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GI2 > Smallies 2 > Flashcards

Smallies 2 Flashcards

1
Q

What gastric/oesophageal diseases require surgical management?

A 
Foreign bodies (that can't be removed endoscopically)
GDV
Hiatal hernia
Vascular ring anomaly
Pyloric outflow obstruction
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2
Q

List general support of a GI patient

A 
Oral fluids - small volumes frequently
SC fluids - for mild dehydration
Starve 24h/small volume liquid diets
Bland, highly digestable food
Anti-emetics +/- gastroprotectants
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3
Q

What are the benefits of enteral nutrition?

A

Supports mesenteric perfusion (include pancreas)
Provides trophic factors to repair and maintain intestinal mucosa
Helps normalise intestinal motility

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4
Q

How long does a cat need to be anorexic for to get metabolic consequences?

A

<4 days

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5
Q

What is cachexia?

A

Metabolic derangement - not ‘just’ severe weight loss
Catabolic loss of muscle
Have reduced energy intake with increased requirements
Pro-inflammatory state

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6
Q

How do you calculate resting energy requirement?

A

RER in kcal = 10 x BW in kg^(0.75)

or RER = (30 x BW in kg) + 70

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7
Q

What are risks of tempt feeding by hand?

A

Food aversion
Aspiration
Further weight loss
False sense of security

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8
Q

Name an appetite stimulant?

A

Mirtazapine

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9
Q

What types of feeding tubes are there?

A

Naso-oesophageal
Oesophagostomy
Gastrostomy

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10
Q

Which of the 3 feeding tubes require anaesthesia to place?

A

Oesophagostomy and Gastrostomy

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11
Q

What specialised equipment is required when placing the 3 types of feeding tubes?

A

None for naso-oesophageal and oesophagostomy

Flexible endoscopy for gastrostomy

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12
Q

How long do the 3 types of feeding tubes last?

A

Naso-oesophgeal - days
Oesophagostomy - days to weeks
Gastroscopy - weeks to months

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13
Q

What are possible complications of the 3 types of feeding tubes?

A

Naso-oesophageal - nasal irritation
Oesophagostomy - local cellulitis
Gastrostomy - peritonitis possible

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14
Q

Is home feeding possible with any of the 3 feeding tubes?

A

Yes - naso-oesophageal

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15
Q

Can animals still eat with an oesophageal tube in place?

A

Yes

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16
Q

What are the advantages and disadvantages of postural feeding?

A

Very important for oesophageal motility problems (using gravity)
But there is a risk of aspiration pneumonia (can lead to guarded prognosis)

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17
Q

Defin adverse food reactions

A

Any clinically abnormal response attributed to the ingestion of a food or food additive (can be an allergy or an intolerance)

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18
Q

Define food allergy reactions

A

An immunologically mediated adverse reaction to food unrelated to any physiologic response to a food or food additive

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19
Q

Define food intolerance reactions

A

An abnormal physiologic response to a food that is not believed to be immunologic in nature and may include food posioning, food idiosyncrasy, pharmacologic reaction or metabolic reaction

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20
Q

What do we usually select a therapeutic diet based on?

A

Previous diet history
Careful application of trial and error
Trial diets
Exclusion diets

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21
Q

How long shold an exclusion diet be used for?

A

Minimum of 2-8 weeks (if no improvement after 4 weeks, may need to reconsider)

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22
Q

What signs does a 5-6% dehydrated patient show?

A

Subtle loss of skin elasticity

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23
Q

What signs does a 6-8% dehydrated patient show?

A

Definite delay in return of skin to normal position (skin turgor), sligh increase in CRT, eyes may be slightly sunken into orbits

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24
Q

What signs does a 10-12% dehydrated patient show?

A

Extremely dry mm, complete loss of skin turgor, eyes sunken into orbits, dull eyes, possible signs of shock (tachycardia, cool extremities, rapid/weak pulses), posisble alterations of consciousness

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25
Q

What signs does a 12-15% dehydrated patient show?

A

Definite signs of shock, death is imminent

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26
Q

How can you calculate fluid deficit?

A

BW in kg x percent dehydration (as a decimal) = fluid deficit in ml

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27
Q

What are maintenance fluids?

A

The required volume needed per day to keep the patient in balance, with no chance in total body water

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28
Q

What is shock rate bolus of a colloid fluid?

A

10-20ml/kg for dogs

5-10ml/kg for cats

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29
Q

What is shock rate of a crystalloid solution?

