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VET377B SPAM Second Half > Alimentary Tract (GI) > Flashcards

Alimentary Tract (GI) Flashcards

1
Q

How do we assess the intestinal function and pathology?

  • Lab detection of malassimilation (maldigestion/malabsorption) - Eating normal, losing weight, Diarrhoea
A
  • Faecal analysis - Microscopy of faecal smears, Faecal fat, starch and fibre, total faecal fat, Faecal proteolytic (Trypsin) activity - All not very reliable or sensitive. Use with caution.
  • Trypsin like immunoreactivity (TLI) - Detects canine EPI (Exocrine Pancreatic Insufficiency)
    • Rule out Pancreatic Insufficiency first as a cauase of Malassimilation!
    • Looking for figures below the reference range = EPI, if its close test it again in a few months.
  • Intestinal absorption and tolerance tests - Used to detect increased intestinal permability realitive to reduced Surface Area/Enterocyte dysfunction (IBD/Neoplasia) - Feed an item Sample the Blood and test the serum for the presence of that item = absorption. (Lipids or Carbohydrates) can also show increased absorption
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2
Q

What is dysphagia?

A

Difficulty in swallowing/ Difficulty in Prehension, Mastication and Swallowing

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3
Q

What is an increase in serum folate indicitive of?

What is a decrease in serum folate indictive of?

A

SIBO - Bacteria synthesise folate

Proximal or diffuse Small intestinal disease (carriers necessary for absorption are only present in the proximal SI.)

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4
Q

What is Stomatitis?

A

Inflammation of the Oral Cavity

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5
Q

Describe the mechanisms involved in the digestion and absorption of Lipids in the small intestine?

A
  • Lipids Absorption
  • Triglycerides are first emulsified by bile salts breaking them into small droplets which cannot coalesce and the surface area is increased allowing pancreatic lipase to hydrolyzes them into monoglycerides and Free Fatty Acids.
  • These water insoluable products are then carried into the interior of hte water soluable michelles (formed by Bile Salts and other bile constituents) to the luminal surface of the small intestine epithlial membrane
  • When a michelle approaches the absorptive epithlial surface, the monoglycerides and Free Fatty Acids leave the michelle and passively diffuse through the lipid bilayer of the luminal membrane.
  • The Monoglycerides and FFA are resynthesized into triglyceride inside the epithlial cells
  • These triglycerides are covered in a layer of lipoprotien to form water soluable Chylomicrons. These cannot cross the basement membrane of blood capillaries so instead the enter the lympathic vessels
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6
Q

What pathway do the Visceral Nociceptive signals travel from the GI tract?

A

Spinothalamic pathway

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7
Q

Johne’s Disease causes what kind of diarrhoea and why?

A
  • Johnes Disease is a chronic enteric disease that due to its chronic inflammation causes increased intestinal permeabilty causing diarrhoea.
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8
Q

Describe in detail the mechanisms involved in the intestinal absorption of Sodium via Nutrient-Coupled Sodium Transport

A
  • in the small intestine nutrient couple Na transport occurs via SGLT1 (2Na:1Glucose) and Amino Acid on the lumenial surface.
  • Transport driven by down hill electrochemical Na gradient generated by basolateral Na/K-ATPase pump (secondary active transport)
  • Cl absorbed passively via paracellular pathway in response to lumen-negative transepithlial potential difference generated by movement of other ions.
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9
Q

What is the difference between Regurgitation and Vomiting

A
  • Regurgitation has no:-
    • Nausea
    • Abdominal contractions
    • Conscious Effort
    • Bile
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10
Q

Explain Secretory Diarrhoea

A
  • Increase in active ion transport mechanisms, especially chloride, in both small intestine and colon
  • No demonstratable intestinal lesions
  • Biochemical lesion
  • Diarrhoea associated with fluid overload of large intestine +? large intestinal secretion
  • Typically high-volume diarrhoea
  • Diarrhoeal fluid isotonic
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11
Q

What are exogenous non-metabolisable Probes used for?

What is the advantage of Various Sugar Probes over exogenous non-metabolisable Probes?

