very rare (G. Shep, congenital)

• EPI
• Insufficient synthesis and secretion of digestive enzymes by exocrine portion of pancreas.  
• Weight loss, ravenous appetite, voluminous loose greasy stool, poor hair coat

• weight loss with ravenous appetite
• voluminous pale loose greasy stools
• poor hair coat

voluminous pale greasy loose stools

• decreased TLI (dogs < 2.5, cats < 8.0)
• treat with pancreatic enzymes for life

• Congential EPI caused by lack of pancreatic enzymes
• common in young adult G. Shep
• Recognize, diagnose and treat like EPI

• 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)

• +/- 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

will eat ANYTHING, doesn't have to be food

• 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)

• 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

• 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.

increased or normal folate, decreased cobalamine

increased folate decreased cobalamine

decreased folate and normal cobalamine

normal folate and decreased cobalamine

both decreased

• TLI (to differentiate from EPI)
• Theraputic trials (deworming, antiprotozoals, antibiotics, pancreatic enzymes, food trial)
• Intestinal biopsy (definitive diagnosis)

• 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)

• 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

• 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

• undigested and digested fat in feces (stain is sudan III or IV)
• + direct fecal fat very specific for EPI.  
• Insensitive

• undigested striated muscle fibers, stain with Lugol.  
• Not senstive

suggests maldigestion, but not terribly accurate.

• fecal fat/starch/muscle fiber
• fecal proteolytic activity
• TLI, PLI

• measures protease activity in stool (trypsin, chymotrypsin, and carboxypeptidase)
• Historically was the test for EPI in small animals, but TLI is better and easier.

• chemical substances that separate in solution to form electrically charged ions.  
• anions: Cl^-, HCO₃^-, HPO₄^2-
• cations: Na⁺, K⁺, Ca²⁺
• Function in energy production, enzyme reactions, acid base balance, osmosis and diffusion, and muscle contractions

• 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.

• 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

• Hypernatremia
• increase in aldosterone causes Na retention.
• Cushings.

• decrease in aldosterone causes Na eliminationa and K retention.  
• Hyponatremia, Hyperkalemia.  
• Addison's.
• Plasma Na:K < 27:1 (normal 27:1- ~40:1)

generated in body (lungs, gastric mucosa, kidneys and erythrocytes), altered by other electrolytes and acid-base balance

• 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

• 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

• 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).

• 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.

• 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

• hypernatremia causes decreased aldosterone, and therefore less resorption
• hyponatremia causes increased aldosterone and sodium retention
• Affected by plasma K+ levels and effective blood volume

aldosterone

• dietary/fluid intake
• renal H2O/Na resorption and secretion
• aldosterone

• 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

• lethargy
• muscle weakness
• confusion
• seizures
• dullness
• coma
• nausea, vomiting
• DECREASED blood pressure
• increased aldosterone

• 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.

decreased aldosterone production or nonfunctioning receptors in kidney for aldosterone.

Washout of osmotic gradient in loop of Henle, washed out by too many diuretics.

• lethargy
• weakness
• MUSCLE FASCICULATIONS
• disorientation
• behavior changes
• ataxia
• seizures
• stupor
• coma
• fluid retention (third-spacing)
• INCREASE in blood pressure.

• 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).

• Hyperkalemia and angiotensin II stimulate aldosterone, trade Na for K, so K goes into urine.  
• Hypokalemia lowers aldosterone secretion.

• shift from ECF to ICF
• decreased intake--anorexic
• increased loss: increased insulin activity, diuretics, VDA, sweating in horses, hyperaldosteronism
• alkalosis

increased pH causes ECF to want to lose H+, swaps with K+ so less K+ in ECF

• Profound muscle weakness
• In cats: ventroflexion of neck, forelimb hypermetria (goose-step), broad based hind limb stance

• 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)

Cardiac effects.  Life-threatening bradycardia can lead to arrest.  Addisons often presents with bradycardia.

• 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

• follows Na passively.  
• Principle anion in ECF
• Maintains neutrality/balance

• 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

• 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.

• ionized (50%)
• protein bound-bound primarily to albumin to minimize changes in body (40%)
• chelated-complex with phosphate, citrate, bicarb, sulfate or acetate (10%)

• 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.

• 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

released by thyroid in response to rising blood Ca levels.  Lowers levels by sending to bone and stopping kidney resorption.

• 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.

• skeletal structure and function
• muscle contraction
• blood coagulation (clotting cascade)
• nerve impulses

• Skeletal structure and function
• energy reactions (ADP, ATP)

• GOSHDARNIT
• Granolomatous
• Osteolytic
• Spurious
• Hyperparathyroidism
• D hypervitaminosis
• Addisons
• Renal failure
• Neoplasia (LYMPHOMA)
• Idiopathic
• Temperature

• PU/PD
• CARDIAC ARRHYTHMIAS
• lethargy
• anorexia
• vomiting
• constipation
• weakness
• renal failure (mineralizing)

• 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

3.5 - albumin + calcium

• nervousness
• behavioral changes
• focal muscle twitching
• tetany
• seizures
• cardiac arrhythmias

• 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)

• 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

• Cl-/HCO3- (resorbed/excreted in direct opposition)
• Na+/H+ (energy from Na+ gradient moves H+ out of cell in exchange for K+)

• 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.

• 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.

• increase in partial pressure of CO2
• hypoventilating.  Anesthesia.

• decrease in partial pressure of CO2
• hyperventilating

• decrease in HCO3
• Can be caused by chronic renal failure

increase in HCO3

• 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.