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VTS(ECC) Study > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

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

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2
Q

Non-abdominal rule out for acute abdomen

A

IVDD

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3
Q

Young adult GSD with pancreatic exocrine insufficiency is predisposed to?

A

Mesenteric volvulus

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4
Q

Increased PCV and increased TS indicative of

A

Hemoconcentration, dehydration

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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

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6
Q

High PCV and normal to low TS indicative of

A

HGE in dogs with acute onset vomiting and bloody diarrhea

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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

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8
Q

Increased BG in a dog with acute abdomen may be suggestive of

A

Diabetes or transient diabetes due to severe pancreatitis

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9
Q

Blood glucose in severely hypovolemic dogs is rarely?

Why?

A

> 200mg/dL

Result of catecholamines on glycogenolysis and gluconeogenesis

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10
Q

Elevated blood glucose in cats with acute abdomen is indicative of

A

May be due to stress or diabetes - non specific

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11
Q

Decreased BG in acute abdomen is indicative of?

A

Usually sepsis
Within 40-60mg/dL range
Potentially hypoadrenocorticisim

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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

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13
Q

Hypochloremic metabolic alkalosis in vomiting animal is indicative of

A

Foreign body

Usually also has hypokalemia and hyponatremia

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14
Q

Metabolic acidosis in an acute abdomen may indicate

A

Severe diarrhea or lactic acidosis due to hypoperfusion

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15
Q

Evidence of free gas in the abdomen is usually located

A

Between stomach or liver and diaphragm on lateral radiograph

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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

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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

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18
Q

On radiographs segmental gaseous or fluid distention of small bowel suggests?

A

Intestinal obstruction

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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

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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)

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21
Q

Radiographic evidence of generalized small bowel distention suggests?

A

Generalized small bowel ileus or distal GI obstruction

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22
Q

Risks associated with positive contrast studies - especially with barium

A

Severe intraperitoneal inflammation and granuloma formation

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23
Q

Reasons for radiographic loss of abdominal detail

A

Lack of abdominal fat, free fluid, pancreatitis, large masses, carcinomatosis

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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

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25
Q

Septic peritonitis glucose and lactate gradients

A

Glucose >20mg/dL of peripheral blood to abdominal fluid

Lactate 2mmol/L or more

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26
Q

Diagnostic quality of free fluid associated with bile peritonitis

A

Abdominal fluid bilirubin higher than peripheral blood

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27
Q

Characteristics of a pure transudate and possible causes (free abdominal fluid)

A

clear
TP <2.5g/dL
Low cell count
Cells are either nondegenerate neutrophils or reactive mesothelial cells
Hypoalbuminemia, portal venous obstruction

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28
Q

Characteristics of a modified transudate and possible causes (free abdominal fluid)

A

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

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29
Q

Characteristics of an exudate and possible causes (free abdominal fluid)

A

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

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30
Q

What is the cause of acute pancreatitis?

A

Usually idiopathic

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31
Q

What is the pathophysiology associated with pancreatitis?

A

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.

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32
Q

What is the canine breed disposition for acute pancreatitis?

A

Yorkshire terriers, mini schnauzers, and other terriers

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33
Q

What is a frequent clinical finding in cats with acute pancreatitis?

A

Icterus

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34
Q

What is not a frequent clinical finding in cats with acute pancreatitis?

A

Vomiting, abdominal pain

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35
Q

What are frequent clinical signs in dogs with acute pancreatitis?

A

Vomiting, abdominal pain, anorexia, depression, sometimes diarrhea.
Potentially febrile, dehydrated, icteric

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36
Q

What is the most reliable serum chemistry finding that correlates with acute pancreatitis?

A

Serum pancreatic lipase immunoreactivity

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37
Q

Which platelet abnormality is frequently noted in acute pancreatitis?

A

Thrombocytopenia

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38
Q

Azotemia related to acute pancreatitis is often?

A

Prerenal

Potential for ARF

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39
Q

Glucose in patients with acute pancreatitis is often?

A

Elevated

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40
Q

Decreased blood glucose in patients with acute pancreatitis can be an indication of?

A

Hepatic dysfunction, SIRS, sepsis

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41
Q

Ionized hypocalcemia is common in which breed with acute pancreatitis? What is the clinical significance of this?

A

Cats.

Associated with worse clinical outcome.

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42
Q

Why is an elevated serum lipase and amylase of limited diagnostic use for acute pancreatitis?

A

Often elevate for extrapancreatic reasons (azotemia, glucocorticoid administration, etc.). Often normal in cats who have confirmed pancreatitis

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43
Q

Which coagulation disorders are common in severe acute pancreatitis in both dogs and cats?

A

Thromboses, DIC

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44
Q

What is true about fluid therapy in acute pancreatitis?

A

Large volumes of initial replacement fluids and ongoing maintenance fluids may be required due to large volumes of loss.

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45
Q

When should calcium be supplemented in acute pancreatitis?

A

Only if tetany is present

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46
Q

What effects can calcium supplementation have?

A

Exacerbation of free radical production

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47
Q

Which patients require analgesic therapy when diagnosed or suspected of acute pancreatitis?

A

All patients. Even those that do not seem clinically painful

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48
Q

What benefits does providing analgesic therapy in acute pancreatitis have?