A
  • Are given to an animal orally and they do not undergo any metabolisation, serum and urine is tested and if any markers show then these it indicates an increased permability of the GIT however its unknown where. eg CR -EDTA, PEG)
  • Sugar probes are metabolised at different locations along the GIT therefore a mixture of these can help localise where along the GIT the permability increases.
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12
Q

Explain in detail the mechanism of diarrhoea, relating this to any pathologic changes that occur in the intestinal wall: overfeeding milk replacer to calves

A
  • When over feeding milk replacer this is poorly digestible and remains in the lumen of the intestines. This solute causes excess water to move into the intestinal lumen.
  • This maldigested material reaches the large intestine, undergoing fermentation further increasing the osmotic drag of water.
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13
Q
  • What could a decrease of Serum Cobalamin (B12 and in increase of serum folate indicate?
  • WHat would be another test to help diganose this disease, what else can this test indicate for?
A
  • Small Intestine Bacterial overgrowth
  • Breath Hydrogen - Bacteria metabolise Carbohydrate to Hydrogen. Can also indicate Malabsorption
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14
Q

What is a decreased serum cobalamin (B12) indicitive of?

A
  • Distal of diffuse small intestinal disease involving the ileum
  • SIBO
  • Exocrine Pancreatic Insufficiency
  • Hereditary cobalamin malabsorbtion
  • Low Dietary intake (Vegetarian Diet)
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15
Q

What is Peritonitis?

A

Inflammation of the peritoneum and sructures contained therein

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16
Q
  • What can increased permeability of the GI tract result from?
  • What is the mechanisms of Increased permeability, protein loss and PLE
A
  • Acute inflammation - acute enteroinvasive/necrotising enteritis (typically bacterial diseases eg salmonella)
  • Chronic inflammation - increased pressure in the lamina propria (Eg Johne’s disease, Eosinophillic Enteritis (horses) Histiocytic Ulcerative Colitis (boxer dogs))
  • Mechanisms
    • Increased vascular permeability (acute and chronic permeability)
    • Increased venous pressure
    • Lymphatic obstruction (often with chronic inflammation, neoplasia)
    • Decreased osmotic pressure
  • Leads to increased capillary and/or epithelial permeability –> alter normal osmotic/hydrostatic pressure gradients –> water/electrolytes move from blood to GI lumen
  • If sever –> Plasma protein loss
  • Severe intestinal Protein loss –> Hypoalbuminaemia
  • Any enteric disease causing serum aberratios = protein-losing enteropathy (PLE)
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17
Q

In the Small intestine what products have a net absorption and what has a net Secretion?

A

Net Absorption

  • Water
  • Sodium (active)
  • Potassium (Passive)
  • Chloride (in exchange for bicarbonate)
  • Non-Electrolytes such as glucose, amino acids, lipids and bile salts

Net Secretion

  • Bicarbonate (in exchange for chloride)
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18
Q

If you had a patient with a GI issue that you were working up. What tests would you normally do first?

A

Haematology, Serum Biochem and Urine Analysis

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19
Q

What are the pathologic mechanisms for Diarrhoea?

A
  • Maldigestion/malabsorption (Malassimilation)
    • Ingestion of poorly absorbed soluted (Increase osmotic pressure in lumen)
    • Disease causing loss of mucosal surface area (Villous atrophy)
  • Increased secretion of ions (Hypersecretion)
    • Bacterial toxins
    • Inflammatory mediators
    • Endogenoug laxatives
  • Increased Intestinal Permeability (PLE)
    • Acute inflammation (enteroinvasive bacteria)
    • Chronic inflammation
    • Neoplasia
    • Lymphatic obstruction
  • Changes in intestinal motility
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20
Q

Outline the limitations and indications of Faecal Culture and Sensitivity

A
  • If you suspect a specific pathogen (eg Salmonella spp.)
  • Indications :
    • Clinical signs - Acute GI signs - haemorrhagic, diarrhoea, pyrexia, inflammatory leukogram, neutrophils on rectal cytology
  • Limitations
    • Must be fresh faeces
    • Avoid Refrigeration (kills organisms)
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21
Q
  • What are the two possible mechanisms for Malassimilation?
  • How can malassimination manifest?
A
  • Due to faulty digestion (MalDigestion)
  • Impaired intestinal mucosal transport (MalAbsorption
  • Diarrhoea
    • In carnivores, voluminous watery/pasty faeces, often loaded with undigested fat (steatorrhoea)
    • In horses with SI disease only, diarrhoea may not occur
  • Weight Loss
    • Usually occurs despite normal to ravenous appetite
    • Some agents cause pyrexia and pain –> inappetance
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22
Q

If we have a PLE what blood results would we see?

