Smallies 2 Flashcards

(100 cards)

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
What signs does a 12-15% dehydrated patient show?
Definite signs of shock, death is imminent
26
How can you calculate fluid deficit?
BW in kg x percent dehydration (as a decimal) = fluid deficit in ml
27
What are maintenance fluids?
The required volume needed per day to keep the patient in balance, with no chance in total body water
28
What is shock rate bolus of a colloid fluid?
10-20ml/kg for dogs | 5-10ml/kg for cats
29
What is shock rate of a crystalloid solution?
80-90ml/kg for dogs | 40-60ml/kg for cats
30
Compare pancreatic ducts in dogs and cats
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
31
What is pancreatitis?
Inflammation of the exocrine pancreas
32
What are features of acute pancreatitis?
Variable neutrophilic inflammation, oedema and necrosis Severe necrosis High mortality Reversible
33
What are features of chronic pancreatitis?
Inflammation more likely to be mononuclear or mixed Leads to fibrosis and acinar loss Permanent and irreversible
34
Describe the pathophysiology if acute pancreatitis
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
35
What are risk factors for pancreatitis in dogs?
- 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
36
What breed predispositions are related to pancreatitis in dogs?
- acute disease - terrier and cocker spaniel - chronic disease - CKCS, boxers, cocker spaniels, collies - Schnauzers
37
What are risk factors for pancreatitis in cats?
- no breed predispositions - association with IBD +/- inflammatory liver disease - chronic more likely than acute - duodenal reflex
38
List non-specific signs of pancreatitis
Mild intermittent abdominal pain Pain after eating Anorexia Weakness
39
What are common clinical signs of pancreatitis?
Vomiting | Cranial abdominal discomfort (praying posture)
40
What are physical exam findings with pancreatitis?
``` Hyperthermia Cranial abdominal pain (tachycardia/pnoea) Ascites Dehydration Icterus ```
41
What are clinical signs of acute pancreatitis in the cat?
``` Really ill cat Anorexia, lethargy, Collapse Tachycardia/pnoea Hypothermia Potential pulmonary oedema or jaundice ```
42
What are the clinical signs of chronic pancreatitis in the cat?
``` Triaditis Anorexia Vomiting Weight loss Diarrhoea Jaundice Abdominal pain ```
43
What may you see on biochemistry for pancreatitis?
``` Mild hepatobiliary enzyme elevations (ALT and ALP) Hyperbilirubinaemia Azotaemia Hypokalaemia Hypocalcaemia Hyperglycaemia Hypercholesterolaemia Amylase and lipase ```
44
What might you see on haematology for pancreatitis?
Mild leucocytosis or leucopenia Mild anaemia or haemoconcentration Thrombocytopenia
45
Name a specific test for pancreatitis
Pancreatic Lipase Immunoreactivity (PLI, SpecPL)
46
Discuss the pros and cons of using abdominal radiography for diagnosing pancreatitis
Pros - rules out other differentials e.g. fb causing secondary pancreatitis Cons - pancreatic changes are very subtle
47
Discuss the use of ultrasonography when diagnosing pancreatitis
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
Discuss the use of biopsy when diagnosing pancreatitis
Gold standard but barely performed due to patient stability and post-biospy complications
49
Describe the diagnostic approach to pancreatitis
High clinical index of suspicion from signalment, history and physical exam Appropriate changes on haematology and biochemistry Ideally biopsy
50
What is the management for a chronic low grade pancreatitis
``` Short period of self starve Low fat diet Analgesia Metronidazole Cobalamin/B12 ```
51
What is the management for acute pancreatitis?
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
Discuss the differences in the management of mild, severe and critical cases of acute pancreatitis?
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
What is the prognosis for mild acute pancreatitis and chronic pancreatic disease?
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
What is a pancreatic pseudocyst?
A collection of enzyme rich pancreatic fluid from autodigestion during acute necrotising pancreatitis. Can sponataneously resolve (or rupture)
55
What is a pancreatic abscess?
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
What are poor prognostic indicators in acute pancreatic disease?
Rapid deterioration Evidence of SIRS/pulmonary oedema Clinical signs of bleeding/DIC Intractable pain/vomiting
57
List tissue related reasons for abdominal enlargement in dogs
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
List fluid related reasons for abdominal enlargement in dogs
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
List gas related reasons for abdominal enlargement in dogs
In GIT e.g. GDV/gastric dilation Free gas e.g. perforated gastric/duodenal ulcer Trapped in diseased organs e.g. emphysematous cystitis
60
What is digestion?
The orderly process by which proteins, fats and carbohydrates are broken down into absorbale units
61
What are the two phases of digestion?
Luminal and mucosal/membranous
62
Describe luminal digestion
Relies on digestive enzymes from the salivary glands, stomach and exocrine pancreas
63
Desribe mucosal and membranous digestion
Relies on snzymes in the membranes and cytoplasm or the intestinal mucosal cells
64
What happens during absorption in the SI?