A

Maintain comfort, reduce stress hormones, improve ventilation, may improve GI motility if ileus due to pain

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49
Q

Which systemic analgesic may provide GI motility effects?

A

Low-dose systemic lidocaine

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50
Q

When should enteral nutrition be initiated in patients with acute pancreatitis?

A

Within 24 hours of hospitalization

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51
Q

What benefits does early enteral nutrition have?

A

Improved gut mucosal structure and function, decreased bacterial translocation - leading to decreased risk of SIRS from fewer inciting causes

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52
Q

Which acute pancreatitis patients are proven to be in a hypercatabolic state?

A

Those with moderately severe and severe acute pancreatitis

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53
Q

Which patients with acute pancreatitis warrant antibiotic treatment?

A

Those with documented infections

OR those who initially improve and then deteriorate OR those that do not respond at all

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54
Q

What are indications for surgery in cases of acute pancreatitis?

A

Extrahepatic biliary obstruction, infected pancreatic necrosis, or patients who deteriorate despite aggressive therapy

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55
Q

What surgical procedure MAY be recommended for acute pancreatitis?

A

Debridement and/or drainage for infected necrosis

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56
Q

Cholecystitis

A

Inflammation of the gallbladder

May be used to ID diseases that mimic gallbladder inflammation

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57
Q

What are clinical findings of cholecystitis

A

Nonspecific, vomiting, inappetance, diarreha, lethargy

Physical exam may reveal icterus, abdominal pain, fever

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58
Q

What laboratory findings are common with cholecycstitis

A

Increased ALT, AST, ALP, GGT

May also have elevated TBili and cholesterol

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59
Q

What is the most common infectious cause of cholecystitis?

A

Bacteria

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60
Q

What is the most common type(s) of bacteria associated with cholecystitis?

A

E. Coli, enterococcus, bacteroides, clostridium

Usually enteric in origin

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61
Q

What are the three types of necrotizing cholecystitis?

A

I - Necrosis without rupture
II - Acute inflammation with rupture
III - Chronic inflammation with adhesions and/or fistulae to adjacent organs

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62
Q

What is true of most dogs with necrotizing cholecystitis?

A

Most have had bacterial infection

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63
Q

When is surgical intervention required for cholecystitis?

A

In case of rupture or impending rupture

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64
Q

What is the general prognosis for gallbladder diseases?

A

Poor to guarded prognosis with or without surgery

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65
Q

Which species is more likely to be infected with parasitic infection causing cholecystitis?

A

Cats

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66
Q

How do cats become infected with platynosomum concinnum or amphimerus pseudofelinus?

A

Liver flukes/ liver worms
Eating an intermediate host or second intermediate host
Snails, lizards, frogs, some fish and bugs

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67
Q

What is the recommended treatment for liver parasites?

A

Praziquantel

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68
Q

How long does it take to form complete extrahepatic bile duct obstruction resulting in dilation of gallbladder and cystic duct?

A

Within 24 hours

Dilation of intrahepatic bile duct within 5-7 days

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69
Q

What is true of cholelithiasis in dogs and cats?

A

Rare. And if found rarely the primary problem, usually incidental finding.

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70
Q

When should cholelithiasis be surgically removed?

A

In case of ultrasonographic findings correlating with obstruction - duct distention or patient clinically symptomatic

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71
Q

Which species suffers from gallbladder mucocele?

A

Dogs

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72
Q

What is the breed predisposition for gallbladder mucocele?

A

Shetland sheepdogs, Cocker spaniels, miniature schnauzers

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73
Q

What is a common concurrent disease of gallbladder mucocele?

A

Hyperadrenocorticisim

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74
Q

What lab findings are common with gallbladder mucocele?

A

Similar to cholecystitis

Elevated liver enzymes, hypercholesterolemia, and/or hyperbilirubinemia

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75
Q

What does a gallbladder mucocele look like on ultrasound?

A

Either like a kiwi fruit or finely striated with static bile sludge

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76
Q

What is a risk of gallbladder mucocele?

A

Rupture

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77
Q

What is the recommended treatment for gallbladder mucocele?

A

Cholecystectomy

Medical management may be attempted

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78
Q

What is the effect of ursodeoxycholic acid?

A

Ursodiol - causes choleresis, immunomodulation, may decrease mucin secretion, may improve gallbladder motility

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79
Q

How much is the liver capable of regenerating?

A

About 75% of functional capacity over several weeks

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80
Q

What are common physiologic features of liver failure?

A

Hypotension, lactic acidosis, electrolyte alterations, hepatic encephalopathy, coagulopathy

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81
Q

At what amount of liver function loss does hepatic encephalopathy become evident?

A

More than 70%

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82
Q

What are some of the important neurotoxic substances active in hepatic encephalopathy?

A

Ammonia, aromatic amino acids, endogenous benzodiazapines, GABA, tryptophan

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83
Q

Where is ammonia produced?

A

In the GI and is converted by the liver to urea and glutamine via urea cycle

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84
Q

What is glutamine?

A

Amino acid - One of the major excitatory neurotransmitters in the brain

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85
Q

What is one implication for seizures in hepatic encephalopathy

A

Over-activation of the glutamine receptors

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86
Q

What happens after chronic stimulation of glutamine receptors in hepatic encephalopathy?

A

Depression and coma symptoms become more common.

Due to inhibitory factors like GABA and endogenous benzodiazepines

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87
Q

Which clinical signs more likely to occur in acute hepatic failure with hepatic encephalopathy?