A
  • Panhypoproteinaemia (low albumin and globulin)
    • Hypoalbuminaemia would be hepatic insufficiency or PLN typically)
  • Low Choloesterol ??
  • Low Lymphatics ??
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23
Q
  • What type of test is a Canine Faecal parvoviral antigen test?
  • What are some of the tests indications/reasons for running the test??
  • What are its limitations?
A
  • ELISA test - from fresh faeces
  • Indications
    • Signalment/Hx: Young, unvaccinted, exposure
    • Clinical Signs: Acute diarrhoea +/- anorexia, haematemesis, melaena/haematochaezia, pyrexia, leukopaenia/neutropaenia
  • Limitations
    • False Negatives - Virus only sheds in faeces briefly - rately detected after 10-12days post infection (5-7days clinical illness)
    • False Positives - Modified live vaccines results in transient faecal shedding, may give a weak positive result 5-15days post-vacc
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24
Q

What is intussusception?

  • What are some causes?
A

Altered intestinal motility where the intestine folds like a telescope on itself.

  • Dysautonomia
  • Postoperative ileus
  • Opioid induced bowel dysfunction
  • Muscular Dystrophy
  • Visceral Myopathy
  • Viral Enteritis
  • Radiation Enteritis
  • Idiopathic psuedoobstruction
  • Hypothyroidism
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25
Q

What would we expect to see with persistent vomiting, intestinal obstruction of secretory diarrhoea?

A

Electrolyte abnormalities

K

NA

Cl

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26
Q

Explain the 2 main transpot channels :-

  • Cellular
  • Parracellular
A
  • Cellular - through the enterocyte
  • Paracellular - between the enterocytes
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27
Q

Describe in detail the mechanisms involved in the intestinal absorption of Sodium-Hydrogen Exchanger

A
  • In the small intestine and Colon extracellular Na is exchanged for intracellular H+ via NHE3 exchanger
  • Driven by electrochemical Na gradient generated by basolateral Na/K-ATPase pump and pH gradient resulting from moderately acidic intracellular environment
  • Na-H exchange enhanced by decreased intracellular pH and increased luminal pH
  • NH3 inhibited by both cAMP and cGMP (+ the diuretic amiloride.
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28
Q

What is Haematochaezia?

A

Fresh Blood in the faeces

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29
Q

Describe in detail the mechanisms involved in the intestinal absorption of Sodium

A
  • Nutrient-coupled Sodium Transport
    • in the small intestine Na coupled with Glucose can be tranposted via a SGLT1 transporter and also Na coupled with Amino Acid from the apical membrane fo the cell
  • Sodium-Hydrogen Exchanger
    • Small intestine (& Colon) Extracellular Na is exchanged for intracellular H+ via NHE3
  • Parallel Na-H and Cl-HCO3 Exchange
    • ileum and proximal colon, Na+ absorption coupled to movement of Cl thought a Cl-HCO3 anion exchanger
  • Electrogenic Sodium Absorption
    • In Distal Colon, electrogenic Na+ absorption occurs via NA+ sepcific aldosterone sensitive ion channel (blocked by amiloride)
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30
Q

Outline the Basic clinical approach to an animal with dysphagia

A
  • Can animal prehend
    • No elevuate lips, facial muscles, incisor teeth, tongue
  • Can animal Masticate
    • No: Check teeth, tongue, jaws and muscles of masitcation
  • Can animal Swallow
    • No: Rvaluate pharyngeal and esophageal function
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31
Q

During Prehension and Mastication what Crainal Nerves are providing Motor and Sensory?

A
  • Prehension
    • Motor
      • CN V, VII, XII
    • Sensory
      • CN VII, IX, X, I, II, V
  • Mastication
    • Motor
      • CN V, VII, XII
    • Sensory
      • CN V, VII, IX
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32
Q

Explain what Osmotic Diarrhoea is

A
  • Component of most diarrhoeal disease
  • Increased amounts of solute (mainly ions and organic molecules) raise effective osmotic pressure of the intestinal contents
  • Water drawn into intestinal lumen, down osmotic gradient
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33
Q

What are some Clinical signs of Abdominal Pain in dogs

A
  • Obvious discomfort
  • Depression
  • Continually shifting positions
  • lickin or look at abdomen
  • whine
  • growl
  • snap (if touched)
  • Tense abdomen
  • grunts or tries to walk away when palpated
34
Q
  • When you have malassimilation (malabsorption/maldigestion) what type of diarrhoea will you expect to see?
  • Give some disease that would be associated with Malassimilation
A
  • Osmotic Diarrhoea
  • Malassimilation
    • Maldigestion
      • Exocrine Pancreatic insufficiency
      • Complete Billary Obstruction
    • Malabsorption
      • Villous Atrophy : Canine Parvovirus
35
Q

