Gastrointestinal Flashcards
(326 cards)
1
Q
General causes of acute abdomen
A
Distention of hollow viscus or organ capsule, ischemia, traction, and inflammation secondary to a variety of causes
2
Q
Non-abdominal rule out for acute abdomen
A
IVDD
3
Q
Young adult GSD with pancreatic exocrine insufficiency is predisposed to?
A
Mesenteric volvulus
4
Q
Increased PCV and increased TS indicative of
A
Hemoconcentration, dehydration
5
Q
Normal or increased PCV and low to normal TS indicative of
A
Protein loss from vasculature - often associated with protein loss from peritonitis
6
Q
High PCV and normal to low TS indicative of
A
HGE in dogs with acute onset vomiting and bloody diarrhea
7
Q
Decreased PCV and TS is indicative of
A
Hemorrhage
In dogs splenic contraction makes PCV less reliable
Dogs: Splenic rupture, severe hemorrhage from GI ulcer
Cats: Non-neoplastic more common than neoplastic
8
Q
Increased BG in a dog with acute abdomen may be suggestive of
A
Diabetes or transient diabetes due to severe pancreatitis
9
Q
Blood glucose in severely hypovolemic dogs is rarely?
Why?
A
> 200mg/dL
Result of catecholamines on glycogenolysis and gluconeogenesis
10
Q
Elevated blood glucose in cats with acute abdomen is indicative of
A
May be due to stress or diabetes - non specific
11
Q
Decreased BG in acute abdomen is indicative of?
A
Usually sepsis
Within 40-60mg/dL range
Potentially hypoadrenocorticisim
12
Q
Dipstick BUN elevation in acute abdomen may be indicative of?
A
Pyelonephritis, ureteral or urethral obstruction
If disproportionately high BUN compared to creatinine - GI bleed
13
Q
Hypochloremic metabolic alkalosis in vomiting animal is indicative of
A
Foreign body
Usually also has hypokalemia and hyponatremia
14
Q
Metabolic acidosis in an acute abdomen may indicate
A
Severe diarrhea or lactic acidosis due to hypoperfusion
15
Q
Evidence of free gas in the abdomen is usually located
A
Between stomach or liver and diaphragm on lateral radiograph
16
Q
Large volumes of free gas in the abdomen may indicate?
A
Pneumocystography of a ruptured urinary bladder, ruptured vagina, recent abdominal surgery, ruptured GDV, pneumoperitoneography, or extension of pneumomediastinum
17
Q
Small volumes of free gas in the abdomen may indicate?
A
Rupture of GI tract or infection with gas-forming organism
Gas in gallbladder wall, liver, or spleen is most often associated with clostridia spp. Infection
18
Q
On radiographs segmental gaseous or fluid distention of small bowel suggests?
A
Intestinal obstruction
19
Q
Normal diameter of small intestine of dog on radiographs?
A
2-3x width of rib or less than width of an intercostal space
Should be no more than 50% larger than any other segment of small bowel
20
Q
Normal diameter of small intestine of cat on radiographs?
A
Should not exceed twice the height of central portion of L4 vertebral body (12mm)
21
Q
Radiographic evidence of generalized small bowel distention suggests?
A
Generalized small bowel ileus or distal GI obstruction
22
Q
Risks associated with positive contrast studies - especially with barium
A
Severe intraperitoneal inflammation and granuloma formation
23
Q
Reasons for radiographic loss of abdominal detail
A
Lack of abdominal fat, free fluid, pancreatitis, large masses, carcinomatosis
24
Q
Diagnostic qualities of free fluid associated with uroabdomen
A
Higher creatinine (2:1) and potassium (1.4:1) in abdominal fluid than peripheral blood
25
Septic peritonitis glucose and lactate gradients
Glucose >20mg/dL of peripheral blood to abdominal fluid
| Lactate 2mmol/L or more
26
Diagnostic quality of free fluid associated with bile peritonitis
Abdominal fluid bilirubin higher than peripheral blood
27
Characteristics of a pure transudate and possible causes (free abdominal fluid)
clear
TP <2.5g/dL
Low cell count
Cells are either nondegenerate neutrophils or reactive mesothelial cells
Hypoalbuminemia, portal venous obstruction
28
Characteristics of a modified transudate and possible causes (free abdominal fluid)
serous to serosanguinous
TP 2.5-5.0g/dL
Moderate total cell count
Depending on cause: Variable numbers of RBCs, nondegenerate neutrophils, mesothelial cells, macrophages, lymphocytes
Often due to passive congestion of liver and viscera and impaired drainage of the lymphatic vessels
Most common causes – right-sided heart failure, dirofilariasis, neoplasia, and liver disease
29
Characteristics of an exudate and possible causes (free abdominal fluid)
often cloudy
TP >3.0g/dL
Cell count >5-7k/uL
Predominately neutrophils usually, numerous other cells may also be present
Most common type of free fluid associated with acute abdomen
May be septic or nonseptic
30
What is the cause of acute pancreatitis?
Usually idiopathic
31
What is the pathophysiology associated with pancreatitis?
Intrapancreatic activation of digestive enzymes leads to autodigestion of pancreas. Premature activation of trypsinogen to trypsin activates other proenzymes and the other local and systemic effects responsible for the clinical picture.