A

80-90ml/kg for dogs

40-60ml/kg for cats

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30
Q

Compare pancreatic ducts in dogs and cats

A

Dogs:
- accessory duct is the largest
- pancreatic duct is more cranial and sits close to bile duct
- pancreatic ducts don’t join the bile duct before emptying in to the duodenum
Cats:
- usually only one pancreatic duct
- joins bile duct before entering the duodenum
- 20% of cats have a small accessory duct

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31
Q

What is pancreatitis?

A

Inflammation of the exocrine pancreas

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32
Q

What are features of acute pancreatitis?

A

Variable neutrophilic inflammation, oedema and necrosis
Severe necrosis
High mortality
Reversible

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33
Q

What are features of chronic pancreatitis?

A

Inflammation more likely to be mononuclear or mixed
Leads to fibrosis and acinar loss
Permanent and irreversible

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34
Q

Describe the pathophysiology if acute pancreatitis

A
  1. inappropriate early activation of trypsin (acinar cells)
  2. activation of zymogens
  3. autodigestion and severe inflammation
  4. pancreatic inflammation and fat necrosis
  5. gut wall involvement leading to bacterial translocation
  6. pro-inflammatory cytokines
  7. neutrophil and monocyte activation
  8. damage to endothelium
  9. tissue oedema and hypoxia (SIRS –> MODS)
  10. lung injury, acute injury, liver damage
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35
Q

What are risk factors for pancreatitis in dogs?

A
  • Breed predispositions
  • Obesity
  • Sex predisposition (increased incidence with males or FN)
  • Previous surgery (previous abdo surgery leading to a drop in BP –> poor perfusion)
  • Drug treatment
  • Endocrine dz - DM, hyperadrenocorticism
  • Ischaemia - poor perfusion
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36
Q

What breed predispositions are related to pancreatitis in dogs?

A
  • acute disease - terrier and cocker spaniel
  • chronic disease - CKCS, boxers, cocker spaniels, collies
  • Schnauzers
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37
Q

What are risk factors for pancreatitis in cats?

A
  • no breed predispositions
  • association with IBD +/- inflammatory liver disease
  • chronic more likely than acute
  • duodenal reflex
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38
Q

List non-specific signs of pancreatitis

A

Mild intermittent abdominal pain
Pain after eating
Anorexia
Weakness

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39
Q

What are common clinical signs of pancreatitis?

A

Vomiting

Cranial abdominal discomfort (praying posture)

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40
Q

What are physical exam findings with pancreatitis?

A 
Hyperthermia
Cranial abdominal pain (tachycardia/pnoea)
Ascites
Dehydration
Icterus
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41
Q

What are clinical signs of acute pancreatitis in the cat?

A 
Really ill cat
Anorexia, lethargy, 
Collapse
Tachycardia/pnoea
Hypothermia
Potential pulmonary oedema or jaundice
42
Q

What are the clinical signs of chronic pancreatitis in the cat?

A 
Triaditis
Anorexia
Vomiting
Weight loss
Diarrhoea
Jaundice
Abdominal pain
43
Q

What may you see on biochemistry for pancreatitis?

A 
Mild hepatobiliary enzyme elevations (ALT and ALP)
Hyperbilirubinaemia
Azotaemia
Hypokalaemia
Hypocalcaemia
Hyperglycaemia
Hypercholesterolaemia
Amylase and lipase
44
Q

What might you see on haematology for pancreatitis?

A

Mild leucocytosis or leucopenia
Mild anaemia or haemoconcentration
Thrombocytopenia

45
Q

Name a specific test for pancreatitis

A

Pancreatic Lipase Immunoreactivity (PLI, SpecPL)

46
Q

Discuss the pros and cons of using abdominal radiography for diagnosing pancreatitis

A

Pros - rules out other differentials e.g. fb causing secondary pancreatitis
Cons - pancreatic changes are very subtle

47
Q

Discuss the use of ultrasonography when diagnosing pancreatitis

A

Reasonable specificity
Sensitivity depends on technique, machine quality etc
Findings depend on degree of oedema, pancreatic swelling, peripancreatic fat necrosis
Useful for assessing concurrent disease
Less useful for chronic pancreatitic
In acute cases the animal may be to painful to put the probe on

48
Q

Discuss the use of biopsy when diagnosing pancreatitis

A

Gold standard but barely performed due to patient stability and post-biospy complications

49
Q

Describe the diagnostic approach to pancreatitis

A

High clinical index of suspicion from signalment, history and physical exam
Appropriate changes on haematology and biochemistry
Ideally biopsy

50
Q

What is the management for a chronic low grade pancreatitis

A 
Short period of self starve
Low fat diet
Analgesia
Metronidazole
Cobalamin/B12
51
Q

What is the management for acute pancreatitis?