Explain Osmotic Diarrhoea

A
  • Component of most diarrhoeal disease
  • Increased amounts of solute (mainly ions and organic molecules) raise effective osmotic pressure of intestinal contents
  • Water drown into the intestinal lumen, down the osmotic gradient
36
Q

How do you asses SIBO (Small Intestinal Bacterial Overgrowth)?

A
  • Test Serum Cobalamin (B12) - a decrease will be seen with EPI, SIBO (bacteria will bind cobalamin and prevent absorption)
  • Test Serum Folate - Will increase with SIBO(and often with EPI) as synthesised by bacteria
37
Q

If a cow had a Caecal Torsion what side would you hear a ping?

A

Right hand side

38
Q

What are some clinical signs associated with Dysphagia?

A
  • Reduced or no feed intake
  • Excess salivation (ptyalism)
  • Gagging
  • Halitosis
39
Q

What is the purpose of Breath Hydrogen testing?

A
  • Detects carbohydrate malabsorption and/or SIBO
  • There will be an increase of hydrogen with increased large intestine fermentation/increased bacteria in small intestine (SIBO)
40
Q

Explain the mechanism by which chloride ions are secreted by intestinal crypt cells and the relationship of this mechanism to secretory diarrhoea

A
  • In both the small and large intestine Cl- secreted from crypt cells
  • Paracellular movement of Na+ driven by lumen-negative transepithelial voltage
  • Cl- secretion provides main driving force for fluid secretion into lumen
  • In small intestine aldo main source of luminal Cl- for Cl--HCO3- anion exchanger
  • Secretion regulatied by second messengers cAMP, cGMP and Ca2+
  • Stimulation by secretagogues causes opening of preexisting and insertion of new Cl- channels - associated with secretory diarrhoea
41
Q

What is a cPL test for?

A

Tests to see if a dog has Pancreatitis.

Canine Pancreatic Lipase Test

42
Q

What is Halitosis

A

Bad Breathe

43
Q
  1. Give 2 examples where cytology of the alimentary tract (as opposed to faecal cytology) may be useful.
A
  • Differentiating between neoplasia and inflammation
  • IDing potential aetiological agents (low sensitivity)
44
Q

Explain a Oral Glucose Tolerance test and what it detects?

A
  • A normal horse would within 2hours double the baseline level of glucose.
  • If the horse suffers a partial malabosrption it would have between 15-65% rise in 2hours
  • Total Malabsorption = no greater than 15% rise in blood glucose level within 2 hours.
  • Insulin resistance is indicated by a high peak (>2.5tims baseline) and prolonged return to base line (>6-7hours)
45
Q

What are the three basic types of intestinal obstructions?

A
  • Simple Obstruction
  • Closed Loop Obstruction
  • Strangulation Obstruction
46
Q
  • Explain how hypersecretion diarrhoea happens
  • What can cause Hypersecretion?
A
  • ↑cAMP > block NHE3 > blocks NaCl absorption at villous tips; causes crypts to secrete Cl (i.e. absorption blocked AND secretion ↑
  • Enterotoxigenic (enterotoxic) collibacillosis (E.Coli)
47
Q

What type of Abdominal Visceral Nociceptors are there in the GI tract?

A
  • Stretch receptors
    • In muscular layers of hollow viscera, between muscularis mucosa and submucosa
    • In serosa of solid organs
    • In mesentery, espcially associated with large blood vessels
  • Chemoreceptors
    • Respond to variety of chemical stimuli
    • Mainly within mucosa and submucosa of hollow viscera
48
Q

What is the mechanism that can lead to secretory diarrhoea?

A

The principal driving force for the secretiun if fkuid is the movement of Cl- from the serosal to the luminal compartment. Na+ and water follow passively in response to the ensuing electrical and osmotic gradients. Both the small and large intestine exhibit a basal rate of Cl- secretion. Disruption of the regulation of this mechanism can lead to secretory diarrhoea.