32
What is the canine breed disposition for acute pancreatitis?
Yorkshire terriers, mini schnauzers, and other terriers
33
What is a frequent clinical finding in cats with acute pancreatitis?
Icterus
34
What is not a frequent clinical finding in cats with acute pancreatitis?
Vomiting, abdominal pain
35
What are frequent clinical signs in dogs with acute pancreatitis?
Vomiting, abdominal pain, anorexia, depression, sometimes diarrhea.
Potentially febrile, dehydrated, icteric
36
What is the most reliable serum chemistry finding that correlates with acute pancreatitis?
Serum pancreatic lipase immunoreactivity
37
Which platelet abnormality is frequently noted in acute pancreatitis?
Thrombocytopenia
38
Azotemia related to acute pancreatitis is often?
Prerenal
| Potential for ARF
39
Glucose in patients with acute pancreatitis is often?
Elevated
40
Decreased blood glucose in patients with acute pancreatitis can be an indication of?
Hepatic dysfunction, SIRS, sepsis
41
Ionized hypocalcemia is common in which breed with acute pancreatitis? What is the clinical significance of this?
Cats.
| Associated with worse clinical outcome.
42
Why is an elevated serum lipase and amylase of limited diagnostic use for acute pancreatitis?
Often elevate for extrapancreatic reasons (azotemia, glucocorticoid administration, etc.). Often normal in cats who have confirmed pancreatitis
43
Which coagulation disorders are common in severe acute pancreatitis in both dogs and cats?
Thromboses, DIC
44
What is true about fluid therapy in acute pancreatitis?
Large volumes of initial replacement fluids and ongoing maintenance fluids may be required due to large volumes of loss.
45
When should calcium be supplemented in acute pancreatitis?
Only if tetany is present
46
What effects can calcium supplementation have?
Exacerbation of free radical production
47
Which patients require analgesic therapy when diagnosed or suspected of acute pancreatitis?
All patients. Even those that do not seem clinically painful
48
What benefits does providing analgesic therapy in acute pancreatitis have?
Maintain comfort, reduce stress hormones, improve ventilation, may improve GI motility if ileus due to pain
49
Which systemic analgesic may provide GI motility effects?
Low-dose systemic lidocaine
50
When should enteral nutrition be initiated in patients with acute pancreatitis?
Within 24 hours of hospitalization
51
What benefits does early enteral nutrition have?
Improved gut mucosal structure and function, decreased bacterial translocation - leading to decreased risk of SIRS from fewer inciting causes
52
Which acute pancreatitis patients are proven to be in a hypercatabolic state?
Those with moderately severe and severe acute pancreatitis
53
Which patients with acute pancreatitis warrant antibiotic treatment?
Those with documented infections
| OR those who initially improve and then deteriorate OR those that do not respond at all
54
What are indications for surgery in cases of acute pancreatitis?
Extrahepatic biliary obstruction, infected pancreatic necrosis, or patients who deteriorate despite aggressive therapy
55
What surgical procedure MAY be recommended for acute pancreatitis?
Debridement and/or drainage for infected necrosis
56
Cholecystitis
Inflammation of the gallbladder
| May be used to ID diseases that mimic gallbladder inflammation
57
What are clinical findings of cholecystitis
Nonspecific, vomiting, inappetance, diarreha, lethargy
| Physical exam may reveal icterus, abdominal pain, fever
58
What laboratory findings are common with cholecycstitis
Increased ALT, AST, ALP, GGT
| May also have elevated TBili and cholesterol
59
What is the most common infectious cause of cholecystitis?
Bacteria
60
What is the most common type(s) of bacteria associated with cholecystitis?
E. Coli, enterococcus, bacteroides, clostridium
| Usually enteric in origin
61
What are the three types of necrotizing cholecystitis?
I - Necrosis without rupture
II - Acute inflammation with rupture
III - Chronic inflammation with adhesions and/or fistulae to adjacent organs
62
What is true of most dogs with necrotizing cholecystitis?
Most have had bacterial infection
63
When is surgical intervention required for cholecystitis?
In case of rupture or impending rupture
64
What is the general prognosis for gallbladder diseases?
Poor to guarded prognosis with or without surgery
65
Which species is more likely to be infected with parasitic infection causing cholecystitis?
Cats
66
How do cats become infected with platynosomum concinnum or amphimerus pseudofelinus?
Liver flukes/ liver worms
Eating an intermediate host or second intermediate host
Snails, lizards, frogs, some fish and bugs
67
What is the recommended treatment for liver parasites?
Praziquantel
68
How long does it take to form complete extrahepatic bile duct obstruction resulting in dilation of gallbladder and cystic duct?
Within 24 hours
| Dilation of intrahepatic bile duct within 5-7 days
69
What is true of cholelithiasis in dogs and cats?
Rare. And if found rarely the primary problem, usually incidental finding.
70
When should cholelithiasis be surgically removed?
In case of ultrasonographic findings correlating with obstruction - duct distention or patient clinically symptomatic
71
Which species suffers from gallbladder mucocele?
Dogs
72
What is the breed predisposition for gallbladder mucocele?
Shetland sheepdogs, Cocker spaniels, miniature schnauzers
73
What is a common concurrent disease of gallbladder mucocele?