A

Treat any underlying causes/stop any drugs if idiopathic
Manage concurrent disease especially in cats e.g. hepatic lipidosis
Analgesia
Fluids
Ealry enteral nutrition

52
Q

Discuss the differences in the management of mild, severe and critical cases of acute pancreatitis?

A

Mild - can manage at home, starve for 24-48hrs, give water per os and anti-emetics
Severe - hospitalise for fluids (+/- K if hypokalaemic), analgesia (opioids - AVOID NSAIDS)
Critical - fluid therapy is a challange (often hypovolaemia with SIRS but at risk of pulmonary oedema due to endothelial damage = poor prognosis), antibiotics (suspect bacterial translocation)

53
Q

What is the prognosis for mild acute pancreatitis and chronic pancreatic disease?

A

Mild acute - self limiting and can have a good prognosis

Chronic - risk of long term complication e.g. EPI, DM or protein/calorie malnutrition

54
Q

What is a pancreatic pseudocyst?

A

A collection of enzyme rich pancreatic fluid from autodigestion during acute necrotising pancreatitis. Can sponataneously resolve (or rupture)

55
Q

What is a pancreatic abscess?

A

Collection of purulent and nectrotic pancreatic tissue. In severe acute disease it can lead to parenchymal necrosis. Surgery is the treatment of choice but mortality rate is high

56
Q

What are poor prognostic indicators in acute pancreatic disease?

A

Rapid deterioration
Evidence of SIRS/pulmonary oedema
Clinical signs of bleeding/DIC
Intractable pain/vomiting

57
Q

List tissue related reasons for abdominal enlargement in dogs

A

Organ enlargement e.g. liver, spleen, kidney, prostate, uterus
Pregnancy
Fat e.g. obesity, hyperadrenocorticism
Neoplasia e.g. focal organ massess or infiltrating neoplasia
Granulotmatous disease e.g. fungal disease or FIP

58
Q

List fluid related reasons for abdominal enlargement in dogs

A

Free fluid in the abdoment
Fluid trapped in organs e.g. hydronephrosis, pyo/mucometra
fluid filled cysts e.g. perinephric cyst, polycystic kidney/liver

59
Q

List gas related reasons for abdominal enlargement in dogs

A

In GIT e.g. GDV/gastric dilation
Free gas e.g. perforated gastric/duodenal ulcer
Trapped in diseased organs e.g. emphysematous cystitis

60
Q

What is digestion?

A

The orderly process by which proteins, fats and carbohydrates are broken down into absorbale units

61
Q

What are the two phases of digestion?

A

Luminal and mucosal/membranous

62
Q

Describe luminal digestion

A

Relies on digestive enzymes from the salivary glands, stomach and exocrine pancreas

63
Q

Desribe mucosal and membranous digestion

A

Relies on snzymes in the membranes and cytoplasm or the intestinal mucosal cells

64
Q

What happens during absorption in the SI?

A

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

65
Q

Give a summary of carbohydrate digestion

A

Salivary alpha amylase initiates starch digestion
Starch fragments formed: maltose, some glucose, dextrins
Alpha amylase breakdown of starch completed in small intestine by pancreatic amylase
Dissacharides: broken down to monosaccharides by maltase, sucrase and lactase - ‘brush border’ enzymes
Glucose and galactose transported across intestinal mucosa - ‘actively’
Fructose transport is facilitated

66
Q

Give an overview of protein digestion

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

67
Q

Give an overview of lipid digestion

A

Emulsification is crucial and depends on bile
Pancreatic lipase is activated in the intestine
Lipid transport:
- Micelles transport lipids across enterocyte cell membranes
- Chylomicrons (large lipoprotein complexes) are used for transport in lymphatic circulation
- Short chain TGs absorbed directly

68
Q

What can go wrong with digestion and absorption, and what are the consequences?

A

Exocrine pancreatic insufficiency (EPI)
- Inadequate secretion of pancreatic enzymes
- Maldigestion of fat
- Steatorrhoea - presence of excess fat in faeces
- Extreme weight loss
Biliary disease (gall stones, cholestatic liver disease, extrahepatic biliary obstruction)
- Failure of emulsification
- Lipase works but unable to solubilise lipids into micelles
- Maldigestion
Intestinal mucosal abnormalities (inflammation, viral/bacterial infection, neoplastic infiltration)
- Malabsorption

69
Q

What are the beneficial effects of maldigestion and malabsorption?

A

Inhibition of microsomal triglyceride transfer protein - reduces appetite and fatty acid uptake
Inhibition of gastrointestinal lipase - reduces fat absorption

70
Q

What are the two patterns of motility in the SI?

A

Peristalisis and segmentation

71
Q

What is peristalsis?

A

Coordinated reflex response to stretch the gut wall moving from the oesophagus to the rectum
Inflenced by the ANS

72
Q

What is the use of SI segmentation?

