9. Pancreas

Question 1

Which drugs act on intestinal motility?

Answer 1

Parasympathomimetic drugs (cholinergic end plate stimulants), parasympatholytic dugs (cholinergic end plate inhibitors), sympathomimetic drugs (adrenergic
end plate stimulants).

Question 2

What effect does the drugs have on intestinal motility?

Answer 2

These drugs have local and systemic effects.
Locally: through the plexi (plexus myentericus Auerbachi, submucosus Meisneri) and act at
the end plates. Components of the feed (i.e. fibers) and temp of feed are also acting through these plexi and end plates.

Question 3

What is ileus, causes and effects?

Answer 3

Ileus is: Persistent inhibition of aboral transmission of gastric or intestinal contents.)
Cause: Some intestinal irritants (i.e. foreign bodies w. rough surface) cause severe muscular contraction onto them that mediates the development of ileus.
Effects: Severe spastic muscle contraction may cause decreased blood perfusion and necrosis of the intestinal
wall at the site of ileus.

Question 4

Increased parasympathomimetic effect

Answer 4

Stigmosan inj.:
- Local effect: increased smooth muscle contraction (increased peristalsis, and secretory function) – increased intestinal metabolism causes increased gas formation and gas accumulation cranially from the effect)
- Systemic effect: Increased parasymathomimetic and acetylcholine effects – increased muscular (smooth
muscle and striated also) irritability.

Question 5

Increased parasympatholytic effect

Answer 5

Buscopan inj.:
- Local effects: relaxing intestinal muscles (decreased peristalsis) and decreasing secretory function.
-Systemic effect: decreased parasympathetic tone.
These parasympatholytic drugs should not be used in veterinary practice for the treatment of GI-hypermotility, and hypersecretion due to the danger of intestinal bacterial overgrowth and absorption of toxic materials.

Question 6

Drugs used for parasympatholytic effect

Answer 6

• Scopolamin is used to decrease intestinal muscle spasm in order to be able to perform rectal examination in horses or cattle that have colic.
• Atropin is used to inhibit the effects (i.e. salivation, lacrimation, vomiting, diarrhea, convulsions, miosis) of parasympathetic stimulant drugs or toxins or to treat some cardiologic diseases.
• Atropin, scopolamine and similar alkaloids in different plants can cause toxicosis (if ingested) with the signs of mydriasis, xerostomia (dry mucous membrane in the mouth because of decreased saliva secretion) , intestinal, or ruminal atonia, bloat, and in severe cases shock.

Question 7

Increased sympathomimetic effect

Answer 7

Adrenalin (epinephrine)

• Local effect: relaxing intestinal muscles, paralytic ileus.
• Systemic effect: adrenaline is a stress mediator. Increased sympathetic tone is generally caused by increased endogenous adrenalin production due to stress or pain (the consequence can be intestinal or ruminal atonia or even paralytic ileus). Adrenalin injection can save life! It is used for the treatment of severe anaphylactic shock, and for resuscitation in case of asystole to restart heart muscle contractions.

Question 8

Local and general consequences in ileus

Answer 8

• Intestinal spasm onto the irritant
• Intestinal content can not be transmitted further aboraly, starts to be decomposed. Bacteria will overgrow->water influx into lumen.
• Aboraly from the foreign body intestines are empty, walls are attached to each other
• Vessels of the intestinal wall are compressed at site of ileus
• Stasis develops behind the block of the venous flow, and lack of blood after the block of arterial flow
• Local anaerobic GL and local lactic acidosis develops at ileus -> tissue necrosis and inflam. process locally.
• Fluid accumulates in the intestine proximally from the block.
• Some water is filtrated through the vessels and can get into the abd. cavity, causing ascites, and if bacteria-> septic peritoniti.
• Some water is vomited due to the antiperistalsis.
• Due to the accumulation of the intestinal content, bacterial overgrowth is developed. Intestinal wall becomes damaged, endotoxaemia, shock, bacteraemia, sepsis, and peritonitis.
• Dehydration.
• Increased gas accumulation in the loops prox from ileus.
• Intestinal damage->haemorrhage in lumen->blood loss.
• The patients do not eat; their abdominal cavity is painful so there is stress and adrenalin effect. Due to adrenalin there is intestinal atonia, and there is no stimulus for the emptying of the gall bladder. Gall bladder can be very large. Endotoxaemia.
• In some chronic cases pancreatitis and liver damage may develop, due to the intestinal hypoxia, bacterial overgrowth and absorption of bacterial toxins,
• Water loss due to profuse vomiting and water influx into the intestinal lumen cause haemoconcentration and
  hypovolemia, poor tissue perfusion and general anaerobic GL and lactic acid production, and sometimes hypovolemic shock.
• As a consequence of dehydration GFR-will be decreased, decreased renal function also develops
• Loss especially K+ (hypokalaemia) causes muscle weakness, also in the breathing muscles which leads to
  hypoxia, and even death!
• Due to the muscle weakness, respiratory muscles do not work properly, so ventilatory failure also exists, hyperkapnia, hypoxaemia will develope. Ventilartory disorder may cause respiratory acidosis.
• Due to the dehydration, metabolic and respiratory acidosis may develope, hypokalaemia,
  endotoxaemia and bacteraemia causes shock, and death