Hyperadrenocorticisim
74
What lab findings are common with gallbladder mucocele?
Similar to cholecystitis
| Elevated liver enzymes, hypercholesterolemia, and/or hyperbilirubinemia
75
What does a gallbladder mucocele look like on ultrasound?
Either like a kiwi fruit or finely striated with static bile sludge
76
What is a risk of gallbladder mucocele?
Rupture
77
What is the recommended treatment for gallbladder mucocele?
Cholecystectomy
| Medical management may be attempted
78
What is the effect of ursodeoxycholic acid?
Ursodiol - causes choleresis, immunomodulation, may decrease mucin secretion, may improve gallbladder motility
79
How much is the liver capable of regenerating?
About 75% of functional capacity over several weeks
80
What are common physiologic features of liver failure?
Hypotension, lactic acidosis, electrolyte alterations, hepatic encephalopathy, coagulopathy
81
At what amount of liver function loss does hepatic encephalopathy become evident?
More than 70%
82
What are some of the important neurotoxic substances active in hepatic encephalopathy?
Ammonia, aromatic amino acids, endogenous benzodiazapines, GABA, tryptophan
83
Where is ammonia produced?
In the GI and is converted by the liver to urea and glutamine via urea cycle
84
What is glutamine?
Amino acid - One of the major excitatory neurotransmitters in the brain
85
What is one implication for seizures in hepatic encephalopathy
Over-activation of the glutamine receptors
86
What happens after chronic stimulation of glutamine receptors in hepatic encephalopathy?
Depression and coma symptoms become more common.
| Due to inhibitory factors like GABA and endogenous benzodiazepines
87
Which clinical signs more likely to occur in acute hepatic failure with hepatic encephalopathy?
Cerebral edema, increased intracranial pressure, possible herniation of the brain stem
88
Which types of exogenous substances may exacerbate hepatic encephalopathy?
Drugs (i.e. NSAIDs), high protien meals, GI ulceration, constipation, stored blood transfusions
89
What is a mainstay of treatment for hepatic encephalopathy?
Decreasing blood ammonia levels
| But may not be correlated in all cases
90
What is true of hemorrhage in patients with hepatic failure?
Usually not spontaneous. Caused by trauma or other medical issue.
91
What are potential causes of coagulation disorders in hepatic failure?
Decreased factor synthesis or increased utilization, increased fibrinolysis, tissue thromboplastin release, decreased platelet function and number, vitamin K deficiency, increased production of anticoagulants
92
In hepatic failure, when is vitamin K deficiency most likely to occur?
When bile duct obstruction present
93
In hepatic failure, when is portal hypertension most likely to occur?
When cirrhosis present
94
What other systemic issues may be noted in patients with hepatic failure?
Increased risk of infection, systemic hypotension, pulmonary abnormalities, acid base disturbances, renal dysfunction, portal hypertension
95
What are three types of icterus?
Prehepatic (hemolysis), hepatic (intrinsic hepatic injury/failure), or posthepatic (functional or mechanical bile duct obstruction)
96
Why might polyuria and polydipsia be common clinical signs associated with hepatic failure?
Potentially due to the failure of the liver to produce urea leading to defective renal concentrating ability and decreased release or response of renal ducts to ADH
97
Which sign of hepatic encephalopathy is more common in the cat than the dog?
Ptyalism
98
What correlates with a diagnosis of fulminant hepatic failure?
Signs of hepatic encephalopathy, changes in blood chemistry, coagulopathy, and associated history
99
When may nonregenerative anemia be noted in hepatic failure?
Chronic disease, chronic GI bleed, portosystemic shunting
100
When may regenerative anemia be noted in hepatic failure
Gastroduodenal ulceration
101
ALT and AST are both present in hepatocytes and can leak after disruption of cell membrane. Which is more specific for hepatic dysfunction?
ALT - short half life, only in hepatocytes
| AST - shorter half life, also present in liver, muscle, and RBCs
102
Where is ALP located?
Bone, liver, and can be steroid induced in dogs
103
What is an elevation in ALP indicative of?
Increased ALP suggests cholestatic disease
| In cats has short half life and any elevation is suggestive of liver disease
104
What is GGT an indication of? How does it compare to ALP?
Cholestatic disease
| More specific and less sensitive than ALP
105
How high must liver enzymes be to diagnose hepatic failure?
May be normal or only slightly elevated and patient may be in end-stage hepatic failure
106
What causes hyperbilirubinemia
breakdown of hemoglobin, myoglobin, and other cytochromes
107
What must the bilirubin level be to cause clinical icterus?
Minimum of 2.3-3.3mg/dL
108
What is hypoalbuminemia with normal to elevated globulins, hypocholesterolemia, hypoglycemia, and decreased BUN an indication of?
Liver failure - these are liver function parameters
109
Where is albumin produced?
In the liver - decreased production not noted until 66-80% of liver function lost
110
What does hypoalbuminemia indicate?
May indicate PLE, PLN, third-spacing, or liver failure
111
Why does hepatic failure cause hypoglycemia?
Liver helps maintain glucose balance via gluconeogenesis and glycogenolysis
<30% of hepatic function present when hypoglycemia present
112
In which species is some degree of bilirubinuria norma?