A

Cerebral edema, increased intracranial pressure, possible herniation of the brain stem

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88
Q

Which types of exogenous substances may exacerbate hepatic encephalopathy?

A

Drugs (i.e. NSAIDs), high protien meals, GI ulceration, constipation, stored blood transfusions

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89
Q

What is a mainstay of treatment for hepatic encephalopathy?

A

Decreasing blood ammonia levels

But may not be correlated in all cases

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90
Q

What is true of hemorrhage in patients with hepatic failure?

A

Usually not spontaneous. Caused by trauma or other medical issue.

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91
Q

What are potential causes of coagulation disorders in hepatic failure?

A

Decreased factor synthesis or increased utilization, increased fibrinolysis, tissue thromboplastin release, decreased platelet function and number, vitamin K deficiency, increased production of anticoagulants

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92
Q

In hepatic failure, when is vitamin K deficiency most likely to occur?

A

When bile duct obstruction present

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93
Q

In hepatic failure, when is portal hypertension most likely to occur?

A

When cirrhosis present

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94
Q

What other systemic issues may be noted in patients with hepatic failure?

A

Increased risk of infection, systemic hypotension, pulmonary abnormalities, acid base disturbances, renal dysfunction, portal hypertension

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95
Q

What are three types of icterus?

A

Prehepatic (hemolysis), hepatic (intrinsic hepatic injury/failure), or posthepatic (functional or mechanical bile duct obstruction)

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96
Q

Why might polyuria and polydipsia be common clinical signs associated with hepatic failure?

A

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

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97
Q

Which sign of hepatic encephalopathy is more common in the cat than the dog?

A

Ptyalism

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98
Q

What correlates with a diagnosis of fulminant hepatic failure?

A

Signs of hepatic encephalopathy, changes in blood chemistry, coagulopathy, and associated history

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99
Q

When may nonregenerative anemia be noted in hepatic failure?

A

Chronic disease, chronic GI bleed, portosystemic shunting

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100
Q

When may regenerative anemia be noted in hepatic failure

A

Gastroduodenal ulceration

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101
Q

ALT and AST are both present in hepatocytes and can leak after disruption of cell membrane. Which is more specific for hepatic dysfunction?

A

ALT - short half life, only in hepatocytes

AST - shorter half life, also present in liver, muscle, and RBCs

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102
Q

Where is ALP located?

A

Bone, liver, and can be steroid induced in dogs

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103
Q

What is an elevation in ALP indicative of?

A

Increased ALP suggests cholestatic disease

In cats has short half life and any elevation is suggestive of liver disease

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104
Q

What is GGT an indication of? How does it compare to ALP?

A

Cholestatic disease

More specific and less sensitive than ALP

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105
Q

How high must liver enzymes be to diagnose hepatic failure?

A

May be normal or only slightly elevated and patient may be in end-stage hepatic failure

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106
Q

What causes hyperbilirubinemia

A

breakdown of hemoglobin, myoglobin, and other cytochromes

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107
Q

What must the bilirubin level be to cause clinical icterus?

A

Minimum of 2.3-3.3mg/dL

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108
Q

What is hypoalbuminemia with normal to elevated globulins, hypocholesterolemia, hypoglycemia, and decreased BUN an indication of?

A

Liver failure - these are liver function parameters

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109
Q

Where is albumin produced?

A

In the liver - decreased production not noted until 66-80% of liver function lost

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110
Q

What does hypoalbuminemia indicate?

A

May indicate PLE, PLN, third-spacing, or liver failure

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111
Q

Why does hepatic failure cause hypoglycemia?

A

Liver helps maintain glucose balance via gluconeogenesis and glycogenolysis
<30% of hepatic function present when hypoglycemia present

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112
Q

In which species is some degree of bilirubinuria norma?

A

Dogs - especially male dogs

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113
Q

Which bile acid test is contraindicated in patients with signs of hepatic encephalopathy?

A

Ammonia tolerance test

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114
Q

Which electrolyte abnormality may cause hemolysis?

A

Hypophosphatemia

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115
Q

Which medications are indicated for seizures associated with hepatic encephalopathy?

A

Levetriacetam or propofol

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116
Q

Why are enemas indicated in treatment of hepatic failure?

A

To clear out GI contents and reduce ammonia levels

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117
Q

Which antimicrobials may decrease gut flora - thereby improving signs of hepatic encephalopathy?

A

Metronidazole, neomycin, ampicillin

Caution with neurotoxicity from metronidazole

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118
Q

When might vitamin K be of particular use for treatment of coagulopathy in hepatic failure?

A

If patient has cholestasis and fat malabsorption

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119
Q

Which fluid choice should be avoided in patients with hepatic failure? Why?

A

LRS - lactate undergoes hepatic metabolism to change to bicarbonate

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120
Q

Which types of proteins may be preferred in patients with hepatic encephalopathy?

A

Milk and vegetable - lower in aromatic aminos, higher in branched chain aminos

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121
Q

In hepatic failure, what are poor prognostic indicators?

A

PT > 100 seconds, patient very young or very old, viral or idiosyncratic drug reaction as inciting cause, markedly increased bilirubin

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122
Q

Hepatitis

A

Inflammatory cell infiltrate within hepatic parenchyma

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123
Q

Cholangiohepatitis

A

Inflammation of liver and bile ducts

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124
Q

True or false? A patient with a short course of clinical signs is more likely to have acute liver disease?