Question 9

Some clinical signs and complications of pancreatitis

Answer 9

anorexia, depression, severe abdominal pain, severe vomiting, exsiccosis, sometimes diarrhea, signs of heart failure, vasculitis, kidney failure, liver failure, dyspnoe, sometimes anaemia and/or icterus, sometimes signs of
peritonitis, paralytic ileus, septicaemia, DIC, multi organ failure, abscess formation in the pancreas

Question 10

Laboratory examination of pancreatitis

Answer 10

Haematological, serum biochemical, cytological and microbiological analysis.

Question 11

Haematological analysis

Answer 11

 polycythaemia 
 degradation of red blood cells
 anaemia (in chronic sever cases)
 leukocytosis (or leukopenia in case of abscess)
 neutrophilia (or -penia), left shift
 leukemoid reaction

Question 12

Determination of pancreatic enzymes in the plasma

Answer 12

 alpha-amylase activity
 lipase activity
 phospholipase-a2 activity
 trypsinogene-/trypsine/conc. (RIA or ELISA methods)
 elastase concentration (RIA or ELISA methods)
 Best is: pancreas specific lipase (PSL) (ELISA method)

Question 13

Determination of substrates

Answer 13

 glucose concentration (IDDM)
 concentration of electrolytes
 alpha2-macroglobulin concentration
 alpha1-antitrypsine concentration
 triacylglycerol concentration
 Ca2+ concentration
 kidney, liver parameters and total protein, albumin concentration should be measured in order to diagnose the effects of the complications.

Question 14

normal value of alpha-amylase

Answer 14

< 800-1000 IU/l

Question 15

Alpha-amylase methods

Answer 15

• Starch digestion test

- p-nitrophenol method

Question 16

Increased alpha-amylase activity is found in the following cases

Answer 16

acute pancreatitis
acute, subacute kidney failure
FIP and other immune-mediated diseases, 
lymphoma, myeloma, diabetes mellitus,
ileus,
gastric or intestinal perforation
parotitis,
chronic enteritis

Question 17

Lipase Normal value

Answer 17

< 800 IU/l

Question 18

Lipase method for dogs and cats

Answer 18

ELISA laboratory test - pancreas specific lipase

Question 19

Determination of lipase activity

Answer 19

Turbidimetric method

Question 20

Alpha-amylase/creatinin-ratio
Measurement of urine amylase, urine creatinine and plasma amylase and plasma creatinin for…
1. Pancreatitis
2. Kidney failure

Answer 20

1. pancreatitis: urine amylase+urine creatinin: incr
   plasma amylase: incr, plasma creatinin: incr/same
2. kidney failure: urine amylase+urine creatinin: decr,
   plasma amylase+plasma creatinin: incr

Question 21

Alpha-amylase/creatinin-ratio normal value

Answer 21

Normal value 1-6%

Values above 6 % means pancreatitis

Question 22

EPI is developed due to?

Answer 22

Chronic necrotic or atrophic damage to the pancreas, or sometimes it is an inherited disease.

Question 23

Feature of EPI?

Answer 23

Decreased production of digestive enzymes, or the enzymes do not get out from the organ into the intestines

Question 24

Effects of EPI

Answer 24

-Maldigestion
-pancreatogenous dyspepsia
-loose weight, despite they are always very hungry, and they eat remarkably more than normal.
-Some animals overeat and vomit some of the food, then eat it again
-coprophagia, and/or allotriophagia (pica).
-intermittent chronic diarrhoea, bacterial enteritis and frequent flatulence.
-Faeces: very bad small, color can be very light grey. -vitamin deficiencies->skin and fur problems, increased hair loss, unkempt hair coat, and sometimes
mild anaemia
-IDDM sometimes follows EPI

Question 25

Treatment of EPI

Answer 25

These animals usually need lifelong treatment with pancreatic enzymes (given orally), and easily digestible diet-food, and regular parenteral (!) vitamin supplementation, and sometimes, when they suffer from enteritis they need symptomatic treatment (maintenance of electrolyte, water and acid-base balance) and (if it is bacterial enteritis) targeted antibiotic therapy, also.

Question 26

Laboratory examination of EPI

Answer 26

• TLI-concentration: EPI if; TLI conc. is less than 2,5 µg/l
• BT-PABA test
• Dyed agar-gel digestion and Schwachmann-filmtest
• Lipid absorption test
• Faecal elastase test
• Examining undigested particles in faecal sample