Dogs - especially male dogs
113
Which bile acid test is contraindicated in patients with signs of hepatic encephalopathy?
Ammonia tolerance test
114
Which electrolyte abnormality may cause hemolysis?
Hypophosphatemia
115
Which medications are indicated for seizures associated with hepatic encephalopathy?
Levetriacetam or propofol
116
Why are enemas indicated in treatment of hepatic failure?
To clear out GI contents and reduce ammonia levels
117
Which antimicrobials may decrease gut flora - thereby improving signs of hepatic encephalopathy?
Metronidazole, neomycin, ampicillin
| Caution with neurotoxicity from metronidazole
118
When might vitamin K be of particular use for treatment of coagulopathy in hepatic failure?
If patient has cholestasis and fat malabsorption
119
Which fluid choice should be avoided in patients with hepatic failure? Why?
LRS - lactate undergoes hepatic metabolism to change to bicarbonate
120
Which types of proteins may be preferred in patients with hepatic encephalopathy?
Milk and vegetable - lower in aromatic aminos, higher in branched chain aminos
121
In hepatic failure, what are poor prognostic indicators?
PT > 100 seconds, patient very young or very old, viral or idiosyncratic drug reaction as inciting cause, markedly increased bilirubin
122
Hepatitis
Inflammatory cell infiltrate within hepatic parenchyma
123
Cholangiohepatitis
Inflammation of liver and bile ducts
124
True or false? A patient with a short course of clinical signs is more likely to have acute liver disease?
False - the liver has a large reserve capacity - may have been deteriorating for a long time
125
What are clinical signs that are more likely to be from acute rather than chronic liver disaese?
Fever, abdominal pain
126
Which clinical sign more likely to be linked to cholangiohepatitis rather than hepatitis?
Ascities
127
Why is the liver particularly susceptible to anoxia?
Due to mixture of venous and arterial blood which supplies the liver
128
What factor may be an important factor in initiation and perpetuation of hepatitis?
Tumor necrosis factor alpha
129
What is one of the most common hepatobiliary disorders in cats?
Feline cholangitis complex - may be neutrophilic or lymphocytic
130
What other disorders are associated with neutrophilic feline cholangitis complex?
IBD and pancreatitis
131
When trying to obtain diagnostic samples for culture and sensitivity in feline cholangitis complex, what is the preferred specimen?
Gallbladder bile
132
What is the suspected cause of lymphocytic feline cholangitis complex?
Immune mediated
133
Canine chronic hepatitis
Progressive, idiopathic, necroinflammatory disease
134
What is the suspected cause of canine chronic hepatitis?
Immune mediated - either primary or secondary
135
Which breeds are more likely to develop canine chronic hepatitis?
Cocker spaniel, Bedlington terrier, Dalmatian, Doberman, Springer Spaniel, Labrador retriever, Skye terrier, standard poodle, west highland terrier
136
What is the preferred treatment for canine chronic hepatitis?
No well studied protocol but the mainstay of treatment involves immunosuppresive therapy
137
When is copper chelation indicated in canine chronic hepatitis?
When evidence of copper storage diseases - may be present, or may have copper storage issue due to liver deterioration
138
Which drugs are used for copper chelation in dogs?
D-penicillamine and trientine
139
What is true of most viral causes of hepatitis or cholangiohepatitis?
Uncommon in both dogs and cats, usually have poor prognosis
140
Infectious canine hepatitis
Canine adenovirus type I - rare.
141
Which animals are most likely to develop canine adenovirus?
Young, unvaccinated dogs
142
What may be seen in animals that recover from canine adenovirus type I (infectious canine hepatitis)?
Anterior uveitis and corneal edema
143
Feline infectious peritonitis
Cause by feline enteric coronavirus and can affect any organ in the body
144
Which liver values increase with hepatic involvement of FIP?
ALT, AST, hyperbilirubinemia
145
Which serovars are normally isolated in animals that have hepatic involvement from leptospirosis?
L. icterohaemorrhagiae and L. pomona
146
What is leptospirosis and what does it cause?
Bacterial infection usually resulting in ARF but may involve pulmonary hemorrhage, uveitis, and acute fever
147
Do cats contract leptospirosis?
Not usually, but rarely they may develop some clinical signs
148
What antibiotic protocol is used to treat both leptospiremic stage and carrier state of leptospirosis?
Doxycycline
| Historically penicillin for leptopiremic state then doxy for carrier state
149
Which bartonella strains have been associated with liver disease in dogs?
Bartonella henselae and Bartonella clarridgeiae
150
What is the preferred specimen for diagnosis of bartonella suspected to be causing liver disease?
Liver tissue for DNA PCR
151
What should be suspected in critically ill animals developing evidence of hepatic disease while hospitalized?
Sepsis
152
Gastroenteritis
Broad term to indicate inflammation of stomach and intestinal tract
153
What do parietal cells of the stomach produce?
hydrochloric acid
154
What do cheif cells of the stomach produce?
pepsinogen
155
What do mucous producing cells of the stomach produce?
mucous and bicarbonate
156
What is the suspected cause of histiocytic ulcerative colitis in boxers?
Invasive E. coli in the colonic mucosa
157
Which type of intestinal parasite are usually linked with GI blood loss?