A

False - the liver has a large reserve capacity - may have been deteriorating for a long time

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125
Q

What are clinical signs that are more likely to be from acute rather than chronic liver disaese?

A

Fever, abdominal pain

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126
Q

Which clinical sign more likely to be linked to cholangiohepatitis rather than hepatitis?

A

Ascities

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127
Q

Why is the liver particularly susceptible to anoxia?

A

Due to mixture of venous and arterial blood which supplies the liver

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128
Q

What factor may be an important factor in initiation and perpetuation of hepatitis?

A

Tumor necrosis factor alpha

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129
Q

What is one of the most common hepatobiliary disorders in cats?

A

Feline cholangitis complex - may be neutrophilic or lymphocytic

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130
Q

What other disorders are associated with neutrophilic feline cholangitis complex?

A

IBD and pancreatitis

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131
Q

When trying to obtain diagnostic samples for culture and sensitivity in feline cholangitis complex, what is the preferred specimen?

A

Gallbladder bile

132
Q

What is the suspected cause of lymphocytic feline cholangitis complex?

A

Immune mediated

133
Q

Canine chronic hepatitis

A

Progressive, idiopathic, necroinflammatory disease

134
Q

What is the suspected cause of canine chronic hepatitis?

A

Immune mediated - either primary or secondary

135
Q

Which breeds are more likely to develop canine chronic hepatitis?

A

Cocker spaniel, Bedlington terrier, Dalmatian, Doberman, Springer Spaniel, Labrador retriever, Skye terrier, standard poodle, west highland terrier

136
Q

What is the preferred treatment for canine chronic hepatitis?

A

No well studied protocol but the mainstay of treatment involves immunosuppresive therapy

137
Q

When is copper chelation indicated in canine chronic hepatitis?

A

When evidence of copper storage diseases - may be present, or may have copper storage issue due to liver deterioration

138
Q

Which drugs are used for copper chelation in dogs?

A

D-penicillamine and trientine

139
Q

What is true of most viral causes of hepatitis or cholangiohepatitis?

A

Uncommon in both dogs and cats, usually have poor prognosis

140
Q

Infectious canine hepatitis

A

Canine adenovirus type I - rare.

141
Q

Which animals are most likely to develop canine adenovirus?

A

Young, unvaccinated dogs

142
Q

What may be seen in animals that recover from canine adenovirus type I (infectious canine hepatitis)?

A

Anterior uveitis and corneal edema

143
Q

Feline infectious peritonitis

A

Cause by feline enteric coronavirus and can affect any organ in the body

144
Q

Which liver values increase with hepatic involvement of FIP?

A

ALT, AST, hyperbilirubinemia

145
Q

Which serovars are normally isolated in animals that have hepatic involvement from leptospirosis?

A

L. icterohaemorrhagiae and L. pomona

146
Q

What is leptospirosis and what does it cause?

A

Bacterial infection usually resulting in ARF but may involve pulmonary hemorrhage, uveitis, and acute fever

147
Q

Do cats contract leptospirosis?

A

Not usually, but rarely they may develop some clinical signs

148
Q

What antibiotic protocol is used to treat both leptospiremic stage and carrier state of leptospirosis?

A

Doxycycline

Historically penicillin for leptopiremic state then doxy for carrier state

149
Q

Which bartonella strains have been associated with liver disease in dogs?

A

Bartonella henselae and Bartonella clarridgeiae

150
Q

What is the preferred specimen for diagnosis of bartonella suspected to be causing liver disease?

A

Liver tissue for DNA PCR

151
Q

What should be suspected in critically ill animals developing evidence of hepatic disease while hospitalized?

A

Sepsis

152
Q

Gastroenteritis

A

Broad term to indicate inflammation of stomach and intestinal tract

153
Q

What do parietal cells of the stomach produce?

A

hydrochloric acid

154
Q

What do cheif cells of the stomach produce?

A

pepsinogen

155
Q

What do mucous producing cells of the stomach produce?

A

mucous and bicarbonate

156
Q

What is the suspected cause of histiocytic ulcerative colitis in boxers?

A

Invasive E. coli in the colonic mucosa

157
Q

Which type of intestinal parasite are usually linked with GI blood loss?

A

Hookworms

158
Q

Which intestinal parasites can be indicated in severe GI inflammation, vomiting, and diarrhea?

A

Ascarids (toxo), hookworms, whipworms

159
Q

Most common fungal causes of gastroenteritis

A

Histoplasmosis, pythium

Cause severe PLE

160
Q

What is the minimum PCV required to diagnose HGE?

A

60%

161
Q

What is the cause of HGE?

A

Often idiopathic

162
Q

Why does the TP not increase in HGE?

A

Loss of proteins from GI or redistribution of body water

163
Q

What can a lack of proper perfusion to the GI tract cause?

A

Worsening GI inflammation, bacterial translocation, sepsis, and DIC

164
Q

What is protein losing enteropathy?

A

Broad diagnosis – Any cause of GI disease that causes excessive loss of proteins

165
Q

Most common causes of PLE

A

IBD, lymphangiectasia, diffuse GI fungal disease, and diffuse neoplasia like lymphosarcoma

166
Q

What causes protein loss in PLE?