This regulation is controlled by second messengers cAMP, cGMP and Ca2+

49
Q

Name the voluntary and involuntary phases of deglutition

A
  • Voluntary
    • Oral
  • Involuntary phase (reflex)
  • Pharyngeal
  • Cricophageal
  • Oesophageal
  • Gastro-Oesophageal
50
Q
  • What tests would you run if you believe PLE (Protein Losing Enteropothy) ?
  • What Results would you expect?
A
  • Serum Albumin and total Plasma Protien
    • Most cases are Panhypoproteinaemic though some exhibit hypoalbuminaemia without hypoglobulinaemia. Therefore need A:G ratio
    • 1st rule out : Blood Loss, protien-losing nephropathy, hepatic failure, exudative dermatology, loss into body cavity exduate.
  • Faecal a-1 proteinase inhibitor in faecal samples
    • Similar MW as Albumin (albumin is degraded in the gut but this does not)
  • Cr-albumin recovery in faecal samples
    • Gold Standard - IV administrated radioactive substance
51
Q

What are the 3 basic types of intestinal obstruction

A
  • Simple obstruction
    • Foreign Body
  • Closed Loop Obstruction
    • Herniation - Small intestine entraped through epiploic foreamen
  • Strangulation Obstruction
    • Torsion around pedunculated lipoma
    • GDVD
52
Q

Explain the importance of the intestinal surface area to the digestive and absorptive functions of the small and large intestine.

A
  • Small Intestine
    • Has Villi, Microvilli and crypts.
    • Digestion and absorption of nutrients are faciliated by a large mucosal surface area
    • Crypts are where the enterocytes are produced.
    • Crypt cells are secretory
    • Villous Cells are Absorptive
    • The Enterocytes migrate from the Crypts to the villous tips becomming absorptive and then they undergo apoptosis and slough off
    • Turnover time for these cells is 3-5 days
  • Large Intestine
    • Villi are not present however mature enterocytes still assume an absorptive role
53
Q

If a dog had been vomiting enough to get metabolic Alkalosis what would you give to recify this?

  1. Electrolytes
  2. NaCl
A

NaCl

Electrolytes have Bicarbonate precurses in it and could potentially make it worse.

54
Q

What are the clinical signs or acute abdominal pain in a Horse (colic)

A
  • Agitated appearance
  • Grinding teeth
  • COnstantly looking at flank
  • Sweating
  • Stretching our as if to urinate
  • Constantly going down and getting up
  • Going down and rolling
  • Not eating
  • Foals may throw themselves on the ground
  • Lying in lateral recombency (+/- groaning)
  • Dog-Sigging (Uncommon)
55
Q

Explain the general mechanism and volumes of the daily water turnover in the small and large intestine of a 20Kg dog and a 500kg horse

A
  • The volume of daily water turnover through the Small and Large intestine far exceed the oral intake and faecal output of water.
  • As you move down the intestine towards the colon the the junctions become more tight and therefore the potential difference increases, inturn increasing the absorption efficiency
  • In the Small intestine there is net absorption of water, sodium, chloride and potassium, along with nonelectrolytes such as glucose, amino acids and Bile Salts. Bicarbonate is the main ion secreted into the small intestine (important buffering of material entering the large intestine.)
  • In the large intestine there is net absorption of water, sodium, chloride and short chain fatty acids (SCFA) produced from bacterial fermentation. Bicarbonate is again secreted and Potassium is also secreted.
  • Importantly in the Large intestine the transporters that enable absorption of nutrients such as glucose and amino acids are not present so any of this still in the lumen will undergo bacterial fermentation.
56
Q
  • What test do you use for Canine parvovirus
  • What are some indications to do this test?
A
  • Do an ELISA (fresh faeces (Swab less desirable) for the Canine faecal parvoviral antigen
  • Indications
    • Young, Unvaccinated, and possible exposure
    • Clinical Signs: Acute diarrhoea, +/- anorexia, haematemesis, melanea/haematochaezia, pyrexia, leukopaenia/neutropaenia
57
Q
  • What is SIBO?
  • What are some causes of SIBO?
A
  • Small Intestinal Bacterial Overgrowth
  • Causes
    • Segmental Stasis/hypomotility
    • Neonates prior to commensals becomming established
    • Antibiotic Administration
    • EPI (exocrine pancreatic insufficiency)
  • What can SIBO lead to?
    • Bile Salt depletion - leading to Steatorrhoea (abnormal amounts of fat in faeces/diarrhoea)
    • Decreased Cobalamin (B12) - due to binding and inactiviation of vitamin to bacteria in small intestine
    • Increased folate - due to increased bacterial production
58
Q

What is Anaemia with Hypoalbuminaemia suggestive of?