Hookworms
158
Which intestinal parasites can be indicated in severe GI inflammation, vomiting, and diarrhea?
Ascarids (toxo), hookworms, whipworms
159
Most common fungal causes of gastroenteritis
Histoplasmosis, pythium
| Cause severe PLE
160
What is the minimum PCV required to diagnose HGE?
60%
161
What is the cause of HGE?
Often idiopathic
162
Why does the TP not increase in HGE?
Loss of proteins from GI or redistribution of body water
163
What can a lack of proper perfusion to the GI tract cause?
Worsening GI inflammation, bacterial translocation, sepsis, and DIC
164
What is protein losing enteropathy?
Broad diagnosis – Any cause of GI disease that causes excessive loss of proteins
165
Most common causes of PLE
IBD, lymphangiectasia, diffuse GI fungal disease, and diffuse neoplasia like lymphosarcoma
166
What causes protein loss in PLE?
Disruption of normal enterocyte function and deranged permeability through tight junctions
167
What are two large proteins lost in PLE?
Antithrombin and albumin
168
In addition to protein loss, what is a major sequella of PLE?
Thrombosis formation
169
What extraintestinal disorders may cause gastroenteritis?
Hypoadrenocorticisim, liver or kidney disease, acute pancreatitis, peritonitis
170
Which dog breeds are predisposed to congenital megaesophagus?
Wire-haired fox terrier, mini schnauzer, GSD, Great Danes, Irish setters, Labrador retrievers, Newfoundlands, Shar Pei
171
Which cat breed is predisposed to congenital megaesophagus?
Rare in cats but Siamese may be predisposed
172
What causes congenital megaesophagus in dogs?
Organ specific sensory dysfunction from vagal afferent system in the esophagus
173
What is the most likely cause of acquired (or adult onset) megaesophagus?
Usually idiopathic
| If known cause - most commonly myasthenia gravis
174
What cat breeds are at increased risk of developing acquired megaesophagus?
Abyssinians and Somali
175
What are conditions that put an animal at increased risk of developing acquired megaesophagus?
peripheral neuropathies, laryngeal paralysis, myasthenia gravis, esophagitis, and chronic or recurrent gastric dilation with or without volvulus at increased risk
176
What dog breeds are at increased risk of developing acquired megaesophagus?
GSD, Golden retrievers, Irish setters
177
True or False - Prokinetic drugs are useful in treating congenital megaesophagus
False
178
What are medications used for myasthenia gravis?
Pyridostigmine, prednisone, azothioprine
179
What is the prognosis for megaesophagus?
Poor without a definitive diagnosis - due to recurrent complications
180
In cats, what is a common condition that may both cause and be caused by gastric obstruction or disturbed motility?
Hairballs
181
What is a common presenting complaint of delayed gastric emptying or gastric obstruction
Chronic, intermittent vomiting occurring more than 8 hours after eating
182
How are functional disorders of gastric emptying diagnosed?
After imaging with contrast and endoscopy, diagnosis of exclusion
183
What is the preferred dietary treatment for delayed gastric emptying?
Frequent, small, low-fat, high carbohydrate meals
184
What is a pseudo-obstruction
Functional obstruction caused by hypomotility and ileus - usually idiopathic
185
What is a potential sequela of ileus?
Bacterial translocation - endotoxemia, sepsis
186
What is the most common cause of megacolon in middle-aged cats?
Usually idiopathic - generally a dysfunction of colonic smooth muscle
187
What are some metabolic causes of constipation?
Dehydration, hypokalemia, hypocalcemia
188
Where is >95% of the body's serotonin stored?
In the GI tract, mostly in endochromaffin cells
189
What is a limiting factor in use of serotonergic drugs?
They do not work if enteric nerves are degenerated or non-functional
190
On which organs does cisapride encourage motility
colon, esophagus, stomach, and small intestine
191
When should you administer cisapride in relation to feeding?
15 minutes before a meal - oral absorption increases with food
192
On which organs does metoclopramide encourage motility
coordinates and stimulates esophageal, gastric, pyloric, and duodenal motor activity
Also - Increases lower esophageal sphincter tone, stimulates gastric contractions. Relaxes pylorus and duodenum
193
What are the characteristics of postoperative ileus?
Decreased GI myoelectric activity and motility
194
What effects does metoclopramide have on the brain?
Crosses blood-brain barrier
Dopamine antagonism at chemoreceptor trigger zone produces an antiemetic effect
dopamine antagonism in striatum causes extrapyramidal signs
195
Extrapyramidal signs
Involuntary muscle spasms, motor restlessness, inappropriate aggression
196
What is the treatment for extrapyramidal signs initiated by metoclopramide?
Diphenhydramine IV if noted in time
| Restores dopamine to ACH balance due to anticholinergic action
197
When should oral metoclopramide be given in relation to food?
At least 30 minutes before a meal, often given at bedtime as well
198
Which antibiotics are used as prokinetic agents?
Macrolides - erythromycin and clarithromycin
| Motilin receptors
199
Which antacids have prokinetic effects?
The H2 blockers ranitidine and nizatidine
200
What are some 5-HT3 antagonist drugs?
