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Small Animal Final Year > Intro To Intestinal Disease > Flashcards

Intro To Intestinal Disease Flashcards

1
Q

Define digestion

A

The orderly process by which proteins, fats and carbohydrates are broken down in to absorbable units

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2
Q

What are the two phases of digestion?

A
  • Luminal to start with
  • Then at the level of the mucosal/membranous
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3
Q

Define absorption

A

The process by which products of digestion and vitamins, minerals and water cross the mucosa to enter blood or lymph

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4
Q

What is the role of the mouth in digestion of CHO?

A

Salivary alpha-amylase begins starch digestion to mainly maltose, some glucose and dextrins

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5
Q

What is the surface area of the SI provided by (3)

A
  • villi
  • Microvilli
    • Increase SA further = optimising
  • brush border
    • protective glycocalyx layer
    • brush border enzymes
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6
Q

What happens in the luminal phase in the SI?

A

Starch breakdown continued by pancreatic amylase to maltose…

…cannot yet be absorbed

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7
Q

What happens in the membranous phase in the SI?

A

Dissacharides to monosaccharides by glucosidase enzymes (maltase, sucrase and lactase) located in intestinal brush border

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8
Q

Monosaccarides transported across intestinal mucosa, what is glucose and maltose limited by the rate of?

A

Epithelial transport

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9
Q

Monosaccarides transported across intestinal mucosa, what is lactose limited by the rate of?

A

Rate of hydrolysis

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10
Q

What does CHO active transport require energy from?

A

Na+K+ATPase (sodium pump)

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11
Q

How does the sodium pump work?

A

Na+linked glucose transporter. 2 binding sites, 1 for glucose and 1 for sodium.

  1. Generate gradient
  2. Transport nutrient

H+linked transporter:

Some dipeptides

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12
Q

How does CHO facilitated trasport work? What is it used for?

A

Does not require energy but instead uses concentration gradient of substrate to activate pumps

Fructose

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13
Q

Glucose

Mannose

Xylose

Galactose

Fructose

What is the rate of absorption in order?

A

galactose > glucose > fructose > mannose > xylose

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14
Q

How is protein digested?

A

Protein first denatured by stomach acid then passes to small intestine

Luminal phase: specific proteases hydrolyse protein to short chain peptides

Membranous phase: hydrolysed further to mainly di/tripeptides but some free amino acids

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15
Q

How are amino acid actively trasported?

A

Specific membrane proteins then transport across gut wall by secondary active transport (as for CHO)

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16
Q

There is a risk of autolysis by pancreatic proteolytic enzymes. What is the defence mechanism for this?

A
  • inactive enzymes secreted in to the pancreatic duct in zymogen granules
  • activation only occurs in the intestinal lumen eg trypsinogen to trypsin
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17
Q

How is lipids transported?

A

–Micelles transport lipids across enterocyte cell membranes

–Chylomicrons (large lipoprotein complexes) are used for transport in lymphatic circulation

–Short chain tgs absorbed directly

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18
Q

How is lipid digested?

A
  • Emulsification is crucial and depends on bile
  • Pancreatic lipase is activated in the intestine
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19
Q

What is EPI?

What are the signs?

A

–Inadequate secretion of pancreatic enzymes

–Maldigestion

–Steatorrhoea

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20
Q

What does biliary disease cause? (gall stones, cholestatic liver disease, extrahepatic biliary obstruction)

A

–Failure of emulsification

–Lipase works but unable to solubilise lipids into micelles

–Maldigestion

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21
Q

What is the problem with intestinal mucosal abnormalities?

(inflammation, viral/bacterial infection, neoplastic infiltration).

A

Malabsorption

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22
Q

What drug inhibits GI lipase and reduces fat absorption? Licensed?

A

–Orlistat (xenical)- not licensed

  • Toxicity studies in dogs
  • Predictable adverse effects….
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23
Q

Name a drug that inhbitis microsomal TAG transfer protein? Reduces appetite and FA uptake (2) Is it authoriseed?

A

–Mitratapide (yarvitan) -no longer authorised

–Dirlotapide (slentrol)-no LONGER AUTHORISED

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24
Q

Is the gut lumen inside or outside the body?