A

Disruption of normal enterocyte function and deranged permeability through tight junctions

167
Q

What are two large proteins lost in PLE?

A

Antithrombin and albumin

168
Q

In addition to protein loss, what is a major sequella of PLE?

A

Thrombosis formation

169
Q

What extraintestinal disorders may cause gastroenteritis?

A

Hypoadrenocorticisim, liver or kidney disease, acute pancreatitis, peritonitis

170
Q

Which dog breeds are predisposed to congenital megaesophagus?

A

Wire-haired fox terrier, mini schnauzer, GSD, Great Danes, Irish setters, Labrador retrievers, Newfoundlands, Shar Pei

171
Q

Which cat breed is predisposed to congenital megaesophagus?

A

Rare in cats but Siamese may be predisposed

172
Q

What causes congenital megaesophagus in dogs?

A

Organ specific sensory dysfunction from vagal afferent system in the esophagus

173
Q

What is the most likely cause of acquired (or adult onset) megaesophagus?

A

Usually idiopathic

If known cause - most commonly myasthenia gravis

174
Q

What cat breeds are at increased risk of developing acquired megaesophagus?

A

Abyssinians and Somali

175
Q

What are conditions that put an animal at increased risk of developing acquired megaesophagus?

A

peripheral neuropathies, laryngeal paralysis, myasthenia gravis, esophagitis, and chronic or recurrent gastric dilation with or without volvulus at increased risk

176
Q

What dog breeds are at increased risk of developing acquired megaesophagus?

A

GSD, Golden retrievers, Irish setters

177
Q

True or False - Prokinetic drugs are useful in treating congenital megaesophagus

A

False

178
Q

What are medications used for myasthenia gravis?

A

Pyridostigmine, prednisone, azothioprine

179
Q

What is the prognosis for megaesophagus?

A

Poor without a definitive diagnosis - due to recurrent complications

180
Q

In cats, what is a common condition that may both cause and be caused by gastric obstruction or disturbed motility?

A

Hairballs

181
Q

What is a common presenting complaint of delayed gastric emptying or gastric obstruction

A

Chronic, intermittent vomiting occurring more than 8 hours after eating

182
Q

How are functional disorders of gastric emptying diagnosed?

A

After imaging with contrast and endoscopy, diagnosis of exclusion

183
Q

What is the preferred dietary treatment for delayed gastric emptying?

A

Frequent, small, low-fat, high carbohydrate meals

184
Q

What is a pseudo-obstruction

A

Functional obstruction caused by hypomotility and ileus - usually idiopathic

185
Q

What is a potential sequela of ileus?

A

Bacterial translocation - endotoxemia, sepsis

186
Q

What is the most common cause of megacolon in middle-aged cats?

A

Usually idiopathic - generally a dysfunction of colonic smooth muscle

187
Q

What are some metabolic causes of constipation?

A

Dehydration, hypokalemia, hypocalcemia

188
Q

Where is >95% of the body’s serotonin stored?

A

In the GI tract, mostly in endochromaffin cells

189
Q

What is a limiting factor in use of serotonergic drugs?

A

They do not work if enteric nerves are degenerated or non-functional

190
Q

On which organs does cisapride encourage motility

A

colon, esophagus, stomach, and small intestine

191
Q

When should you administer cisapride in relation to feeding?

A

15 minutes before a meal - oral absorption increases with food

192
Q

On which organs does metoclopramide encourage motility

A

coordinates and stimulates esophageal, gastric, pyloric, and duodenal motor activity
Also - Increases lower esophageal sphincter tone, stimulates gastric contractions. Relaxes pylorus and duodenum

193
Q

What are the characteristics of postoperative ileus?

A

Decreased GI myoelectric activity and motility

194
Q

What effects does metoclopramide have on the brain?

A

Crosses blood-brain barrier
Dopamine antagonism at chemoreceptor trigger zone produces an antiemetic effect
dopamine antagonism in striatum causes extrapyramidal signs

195
Q

Extrapyramidal signs

A

Involuntary muscle spasms, motor restlessness, inappropriate aggression

196
Q

What is the treatment for extrapyramidal signs initiated by metoclopramide?

A

Diphenhydramine IV if noted in time

Restores dopamine to ACH balance due to anticholinergic action

197
Q

When should oral metoclopramide be given in relation to food?

A

At least 30 minutes before a meal, often given at bedtime as well

198
Q

Which antibiotics are used as prokinetic agents?

A

Macrolides - erythromycin and clarithromycin

Motilin receptors

199
Q

Which antacids have prokinetic effects?

A

The H2 blockers ranitidine and nizatidine

200
Q

What are some 5-HT3 antagonist drugs?

A

Ondansetron, granisetron

201
Q

5-HT3 antagonist drugs have what effect?

A

Block nausea and vomiting from visceral hypersensitivity

202
Q

How is cisapride metabolized?

A

In the liver by cytochrome P450 enzymes

203
Q

For which species do macrolide antibiotics stimulate colonic smooth muscle?

A

Dogs

204
Q

Where do the macrolide antibiotics encourage motility

A

Initiate motor complex in stomach and antigrade peristalsis in proximal GI

205
Q

Generally, what are causes of GI hemorrhage?

A

Diseases causing ulcers, disease causing coagulopathies, disease associated with vascular anomalies

206
Q

What is the most common cause of GI hemorrage?