Ondansetron, granisetron
201
5-HT3 antagonist drugs have what effect?
Block nausea and vomiting from visceral hypersensitivity
202
How is cisapride metabolized?
In the liver by cytochrome P450 enzymes
203
For which species do macrolide antibiotics stimulate colonic smooth muscle?
Dogs
204
Where do the macrolide antibiotics encourage motility
Initiate motor complex in stomach and antigrade peristalsis in proximal GI
205
Generally, what are causes of GI hemorrhage?
Diseases causing ulcers, disease causing coagulopathies, disease associated with vascular anomalies
206
What is the most common cause of GI hemorrage?
Ulceration
207
What is the main determining factor for coloration of blood in the stool?
Transit time
208
Clinical signs more likely to correlate with upper GI bleed
Hematemesis or melena
209
Clinical sign more likely to correlate with lower GI bleed?
Hematochezia
210
Red blood cell morphology commonly associated with chronic GI bleeding?
Microcytic, hypochromic anemia
211
Red blood cell morphology commonly associated with acute GI bleed?
Normocytic, normochromic anemia
212
Chemistry finding common with GI hemorrhage
High BUN to creatinine ratio (>20)
-Less common with large intestine hemorrhage
From intestinal absorption of proteins into circulatory system
213
Which endocrinopathy is associated with GI hemorrhage?
Hypoadrenocorticism
214
When are antibiotics warranted in GI hemorrhage?
In cases of significant hemorrhage and suspect mucosal barrier compromise
OR
If patient showing signs of sepsis
215
What are some distinguishing features of vomiting vs regurgitation?
Premonitory signs, active abdominal contractions, presence of bile in vomitus as well as frequency and clinical signs
216
Regurgitation
Passive ejection of food, water, or saliva associated with esophageal or less commonly pharyngeal disease
217
Which clinical consequence of regurgitation is most associated with poor prognostic outcome?
Aspiration pneumonia
218
Which drug is most likely to cause esophagitis?
Doxycycline
219
Odynophagia
Pain on swallowing
220
What is true of clinical signs associated with regurgitation?
Usually absent. May have evidence of malnutrition due to frequent regurgitation leading to poor intake
221
What is the most useful imaging technique for regurgitation?
Thoracic radiographs
222
What is the diagnostic test for myasthenia gravis?
Acetylcholine receptor antibody assay
223
What type of muscle is the canine esophagus formed of?
Striated
224
What type of muscle do metoclopramide and cisapride exert effect on?
Smooth muscle
225
What type of feeding tube is contraindicated in patients with regurgitation
Any esophageal feeding tube (NG, NE)
226
Vomiting
Forceful ejection of upper GI tract contents and may occur as result of gastric, intestinal, or systemic disease
227
Which physiologic features contribute to vomiting?
Vomiting center in medulla
Vagal and sympathetic afferent pathways in GI (inflammation or overdistention)
Vestibular system, cerebrum, and chemoreceptor trigger zone
228
Why is the chemoreceptor trigger zone sensitive to some drugs and toxins?
Lack of intact blood-brain-barrier
229
What is the main clinical consequence of vomiting?
Dehydration and electrolyte imbalances
230
How is the differential diagnosis list broken down for vomiting?
Inside vs Outside GI tract and acute vs chronic
231
What is true of clinical signs relating to extragastrointestinal issues that lead to vomiting?
Tend to be major systemic signs - pu/pd, weight loss, etc
| Gastrointestinal related vomiting tends to have only GI related signs
232
What is true of CBC and chemistry results relating to potential causes of vomiting?
Extragastrointestinal causes of vomiting tend to have notable abnormalities while GI causes of vomiting are more likely to have normal blood work
233
Preferred imaging technique for acute vomiting?
Abdominal radiographs - rule out foreign body or obstruction
234
Preferred imaging technique for chronic vomiting?
Ultrasound
235
Diarrhea
Increased fecal mass caused b increase in fecal water or solid content
236
Osmotic diarrhea
From presence of excess luminal osmoles - draws fluid into intestinal lumen
Most causes of diarrhea have osmotic component
237
Secretory diarrhea
Net increase in intestinal fluid secretion
238
Diarrhea from altered permeability
Intestinal mucosa is damaged at epithelial cells or junctions
Causes leak into intestinal lumen - potential for translocation
239
Diarrhea from altered motility
May be from increased or decreased motility - one of least well understood causes
240
Diarrhea - mucous uncommon, hematochezia uncommon, stool volume increased to normal, melena possible, frequency increased to normal, urgency uncommon, tenesmus uncommon
Small bowel diarrhea
241
Diarrhea - mucous common, hematochezia possible, stool volume decreased to normal, melena absent, frequency increased, urgency common, tenesmus common
Large bowel diarrhea
242
What is true of diarrhea relating to adverse food reactions?
Usually self limiting and short term. Rare for true immunologic food reaction
243
How are parvoviruses transmitted? What systems do they affect?
Oronasal exposure - spread to bone marrow, lymphoid organs, intestinal crypts
244
What causes irritable bowel disorder?
Loss of local immune tolerance to normal dietary and bacterial components - upregulation of immune and inflammatory responses
Thickening of intestinal absorptive surface and decreased absorptive capacity
245
Lymphangiectasia
Intestinal lymphatic permeability increased - leakage of protein and fat rich chyle into intestinal lumen
Causes chronic diarrhea and weight loss
246
Why can CHF cause diarrhea?