A

Blood Loss esp from Gastro Intestinal Tract

59
Q

What are the biomarkers of Gastric and intestinal Inflammation, damage and disease?

A
  • Serum Gastrin - R/O Pancreatic Gastrinoma (protonPump inhibitors increase Serum Gastrin so stop using for 10day prior to test)
  • Faecel Occult Blood - Must feed non meat ased diet for 72hrs as this tests for psu\eudoperoxidase activity of heame portion of maemoglobin/myoglobin
  • Plasma Pepsinogen - used in ruminants, indicates damage to abomasum
  • Rumen Fluid pH - For suspected acidosis (normal ph 6-7.5)
  • Lactate in horses with colic
60
Q

How would you test to see if this fluid is urine or some other fluid?

A

Test for Creatinine in the fluid and if the > than the level of creatinine in serum then its urine.

61
Q

What do Chief Cells of the stomach secrete?

A

Pepsinogen

62
Q

In the Large intestine what products have a net absorption and what has a net Secretion?

A

Net Absorption

  • Water
  • Sodium
  • Chloride
  • SCFA’s

Net Secretion

  • Potassium
  • Bicarbonate

Non-Electrolytes such as glucose, amino acids, lipids and bile salts cannot be absorbed in the large intestine - they are fermented

63
Q

Assesment of GIT function and pathology

How do you evaluate GIT motility?

A
  • Survey Radiograph
  • Liquid Barium contrast radiograph
  • Barium Meal contrast radiograph
  • BIPS contrast radiograph (Pill with different size gelatin caps inside. Used to detect obstructions and transit times)
  • Ultrasound
  • Nuclear Scintigraphy
  • Functional MRI
64
Q

What does the parietal cells of the stomach secrete?

A

Hydrochloric Acid

65
Q

What are the 5 phases of swallowing?

A

Oral, pharyngeal, cricopharyngeal, oesophageal and gastro-oesophageal phases

66
Q

WHat is a Paralytic ileus (sometimes just called an ileus)

A

Functional obstruction/ failure of intestinal contents to be propelled aborally along the intestine tract

67
Q

What is the grunt test?

A

By putting pressure to the xiphoid region of a cow, if she grunts, kicks ot acts uncomfortable you can assume she is painful.

Often you have to listen over the trachea during the peak inspiration while simultaneously applying pressure to the xiphoid area to hear a grunt

68
Q

Clinical signs of alimentary tract disease

  • Non-specific with regards to region (both within and without alimentary tract)
  • Specific to upper (oropharynx, Oesophagus, ruminant forestomachs)
  • Specific to lower (stomach/abomasum, intestines anorectum
A
  • Non-specific with regards to region (both within and without alimentary tract)
    • ​Malaise, lethargy and weakness
    • Inappetance, anorexia (Pain?)
    • Weight loss
    • Dehydration
    • Haemorrhage and melaena
    • Abdominal Pain/colic
    • Polyphagia/hyperphagia
  • Specific to upper (oropharynx, Oesophagus, ruminant forestomachs)
    • ​Dysphagia, gagging, rethcing, regurgitaion
    • Ptyalism
    • Halitosis
    • Bloat in ruminants (and diarrhoea secondary to lactic acidosis
  • Specific to lower (stomach/abomasum, intestines anorectum)
    • ​Vomiting and nausea
    • Diarrhoea
    • Haematochaezia
    • Dyschaezia/constipation and tenesmus
    • Gas accumulation, borborygmi, eructation, bloat, flatulence
    • Faecal incontinence
69
Q

The secretion of acid in the stomach is regulated by what 3 agents?

A

Histamine Acetylcholine Gastrin

70
Q

What is Villous Atrophy and what does it do?

How does it come about?

A
  • Villous Atrophy is loss of the Villi in the small intestine
  • Villous atrophy impairs digestion and absorption
  • Can happen as a result of enteric viral disease like
    • Rotavirus
    • Parvovirus
71
Q
  • What are the mechanisms for NSAID’s to cause intestinal ulceration?
  • What are the common sites for these lesions in Dogs and Horses?
A
  • Mechanisms
    • Inhibition of Prostaglandin Synthesis
    • Altered microcirculation
    • Delayed GIT healing (decrease cell turnover and mucous production, stimulate gastin secretion –> increased acid production)
  • Common Sites and lesions
    • Dogs - Colonic perforation
    • Horses - Right dorsal ulcerative colitis and gastroduodenal ulceration
72
Q

Describe the mechanisms involved in the digestion and absorption of carbohydrates in the small intestine?