A

Ulceration

207
Q

What is the main determining factor for coloration of blood in the stool?

A

Transit time

208
Q

Clinical signs more likely to correlate with upper GI bleed

A

Hematemesis or melena

209
Q

Clinical sign more likely to correlate with lower GI bleed?

A

Hematochezia

210
Q

Red blood cell morphology commonly associated with chronic GI bleeding?

A

Microcytic, hypochromic anemia

211
Q

Red blood cell morphology commonly associated with acute GI bleed?

A

Normocytic, normochromic anemia

212
Q

Chemistry finding common with GI hemorrhage

A

High BUN to creatinine ratio (>20)
-Less common with large intestine hemorrhage
From intestinal absorption of proteins into circulatory system

213
Q

Which endocrinopathy is associated with GI hemorrhage?

A

Hypoadrenocorticism

214
Q

When are antibiotics warranted in GI hemorrhage?

A

In cases of significant hemorrhage and suspect mucosal barrier compromise
OR
If patient showing signs of sepsis

215
Q

What are some distinguishing features of vomiting vs regurgitation?

A

Premonitory signs, active abdominal contractions, presence of bile in vomitus as well as frequency and clinical signs

216
Q

Regurgitation

A

Passive ejection of food, water, or saliva associated with esophageal or less commonly pharyngeal disease

217
Q

Which clinical consequence of regurgitation is most associated with poor prognostic outcome?

A

Aspiration pneumonia

218
Q

Which drug is most likely to cause esophagitis?

A

Doxycycline

219
Q

Odynophagia

A

Pain on swallowing

220
Q

What is true of clinical signs associated with regurgitation?

A

Usually absent. May have evidence of malnutrition due to frequent regurgitation leading to poor intake

221
Q

What is the most useful imaging technique for regurgitation?

A

Thoracic radiographs

222
Q

What is the diagnostic test for myasthenia gravis?

A

Acetylcholine receptor antibody assay

223
Q

What type of muscle is the canine esophagus formed of?

A

Striated

224
Q

What type of muscle do metoclopramide and cisapride exert effect on?

A

Smooth muscle

225
Q

What type of feeding tube is contraindicated in patients with regurgitation

A

Any esophageal feeding tube (NG, NE)

226
Q

Vomiting

A

Forceful ejection of upper GI tract contents and may occur as result of gastric, intestinal, or systemic disease

227
Q

Which physiologic features contribute to vomiting?

A

Vomiting center in medulla
Vagal and sympathetic afferent pathways in GI (inflammation or overdistention)
Vestibular system, cerebrum, and chemoreceptor trigger zone

228
Q

Why is the chemoreceptor trigger zone sensitive to some drugs and toxins?

A

Lack of intact blood-brain-barrier

229
Q

What is the main clinical consequence of vomiting?

A

Dehydration and electrolyte imbalances

230
Q

How is the differential diagnosis list broken down for vomiting?

A

Inside vs Outside GI tract and acute vs chronic

231
Q

What is true of clinical signs relating to extragastrointestinal issues that lead to vomiting?

A

Tend to be major systemic signs - pu/pd, weight loss, etc

Gastrointestinal related vomiting tends to have only GI related signs

232
Q

What is true of CBC and chemistry results relating to potential causes of vomiting?

A

Extragastrointestinal causes of vomiting tend to have notable abnormalities while GI causes of vomiting are more likely to have normal blood work

233
Q

Preferred imaging technique for acute vomiting?

A

Abdominal radiographs - rule out foreign body or obstruction

234
Q

Preferred imaging technique for chronic vomiting?

A

Ultrasound

235
Q

Diarrhea

A

Increased fecal mass caused b increase in fecal water or solid content

236
Q

Osmotic diarrhea

A

From presence of excess luminal osmoles - draws fluid into intestinal lumen
Most causes of diarrhea have osmotic component

237
Q

Secretory diarrhea

A

Net increase in intestinal fluid secretion

238
Q

Diarrhea from altered permeability

A

Intestinal mucosa is damaged at epithelial cells or junctions
Causes leak into intestinal lumen - potential for translocation

239
Q

Diarrhea from altered motility

A

May be from increased or decreased motility - one of least well understood causes

240
Q

Diarrhea - mucous uncommon, hematochezia uncommon, stool volume increased to normal, melena possible, frequency increased to normal, urgency uncommon, tenesmus uncommon

A

Small bowel diarrhea

241
Q

Diarrhea - mucous common, hematochezia possible, stool volume decreased to normal, melena absent, frequency increased, urgency common, tenesmus common

A

Large bowel diarrhea

242
Q

What is true of diarrhea relating to adverse food reactions?

A

Usually self limiting and short term. Rare for true immunologic food reaction

243
Q

How are parvoviruses transmitted? What systems do they affect?

A

Oronasal exposure - spread to bone marrow, lymphoid organs, intestinal crypts

244
Q

What causes irritable bowel disorder?

A

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
Q

Lymphangiectasia

A

Intestinal lymphatic permeability increased - leakage of protein and fat rich chyle into intestinal lumen
Causes chronic diarrhea and weight loss

246
Q

Why can CHF cause diarrhea?

A

Especially right sided CHF - causes intestinal and hepatic venous congestion and ascites - decreased absorptive capability

247
Q

What determines intestinal transit time?