Especially right sided CHF - causes intestinal and hepatic venous congestion and ascites - decreased absorptive capability
247
What determines intestinal transit time?
Propulsive peristalsis and segmental contraction
248
When is symptomatic treatment recommended for diarrhea?
If impact on quality of life, fecal scalding, or predisposition to secondary infection from diarrhea (recumbency, catheter infection, etc)
249
What might periumbilical ecchymosis indicate?
AKA Cullen's sign - hemorrhage in peritoneum or retropertoneum
250
What are contraindications for abdominocentesis?
Coagulopathy, organomegaly, distention of abdominal viscus
251
What are the four views for AFAST?
Caudal to xiphoid process, midline over urinary bladder, each flank
252
Why would you utilize open needle vs. closed needle abdominocentesis?
False negatives are more likely if suction is applied - occlusion with omentum or intestinal viscera
253
What is the technique for four-quadrant abdominocentesis
Four open needles placed simultaneously - one in each quadrant around umbilicus
254
What might cause a PCV to be lower than peripheral blood even if intraperitoneal hemorrhage is present?
Hemodilution with urine or fluid from another organ viscus
255
What amount and fluid type is used for diagnostic peritoneal lavage?
22mL/kg warm isotonic saline
256
What is a clear indication of septic peritonitis and warrants immediate surgical exploratory?
Intracellular bacteria from free abdominal fluid or fluid obtained via DPL
257
What is a diagnostic peritoneal lavage sample of >5% indicative of?
Significant hemorrhage - cannot compare directly to peripheral due to dilution
258
Before initiating enteral feeding which vital signs must be stable?
Temperature and blood pressure - hypotension and hypothermia causes poor gut motility
259
What are benefits of early enteral nutrition?
Prevention of villous atrophy, maintenance of intestinal mucosal integrity, preservation of GI immunologic function
260
What are contraindications for enteral feeding
Uncontrolled vomiting, GI obstruction, ileus, malabsorption or maldigestion, inability to protect airway
261
When selecting feeding route, what is the general rule?
Administer food as far proximal in GI tract as possible
262
What medications may be considered for appetite stimulation?
Cyproheptadine, mirtazapine, capromorelin
263
How long should NE or NG tubes be utilized?
Short term feeding - 7-14 days
264
How long should E tubes be utilized?
Longer term - weeks to months
265
How long must you wait after placement of gastrotomy tube to begin feeding?
24 hours to allow return of motility and formation of seal to stoma
266
How long must a gastrotomy tube be in place before it can be taken out?
10-14 days at a minimum - longer if patient was malnourished. Allows stomach to adhere to body wall
267
What is true of feeding via jejunal tube?
Must be liquid elemental diet - best to use CRI to avoid cramping and vomiting
268
How long must you wait until removal of a surgically placed jejunal feeding tube?
At least 5-7 days - waiting for formation of fibrin seal at body wall
269
What are MAJOR possible complications form feeding tubes?
Aspiration, premature dislodgement of tube, infection, metabolic abnormalities
270
What is refeeding syndrome?
A range of electrolyte abnormalities that can occur after initiating feeding after long term anorexia
Hypokalemia, hypophosphatemia, hypomagnesemia
Starts within days of beginning feeding
271
What is the most effective solution for clearing clogs from feeding tubes?
1/4 tsp pancreatic enzyme and 325mg sodium bicarbonate in 5mL warm water
272
When is parenteral nutrition indicated?
When enteral route not feasible (inability to protect airway, continued vomiting, etc) or if gastrointestinal malassimiliation and patient cannot absorb nutrition enterally
273
What is the preferred route of administration for parenteral nutrtition
Via central venous catheter - sterile placement, nonthrombogenic catheter material
274
What type of pareneteral nutrition is most often used
Partial parenteral nutrition - rarely need total, often patients need parenteral nutrition for <1-2 weeks
275
Can parenteral nutrition be administered via peripheral vein?
In some cases with ready made formulas with lower osmolarity
276
What are common complications from administration of parenteral nutrition?
Concern for fluid overload - especially in high risk patients, infection, refeeding syndrome, contamination, extravasation
277
What are general rules for calculation of parenteral nutrition
Utilize lean body weight and administer no more than RER initially, calculate required protein, then calculate required lipid and carbohydrate
278
How much protein does a dog need for parenteral nutrition?
4-6g/100kcal (or 15-25% of calories)
279
How much protein does a cat need for parenteral nutrition?
6g or more/100kcal (or 25-35% of calories)
280
How much of parenteral nutrition is required as lipids if used?
50-70% of non-protein calories
281
How much of parenteral nutrition is required as carbohydrates?
Remainder of non-protein calories after calculating lipids if needed.
282
Which micronutrients might be desirable for parenteral nutrition?
B complex, electrolytes, and zinc
283
What is a benefit to utilization of lipids in parenteral nutrition?
Reduction of dextrose supplementation - less risk of hyperglycemia, concentrated calories
284
What do you need to use with parenteral nutrition, especially if lipid emulsion used?