The process by which products of digestion and vitamines/minerals/water cross the mucosa to enter the blood or lymph
65
Give a summary of carbohydrate digestion
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
Give an overview of protein digestion
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
Give an overview of lipid digestion
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
What can go wrong with digestion and absorption, and what are the consequences?
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
What are the beneficial effects of maldigestion and malabsorption?
Inhibition of microsomal triglyceride transfer protein - reduces appetite and fatty acid uptake Inhibition of gastrointestinal lipase - reduces fat absorption
70
What are the two patterns of motility in the SI?
Peristalisis and segmentation
71
What is peristalsis?
Coordinated reflex response to stretch the gut wall moving from the oesophagus to the rectum Inflenced by the ANS
72
What is the use of SI segmentation?
Slows down transit to allow the mixing of chyme and enzymes
73
Why is peristalsis slower in the colon than the SI?
Enables time for absorption of approximately 90% of the water from intestinal chyme, sodium and some minerals
74
What are clinical signs of SI disease?
``` Weight loss Watery/bulky faeces Increased volume Borborygmi/flatus Abdominal discomfort Defecate 1-3x day No tenesmus or mucus Melena ```
75
What are clinical signs of LI disease?
``` Rarely weight loss Varied faecal types Normal or decreased volume Defecate >6 day Tenesmus Mucus Fresh blood ```
76
What are the categories of diarrhoea?
Osmotic Secretory Inflammatory Motility disorder
77
What are signs of dehydration on biochemistry?
High urea, creatinine, TP
78
What are signs of protein loss in the gut on biochemistry?
Low albumin and globulin
79
what are signs of funcitonal liver disease on biochemistry?
Low urea, cholesterole, albumin, glucose
80
What are the signs od GI bleeding on biochemistry?
High urea +/- low protein
81
How long do clinical signs last with a Campylobacter infection?
Average is 7 days
82
When is radiography indicated for intestinal disease?
Abdominal pain V+D Weight loss Melaena
83
When is thoracic radiography indicated with intestingal diease?
Metastatic spread | Concurrent oesophageal disease
84
What symptomatic management is useful for intestinal diease?
Fluid therapy Electrolytes Anti-emetics Gut protectants
85
How does SI diarrhoea cause metabolic acidosis?
Loss of HCO3- in intestinal fluid | Dehydration --> poor perfusion --> increased lactate --> metabolic acidosis
86
How does vomiting lead to metabolic alkolosis?
Loss of Cl-
87
List causes of acute diarrhoea
``` Diet - change, intolerance, scavenging Drugs - antimicrobials Infections - viral, bacterial, parasitic Inflammatory - IBD Metabolic - Addisons Anatomic - intussusception Neoplasia - lymphoma ```
88
What animals are more likely to get an infectious cause of diarrhoea?
Young animals Animals in colonies/shelters Immunocompromised
89
What are viral causes of acute infectious diarrhoea?
``` Parvovirus Coronavirus Adenovirus Rotavirus Noravirus ```
90
What are bacterial causes of acute infectious diarrhoea?
``` Salmonella Campylobacter E.coli (ETEC, EHEC, EPEC) Clostridium perfringens C. difficile Shigella Yersinia Mycobacteria ```
91
What are parasitic causes of acute infectious diarrhoea?
``` Helminths Protozoa (Giardia, Tritrichomas) ```
92
How does canine parvovirus cause pathology?
Infects rapidly dividing cells e.g. gut crypts, bone marrow, lymphoid tissue
93
What are clinical signs of parvovirus?
``` Vomiting Haemorrhagic diarrhoea Dehydration Panleucopaenia Depressed Anorexic Pyrexic Can lead to septicaemia/endotoxaemia due to loss of mucosal barrier Ileus ```
94
List differentials for a parvovirus case
``` Haemorrhagic enteritis - including neoplasia and idiopathic HGE Salmonella Intussusception FB Addisons ```
95
How can you make a diagnosis of parvo virus?
Signalment and clinical signs are stongly supportive | Faecal analysis - SNAP test
96
What is seen on haematology and biochemistry as a consequence of a parvo case?
Panleucopaenia (consequence of viral replication) Azotaemia Acid-base disturbances Electrolyte disturbances
97
What does the management of a parvo case involve?
``` Fluid therapy Antibiotics Anti-emetics Antacids Ulcer coating medication Immunomodulators and ancillary therapies Oral fluid/nutrients ```
98
Describe fluid therapy management for a parvo case
LRS Be aggressive Maintain electrolytes via supplementation (requires monitoring BP) May need colloid/plasma/whole blood if severe
99
Describe antibiotic management for a parvo case
Broad spectrum E.g. Amoxiclav, metronidazole Care with age of patient (gram -ve cover is hard in young animals)
100
What do you need a broad spectrum antibiotic for a parvo case?
Due to GI translocation of bacteri