A

Slows down transit to allow the mixing of chyme and enzymes

73
Q

Why is peristalsis slower in the colon than the SI?

A

Enables time for absorption of approximately 90% of the water from intestinal chyme, sodium and some minerals

74
Q

What are clinical signs of SI disease?

A 
Weight loss
Watery/bulky faeces
Increased volume
Borborygmi/flatus
Abdominal discomfort
Defecate 1-3x day
No tenesmus or mucus
Melena
75
Q

What are clinical signs of LI disease?

A 
Rarely weight loss
Varied faecal types
Normal or decreased volume
Defecate >6 day
Tenesmus
Mucus 
Fresh blood
76
Q

What are the categories of diarrhoea?

A

Osmotic
Secretory
Inflammatory
Motility disorder

77
Q

What are signs of dehydration on biochemistry?

A

High urea, creatinine, TP

78
Q

What are signs of protein loss in the gut on biochemistry?

A

Low albumin and globulin

79
Q

what are signs of funcitonal liver disease on biochemistry?

A

Low urea, cholesterole, albumin, glucose

80
Q

What are the signs od GI bleeding on biochemistry?

A

High urea +/- low protein

81
Q

How long do clinical signs last with a Campylobacter infection?

A

Average is 7 days

82
Q

When is radiography indicated for intestinal disease?

A

Abdominal pain
V+D
Weight loss
Melaena

83
Q

When is thoracic radiography indicated with intestingal diease?

A

Metastatic spread

Concurrent oesophageal disease

84
Q

What symptomatic management is useful for intestinal diease?

A

Fluid therapy
Electrolytes
Anti-emetics
Gut protectants

85
Q

How does SI diarrhoea cause metabolic acidosis?

A

Loss of HCO3- in intestinal fluid

Dehydration –> poor perfusion –> increased lactate –> metabolic acidosis

86
Q

How does vomiting lead to metabolic alkolosis?

A

Loss of Cl-

87
Q

List causes of acute diarrhoea

A 
Diet - change, intolerance, scavenging
Drugs - antimicrobials
Infections - viral, bacterial, parasitic
Inflammatory - IBD
Metabolic - Addisons
Anatomic - intussusception
Neoplasia - lymphoma
88
Q

What animals are more likely to get an infectious cause of diarrhoea?

A

Young animals
Animals in colonies/shelters
Immunocompromised

89
Q

What are viral causes of acute infectious diarrhoea?

A 
Parvovirus
Coronavirus
Adenovirus
Rotavirus
Noravirus
90
Q

What are bacterial causes of acute infectious diarrhoea?

A 
Salmonella
Campylobacter
E.coli (ETEC, EHEC, EPEC)
Clostridium perfringens
C. difficile
Shigella
Yersinia
Mycobacteria
91
Q

What are parasitic causes of acute infectious diarrhoea?

A 
Helminths
Protozoa (Giardia, Tritrichomas)
92
Q

How does canine parvovirus cause pathology?

A

Infects rapidly dividing cells e.g. gut crypts, bone marrow, lymphoid tissue

93
Q

What are clinical signs of parvovirus?

A 
Vomiting
Haemorrhagic diarrhoea
Dehydration
Panleucopaenia
Depressed
Anorexic
Pyrexic
Can lead to septicaemia/endotoxaemia due to loss of mucosal barrier
Ileus
94
Q

List differentials for a parvovirus case

A 
Haemorrhagic enteritis - including neoplasia and idiopathic HGE
Salmonella
Intussusception
FB
Addisons
95
Q

How can you make a diagnosis of parvo virus?

A

Signalment and clinical signs are stongly supportive

Faecal analysis - SNAP test

96
Q

What is seen on haematology and biochemistry as a consequence of a parvo case?

A

Panleucopaenia (consequence of viral replication)
Azotaemia
Acid-base disturbances
Electrolyte disturbances

97
Q

What does the management of a parvo case involve?

A 
Fluid therapy
Antibiotics
Anti-emetics
Antacids
Ulcer coating medication
Immunomodulators and ancillary therapies
Oral fluid/nutrients
98
Q

Describe fluid therapy management for a parvo case

A

LRS
Be aggressive
Maintain electrolytes via supplementation (requires monitoring BP)
May need colloid/plasma/whole blood if severe

99
Q

Describe antibiotic management for a parvo case

A

Broad spectrum
E.g. Amoxiclav, metronidazole
Care with age of patient (gram -ve cover is hard in young animals)

100
Q

What do you need a broad spectrum antibiotic for a parvo case?

A

Due to GI translocation of bacteri

GI2 (27 decks)

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