1.2 micron filter - prevent lipid embolus
285
How do you stop administration of parenteral nutrition?
Wean off over several hours when patient is receiving at least 50% of daily calories via enteral feeding
286
What must you do if you abruptly discontinue parenteral nutrition?
Administer 5% dextrose solution IV
287
When measuring serial body weights, how can you tell if a patient is malnourished?
Loss of >10% of body weight involuntarily
288
What two measures of body composition are important during nutritional assessment?
Lean body mass and adipose tissue
289
Which body type of patient is more likely to suffer from malnutrition while hospitalized?
Obese patients. Less urgency for nutritional support
290
Cachexia
Lean body mass loss associated with disease
291
Sarcopenia
Lean body mass loss associated with aging
292
Hyporexia
Consumption of <75% of RER
293
If a patient has hypoalbuminemia and inadequate lean body mass, what does it indicate about nutrition?
Poor long term nutrition status - likely hyporexic long term
294
Peritonitis
Inflammation of peritoneal cavity
295
Primary peritonitis
Spontaneous inflammatory condition without underlying abdominal pathology or injury
296
Secondary peritonitis
Most common in small animals
| Secondary to preexisting septic or aseptic intraabdominal condition
297
What is the most common cause of primary peritonitis?
Feline infectious peritonitis
| Possible other causes are usually from blood borne bacteria or parasites
298
Which intraabdominal organ leakage is associated with minimal inflammation? Which are associated with severe inflammation?
Minimal inflammation - bladder and gallbladder (bile)
| Severe inflammation - gastric and pancreatic
299
If a patient had intestinal enterotomy or R&A what is the chance that they will experience dehiscence?
6-15%
300
What is the combination of risk factors that make intestinal leakage more likely?
Preoperative peritonitis, intestinal foreign body, serum albumin 2.5g/dL or less
301
What is an intraoperative risk factor for development of septic peritonitis after GI surgery?
Intraoperative hypotension
302
What are clinical signs associated with peritonitis?
Variable, usually reflect underlying disease process
303
Which clinical signs are a negative prognostic indicator in cats with septic peritonitis?
Bradycardia and hypothermia
304
When is measurement of glucose and lactate unreliable for assessment of intraabodminal fluid?
If postoperative and has closed suction drain. Glucose also unreliable if hemoperitoneum or administering IV dextrose.
305
What are risks associated with open abdominal drainage?
Nosocomial infection potentially leading to superinfection, massive fluid and protein loss, evisceration, organ or omentum strangulation
306
What are poor prognostic indicators in patients with peritonitis?
Refractory hypotension, cardiovascular collapse, DIC, respiratory disease
307
In GDV which occurs first? Dilatation or volvulus?
Either may occur first
308
What physiologic events contribute to cardiovascular compromise during GDV?
Gastric distention causes compression of intraabdominal veins (caudal vena cava, portal vein, splenic veins) leading to decreased venous return (Decreasing CO and MAP)
Decreased venous return and increased venous pressure causes splanchnic pooling and portal hypertension (interstitial edema, loss of IV volume)
309
What is the most immediately life-threatening component of GDV?
Shock
310
What is true of the prognostic indications of gastric necrosis during GDV?
Associated with increased morbidity and mortality
311
Where does gastric necrosis generally start during GDV?
At the fundus, progressing to stomach
312
If hemoabdomen present during GDV - what is a likely cause?
Short gastric artery rupture
313
What are causes of ventricular arrhythmia from GDV?
Myocardial ischemia causing ectopic foci
Release of cardiostimulatory substances - epinephrine
and cardioinhibitory substances - proinflammatory cytokines
314
When do ECG abnormalities frequently start in patients with GDV?
12-24 hours postoperatively
315
Where is the pylorus in a patient with GDV on a right lateral radiograph?
Cranial and dorsal
316
Where is the pylorus in a patient with GDV on a DV radiograph?
Left of midline
317
Why might it be best to avoid VD radiographs in a patient with GDV
Worsening cardiovascular compromise due to compression and VD may encourage aspiration if vomiting or retching
318
When is hyperlactatemia a poor prognostic indicator in GDV?
If it fails to improve with patient stabilization
319
How many hemostatic parameters must be abnormal to indicate poor prognosis in GDV? Why?
3. Correlates with DIC and possibly gastric necrosis.
320
How much does the stomach rotate in a GDV? What is a normal rotation in GDV?
May be 90-360 degrees, usually 180-270 in a clockwise direction
321
When is splenectomy indicated in GDV?
Only if thrombosis or damage from volvulus
322
What is the prognosis for survival of GDV?
With appropriate and aggressive care 70-74% of patients survive to discharge
323
Which method of pexy is associated with higher morbidity?
Tube gastropexy - likely due to premature removal of tube and peristomal cellulitis. Otherwise all methods equal
324
Which perioperative risk factors are associated with mortality prior to suture removal after GDV surgery?
Hypotension at any point during hospitalization, combined splenectomy and partial gastrectomy, peritonitis, sepsis, DIC
325
What is the only substance in bile with a digestive function?
Bile salts - absorb fats and fat-soluble vitamins (A, D, E, and K)
326
What is glycogenolysis?
Glycogen is converted back into glucose by the liver and released into body to be used for energy - triggered by glucagon.