A
  • Carbohydrates need to be hydrolised into monosacchrides (Galactose, Fructose, Glucose) before absorption via specific carrier protiens in the brush border
  • Starch requires amylase to break it down first in the lumen
  • Galactose and Glucose is transported with Sodium in the SGLT1 transporter
  • Fructose is passively transported through a GLUT5 transporter
73
Q

NSAIDS can cause intestinal ulcertion.

Where would you see these in a dog and a horse?

What are the mechanisms for this ulceration?

A
  • Dog
    • Colonic Perforation
  • Horse
    • Right Dorsal Ulcerative Colitis and gastroduodenal ulceration
  • Mechanisms
    • Inhibition of prostaglandin synthesis
    • Altered Microcirculation
    • Delayed GIT healing (decreased cell turnover and mucous production, stimulate gastrin secretion –> increasing acid production)
74
Q

What are some consequences of protracted vomiting?

A
  • Malnutrition
  • Hypovolaemia/dehydration
  • Hypochloraemia
  • Hypokalaemia
  • Metabolic alkalosis
75
Q

What tests would we use to test for intestinal absorptive capability?

A
  • Trypsin-Like immunoreactivity (TLI) - (Canine tests for Exocrine Pancreatic Insufficency)
  • Faecal Analyses -
  • Intestinal absorption and tolerance tests - Detects increased intestinal permeability relative to reduced SA/enterocyte dysfunction (IBD, Neoplasia) - eg Horse Glucose tolerance test
76
Q

What substances activate the chemoreceptors within the GI tract?

A
  • H+, K+, Histamine, serotonin, vasoactive amines, substance P, PG’s and leukotrienes
  • In responce to
    • Inflammation
      • Peritonitis
      • Abscess
      • GI infection of ulceration
      • Acute pancreatitis
    • Tissue ishaemia of necrosis
      • Intestinal volvulus or incarcenation
      • GDV/right sided abomasl torsion
      • INtestinal infarct
      • Splenic torsion
77
Q

What test would we use if we suspect Protien Losing Enteropathy (PLE)?

A

Serum albumin and total plasma protein.

Most cases are panhypoproteinaemic though some patients are hypoabluminaemia without hypoglobulinaemia (due to increased globlin production caused by concurrent/ underlying disease.)

78
Q

Describe the mechanisms involved in the digestion and absorption of Protiens in the small intestine?

A
  • There are multiple pathways for Protiens to be digested and absorbed
  1. Luminal enzymes digest protiens to peptides and then to Amino Acids which are absorbed
  2. Luminal enzymes digest protiens to peptides, Brush Border peptidases digest these to amino acids which are absorbed
  3. Luminal enzymes digest protiens to oligopeptides (mainly Di and Tripeptides) which are taken up by enterocytes where cytosolic peptidases hydolysis produces amino acids that are transported across the basolateral membrane
79
Q

Name the common infectious bacterial, Viral and Fungal causes og prehension and mastication dysfunction

A
  • Bacterial
    • Wooden Tongue
    • Necrotic stomatitis/Calf diphtheria
  • Viral
    • Feline rhinotracheitis virus
    • Calicivirus
    • Vesicular Stomatitides
    • Erosive Stomatitides
  • Fungal
    • Candida glossitis (Foal Thrush)
    • Conidiobulus (Horse)
  • Neoplasia
    • Lymphosarcoma (Dog Tonsil)
    • Fibrosarcoma (Horse)
80
Q

What are the Pathologic mechanisms of Diarrhoea?

A
  • Maldigestgion/Malabsorption (Malassimilation)
    • Ingestion of poorly absorbed solutes (Eg epsom salts cant be absorbed so stays in lumen and diarrhoea is the result)
    • Diseases causing loss of mucosal surface area (villous atrophy)
  • Secretion
    • Bacterial Toxins
    • Inflammatory Mediators
    • Endogenous Laxatives (eg bile salts pass into the large intestin and get fermented)
  • Changes in intestinal permeability
    • Acute inflammation (enteroinvasive bacteria)
    • Chronic inflammation
  • Changes in intestinal motility

VET377B SPAM Second Half (7 decks)

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