A

Outside

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25
Q

What is the function of intestinal microflora?

A

–Complex role of the mucosal immune system

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26
Q

What is the impact of oral antibacterial and diseases on the flora?

A

Interrupt microflora

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27
Q

What is the role of the portal blood flow?

A

•Take blood from gut to the liver without having to dilute in the body. It is then cleaned up and processed. Disruption – you end up knowing the impact. PSS which where the PV doesn’t take to the liver and clinically these animal can be severely affected.

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28
Q

What is the role of the ileocaecal valve?

A

•Between the SI and LI – important to maintain separation here. If you removed thisyouget a lot of problems of dumping SI into the LI = D+

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29
Q

What are the 2 patterns of SI motility, what is the functtion and how do they work?

A

•Peristalsis

–Reflex response to stretch of the gut wall

–Coordinated

–Oesophagus to rectum

–Influenced by autonomic NS

•Segmentation

–Slows down transit

–Enables mixing of chyme & enzymes (gut contents)

30
Q

What are the patterns of motility in the colon? What are the functions of this?

A

•Peristalsis

–Slower rate than in the SI as the colon’s role it to ABSORB WATER (if there isn’t enough time for this you end up with D+)

–Enables time for absorption of

  • Approx 90% of the water from intestinal chyme
  • Sodium
  • Some minerals

–You may not see D+ in bowel disease because the colon may still absorb water. But the SI may be failing to absorb = weight loss

•Segmentation

–Facilitates absorption of water by mixing

31
Q

What is going on here?

A

Ileus: direct inhibition of smooth muscle causing a decrease in intestinal motility.

32
Q

What is going on here in this cat?

A

Dysautonomia contributing to constipation. Other clinical signs include regurgitation due to megoesophagus secondary to oesophageal motility problems and urine retention. Loose ability of smooth muscle

33
Q

What are the general clinical signs of intestinal disease? (10)

A
  • Diarrhoea
  • Vomiting
  • Abdominal pain/discomfort
  • Weight loss – chronic, small bowel
  • Anorexia
  • Flatulence
  • Borborygmi
  • Constipation
  • Tenesmus
  • Melaena or haematochezia
34
Q

How can you differentiate between small and large intestinal diarrhoea?

A
35
Q

Define diarrhoea

A

Passing faeces with:

  • Increased volume
  • And/or increased frequency
36
Q

What are the 4 categories of diarrhoea?

A
  • Osmotic
  • Secretory
  • Inflammatory
  • Motility disorder
37
Q

What is the pathophysiology of osmotic diarrhoea?

A

–Maldigestion (eg EPI, damage to the brush border)

–Malabsorption (eg mucosal damage, villus atrophy, infiltrative disease such as lymphoma)

38
Q

What is the pathophysiology of secretory diarrhoea?

A

–Toxin

–Infection related

39
Q

What is the pathophysioloogy of inflammatory diarrhoea?

A

Inflammatory bowel disease (eg adverse food reaction, idiopathic chronic enteropathy)

40
Q

What do clinical signs of Campylobacter vary with?

A

The strain of organism

41
Q

•Organism may be pathogenic to one species but not another

–Risk of reservoirs of pathogens in healthy animals

–Resistance can be innate or acquired

–Stress effects

Name 2 examples of this.

A

–Campylobacter in a number of wild life and poultry without observable disease.

–E. Coli O157 in cattle

42
Q

Why should you be careful giving anti-diarrhoea tablets?

A

Diarrhoea can be productive

43
Q

How do you initially investigate intestinal disease?

A

•Signalment

–Consider breed, age

–Individual or herd problem?

–Zoonotic implications?

•Full clinical history

–Background history

–Current illness history

–Review the history if necessary!

•Physical examination

–The GI tract is inaccessible

–Look for

44
Q

What could anaemia mean with intestinal disease?

A

Could just be as it is a chronic disease, gi bleeding – iron deficient

45
Q

What does Polycythaemia mean on haematology with GI disease?

A

Dehydration

46
Q

What may an inflammatory leucogram mean on GI disease haematology?