A

Propulsive peristalsis and segmental contraction

248
Q

When is symptomatic treatment recommended for diarrhea?

A

If impact on quality of life, fecal scalding, or predisposition to secondary infection from diarrhea (recumbency, catheter infection, etc)

249
Q

What might periumbilical ecchymosis indicate?

A

AKA Cullen’s sign - hemorrhage in peritoneum or retropertoneum

250
Q

What are contraindications for abdominocentesis?

A

Coagulopathy, organomegaly, distention of abdominal viscus

251
Q

What are the four views for AFAST?

A

Caudal to xiphoid process, midline over urinary bladder, each flank

252
Q

Why would you utilize open needle vs. closed needle abdominocentesis?

A

False negatives are more likely if suction is applied - occlusion with omentum or intestinal viscera

253
Q

What is the technique for four-quadrant abdominocentesis

A

Four open needles placed simultaneously - one in each quadrant around umbilicus

254
Q

What might cause a PCV to be lower than peripheral blood even if intraperitoneal hemorrhage is present?

A

Hemodilution with urine or fluid from another organ viscus

255
Q

What amount and fluid type is used for diagnostic peritoneal lavage?

A

22mL/kg warm isotonic saline

256
Q

What is a clear indication of septic peritonitis and warrants immediate surgical exploratory?

A

Intracellular bacteria from free abdominal fluid or fluid obtained via DPL

257
Q

What is a diagnostic peritoneal lavage sample of >5% indicative of?

A

Significant hemorrhage - cannot compare directly to peripheral due to dilution

258
Q

Before initiating enteral feeding which vital signs must be stable?

A

Temperature and blood pressure - hypotension and hypothermia causes poor gut motility

259
Q

What are benefits of early enteral nutrition?

A

Prevention of villous atrophy, maintenance of intestinal mucosal integrity, preservation of GI immunologic function

260
Q

What are contraindications for enteral feeding

A

Uncontrolled vomiting, GI obstruction, ileus, malabsorption or maldigestion, inability to protect airway

261
Q

When selecting feeding route, what is the general rule?

A

Administer food as far proximal in GI tract as possible

262
Q

What medications may be considered for appetite stimulation?

A

Cyproheptadine, mirtazapine, capromorelin

263
Q

How long should NE or NG tubes be utilized?

A

Short term feeding - 7-14 days

264
Q

How long should E tubes be utilized?

A

Longer term - weeks to months

265
Q

How long must you wait after placement of gastrotomy tube to begin feeding?

A

24 hours to allow return of motility and formation of seal to stoma

266
Q

How long must a gastrotomy tube be in place before it can be taken out?

A

10-14 days at a minimum - longer if patient was malnourished. Allows stomach to adhere to body wall

267
Q

What is true of feeding via jejunal tube?

A

Must be liquid elemental diet - best to use CRI to avoid cramping and vomiting

268
Q

How long must you wait until removal of a surgically placed jejunal feeding tube?

A

At least 5-7 days - waiting for formation of fibrin seal at body wall

269
Q

What are MAJOR possible complications form feeding tubes?

A

Aspiration, premature dislodgement of tube, infection, metabolic abnormalities

270
Q

What is refeeding syndrome?

A

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
Q

What is the most effective solution for clearing clogs from feeding tubes?

A

1/4 tsp pancreatic enzyme and 325mg sodium bicarbonate in 5mL warm water

272
Q

When is parenteral nutrition indicated?

A

When enteral route not feasible (inability to protect airway, continued vomiting, etc) or if gastrointestinal malassimiliation and patient cannot absorb nutrition enterally

273
Q

What is the preferred route of administration for parenteral nutrtition

A

Via central venous catheter - sterile placement, nonthrombogenic catheter material

274
Q

What type of pareneteral nutrition is most often used

A

Partial parenteral nutrition - rarely need total, often patients need parenteral nutrition for <1-2 weeks

275
Q

Can parenteral nutrition be administered via peripheral vein?

A

In some cases with ready made formulas with lower osmolarity

276
Q

What are common complications from administration of parenteral nutrition?

A

Concern for fluid overload - especially in high risk patients, infection, refeeding syndrome, contamination, extravasation

277
Q

What are general rules for calculation of parenteral nutrition

A

Utilize lean body weight and administer no more than RER initially, calculate required protein, then calculate required lipid and carbohydrate

278
Q

How much protein does a dog need for parenteral nutrition?

A

4-6g/100kcal (or 15-25% of calories)

279
Q

How much protein does a cat need for parenteral nutrition?

A

6g or more/100kcal (or 25-35% of calories)

280
Q

How much of parenteral nutrition is required as lipids if used?

A

50-70% of non-protein calories

281
Q

How much of parenteral nutrition is required as carbohydrates?

A

Remainder of non-protein calories after calculating lipids if needed.

282
Q

Which micronutrients might be desirable for parenteral nutrition?

A

B complex, electrolytes, and zinc

283
Q

What is a benefit to utilization of lipids in parenteral nutrition?

A

Reduction of dextrose supplementation - less risk of hyperglycemia, concentrated calories

284
Q

What do you need to use with parenteral nutrition, especially if lipid emulsion used?

A

1.2 micron filter - prevent lipid embolus

285
Q

How do you stop administration of parenteral nutrition?

A

Wean off over several hours when patient is receiving at least 50% of daily calories via enteral feeding

286
Q

What must you do if you abruptly discontinue parenteral nutrition?