A

inflammation – does it look like the body is impacted?, infection, parasites, may have a stress response

47
Q

What may lymphopenia mean on haematology with GI disease?

A

lymphangiectasia

48
Q

What may Eosinophilia, lymphocytosis mean on haematology with GI disease?

A

hypoadenocorticism

49
Q

On biochemsitry what would you see with:
A) Dehydration?

B) Fluid imbalance?

C) Protein loss in the gut?

A

A) Hiigh urea, creatinine, total proteins

B) Electrolyte abnormalities

C) Low albumin globulin

50
Q

On biochemsitry what would you see with:

A) GI bleed

B) Functional liver disease?

C) FIP in in cats?

A

A) High urea +/- low protein

B) Low urea, low cholesterol, low albuin, low glucose

C) High globulin

51
Q

On biochemsitry what would you see with:

A) Hypoadrenocorticism?

B) Malabsorption?

A

A) hyperkalaemia, hyponatraemia

B) low cholesterol +/- albumin

52
Q

What faecal analysis can we do?

A

–Swab or sample?

–Think about pathogenic organisms

–Think when you interpret results

53
Q

What can we look at on faecal parasitology?

A

–Nematodes

–Cestodes

–Protozoa (intermittent shedding?)

  • Giardia – do we need multiple samples?
  • Tritrichomonas in cats
54
Q

What facecal virus tests can we do?

A

–Parvo SNAP test?

–Coronavirus?

55
Q

When would abominal radiography be indicated?

A
  • Abdominal pain?
  • Vomiting and diarrhoea?
  • Weight loss?
  • Melaena?
56
Q

When would you think about doing thoracic radiography?

A
  • Metastatic disease?
  • Concurrent oesophageal disease?
57
Q

what large bowel signs would make us want to conduct a colonoscopy?

A

–Tenesmus

–Mucus

–Fresh blood

–Increased urgency, small volumes

58
Q

What type of test rules out disease?

A

Sensitive

59
Q

What type of test rules in disease?

A

Specific

60
Q

What are the benefits of a gross examination and how do we do this?

A

Can tell if it looks abnormal or not. Ex. Lap. Is the main way we do this. Gross abnormalities may not be present as the external surface isn’t that useful. Internal surface via endoscopy may help.

61
Q

When should we biopsy?

A

Always biopsy, multiple sites- SI, LI and LN

62
Q

Where may a biopsy give a limited info?

A

Submucosal mass e.g. bowel tumours – may only give normal muscos as the thing that is wrong is below the mucosa

63
Q

What is this? How could we treat?

A

Granuloma gastritis

Preds mend this

64
Q

What is this and where is it common?

A

Angular incisa carcinoma

Internal divisions

65
Q

What is this?

A

Worm

66
Q

What is this?

A

Gi lymphoma

67
Q

What is this?

A

Multifocal GI lymphoma
Inflammed
Biopsy may give a neutrophil gastritis and a negative result
So may need to re biopsy

68
Q

What is this?

A

Loss of layers
Eosionophilli enteritis

69
Q

How may you need to manage the consequences of intestinal disease?

A

Symptomatic treatment

70
Q

What 5 things (other than fluid) can an animal loose when vomiting and diarrhoeaing?

A

Na+

K+

Cl-

HCO3-

pH

71
Q

What is the effect of SI diarrhoea on acid base?

What are the 2 main goals of treatment?

What treatment often causes complications?

A
  • common cause of metabolic acidosis
    • loss of HC03- in intestinal fluid
    • dehydration ->poor perfusion->increased lactate-> metabolic acidosis
  • main goals:
    • manage the underlying disease
    • restore renal perfusion
  • treatment with HC03- often causes more complications
72
Q

What is the effect of vomiting on acid-base?

What are the main goals of treatment?

A
  • loss of Cl- ->metabolic alkalosis
    • renal compensatory excretion of HC03- is efficient if renal perfusion is adequate
    • may combine with lactic acidosis
  • main goals:
    • manage the underlying disease
    • restore renal perfusion

Small Animal Final Year (317 decks)

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