A

Administer 5% dextrose solution IV

287
Q

When measuring serial body weights, how can you tell if a patient is malnourished?

A

Loss of >10% of body weight involuntarily

288
Q

What two measures of body composition are important during nutritional assessment?

A

Lean body mass and adipose tissue

289
Q

Which body type of patient is more likely to suffer from malnutrition while hospitalized?

A

Obese patients. Less urgency for nutritional support

290
Q

Cachexia

A

Lean body mass loss associated with disease

291
Q

Sarcopenia

A

Lean body mass loss associated with aging

292
Q

Hyporexia

A

Consumption of <75% of RER

293
Q

If a patient has hypoalbuminemia and inadequate lean body mass, what does it indicate about nutrition?

A

Poor long term nutrition status - likely hyporexic long term

294
Q

Peritonitis

A

Inflammation of peritoneal cavity

295
Q

Primary peritonitis

A

Spontaneous inflammatory condition without underlying abdominal pathology or injury

296
Q

Secondary peritonitis

A

Most common in small animals

Secondary to preexisting septic or aseptic intraabdominal condition

297
Q

What is the most common cause of primary peritonitis?

A

Feline infectious peritonitis

Possible other causes are usually from blood borne bacteria or parasites

298
Q

Which intraabdominal organ leakage is associated with minimal inflammation? Which are associated with severe inflammation?

A

Minimal inflammation - bladder and gallbladder (bile)

Severe inflammation - gastric and pancreatic

299
Q

If a patient had intestinal enterotomy or R&A what is the chance that they will experience dehiscence?

A

6-15%

300
Q

What is the combination of risk factors that make intestinal leakage more likely?

A

Preoperative peritonitis, intestinal foreign body, serum albumin 2.5g/dL or less

301
Q

What is an intraoperative risk factor for development of septic peritonitis after GI surgery?

A

Intraoperative hypotension

302
Q

What are clinical signs associated with peritonitis?

A

Variable, usually reflect underlying disease process

303
Q

Which clinical signs are a negative prognostic indicator in cats with septic peritonitis?

A

Bradycardia and hypothermia

304
Q

When is measurement of glucose and lactate unreliable for assessment of intraabodminal fluid?

A

If postoperative and has closed suction drain. Glucose also unreliable if hemoperitoneum or administering IV dextrose.

305
Q

What are risks associated with open abdominal drainage?

A

Nosocomial infection potentially leading to superinfection, massive fluid and protein loss, evisceration, organ or omentum strangulation

306
Q

What are poor prognostic indicators in patients with peritonitis?

A

Refractory hypotension, cardiovascular collapse, DIC, respiratory disease

307
Q

In GDV which occurs first? Dilatation or volvulus?

A

Either may occur first

308
Q

What physiologic events contribute to cardiovascular compromise during GDV?

A

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
Q

What is the most immediately life-threatening component of GDV?

A

Shock

310
Q

What is true of the prognostic indications of gastric necrosis during GDV?

A

Associated with increased morbidity and mortality

311
Q

Where does gastric necrosis generally start during GDV?

A

At the fundus, progressing to stomach

312
Q

If hemoabdomen present during GDV - what is a likely cause?

A

Short gastric artery rupture

313
Q

What are causes of ventricular arrhythmia from GDV?

A

Myocardial ischemia causing ectopic foci
Release of cardiostimulatory substances - epinephrine
and cardioinhibitory substances - proinflammatory cytokines

314
Q

When do ECG abnormalities frequently start in patients with GDV?

A

12-24 hours postoperatively

315
Q

Where is the pylorus in a patient with GDV on a right lateral radiograph?

A

Cranial and dorsal

316
Q

Where is the pylorus in a patient with GDV on a DV radiograph?

A

Left of midline

317
Q

Why might it be best to avoid VD radiographs in a patient with GDV

A

Worsening cardiovascular compromise due to compression and VD may encourage aspiration if vomiting or retching

318
Q

When is hyperlactatemia a poor prognostic indicator in GDV?

A

If it fails to improve with patient stabilization

319
Q

How many hemostatic parameters must be abnormal to indicate poor prognosis in GDV? Why?

A
  1. Correlates with DIC and possibly gastric necrosis.
320
Q

How much does the stomach rotate in a GDV? What is a normal rotation in GDV?

A

May be 90-360 degrees, usually 180-270 in a clockwise direction

321
Q

When is splenectomy indicated in GDV?

A

Only if thrombosis or damage from volvulus

322
Q

What is the prognosis for survival of GDV?

A

With appropriate and aggressive care 70-74% of patients survive to discharge

323
Q

Which method of pexy is associated with higher morbidity?

A

Tube gastropexy - likely due to premature removal of tube and peristomal cellulitis. Otherwise all methods equal

324
Q

Which perioperative risk factors are associated with mortality prior to suture removal after GDV surgery?

A

Hypotension at any point during hospitalization, combined splenectomy and partial gastrectomy, peritonitis, sepsis, DIC

325
Q

What is the only substance in bile with a digestive function?

A

Bile salts - absorb fats and fat-soluble vitamins (A, D, E, and K)

326
Q

What is glycogenolysis?

A

Glycogen is converted back into glucose by the liver and released into body to be used for energy - triggered by glucagon.

VTS(ECC) Study (30 decks)

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