Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

VET 433a - Small Animal Stream 1 > GI pt. 2 > Flashcards

GI pt. 2 Flashcards

1
Q

Hyperbilirubinemia

A
  • elevated serum bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Jaundice/ Icterus

A
  • yellowing of plasma/ tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Bilirubinuria

A
  • bilirubin in urine (can be physiological in dogs, always abn in cats)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cholestasis

A
  • decreased bile flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Icterus (Physical Exam)

A
  • icterus most nosted in sclera, 3rd eyelid, pinnae, mucous membranes
  • icterus detectable in tissues if serum bilirubin > 2mg/dl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

3 Mechanisms of Icterus

A
  1. Pre-hepatic (hemolytic)
  2. Hepatic
  3. Post-Hepatic (obstructive)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Top Differentials for Pre-hepatic icterus

A
  • IMHA (1 or 2)
  • Heinz body anemia
  • Infectious
  • microangiopathic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Top Differentials for Hepatic Icterus (cats vs dogs)

A 
Cats:
- hepatic lipidosis
- cholangitis
- FIP
- Lymphoma
Dogs (cholestasis):
- Cholangiohepatitis
- chronic hepatitis
- Cu-associated 
- cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Top Differentials for Post-Hepatic Icterus

A
  • obstruction (EHBDO)

- Rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diagnostics for Icterus

A
  • CBC
  • Chem
  • -> Pre - n cholesterol
  • -> hepatic - low cholesterol
  • -> Post - high cholesterol
  • UA (bilirubinuria cats vs dogs)
  • Ultrasound (hepatic vs post-hepatic)
  • Other (coag, FNA, biopsy, CT scan)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Bile composition

A
  • water, bile acids and salts, bilirubin, cholesterol, FA, electrolytes (bile released by CK)
  • Bile acids - steroid acids made by liver
  • Bile salts - salts of bile acids (Na/K)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bile Functions

A
  • fat emulsification and digestion
  • absorption of fat-soluble vitamins
  • bactericidal
  • excretion of waste products (bilirubin and cholesterol)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

2 surgical techniques for liver biopsy

A
  1. suture fracture technique

2. skin punch technique

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Principle diagnostic feature of EHBDO

A
  • hyperbilirubinemia
  • high ALP, ALT< GGT
  • hypoalbuminemia
  • fecal exam - acholic feces, trematode eggs (Cats)
  • bilirubin in the urine (maybe cysts)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Top 2 causes of EHBDO in feline

A
  • Inflammatory (70%)

- Neoplastic (30%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Indications for cholecystectomy in dogs

A
  • biliary mucocele
  • cholelithiasis
  • GB neoplasia or trauma
  • +/- functional EHBO but can catheterize
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Dogs vs Cats Duodenal papilla differences

A

Dogs:
- major duodenal pappila –> exit for CBD + pancreatic duct separately
- minor duodenal pappila –> exit for accessory pancreatic duct
Cats:
- major duodenal pappila –> exit for conjoined CBD + PD
- minor duodenal pappila –> only 20% present

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Understand bilirubin metabolism

A
  1. Spleen - breakdown heme to make biliverdin which is changed to unconjugated bilirubin
  2. unconjugated bilirubin is transported via blood + albumin to liver
  3. Liver - unconjungated –> conjugated bilirubin which is then secreted into bile in gallbladder
  4. Intestines - conj. –> urobilinogen which then gets excreted as stercobilin or reabsorbed and transported to liver or kidney
  5. liver pt2 - recycled
  6. kidney - excreted as urobilin in the urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

T/F: Icterus presents when bilirubin > 2mg/dL

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Icterus:
Pre-hepatic = hemolysis (CBC)
Hepatic = intrahepatic cholestasis (Chem, n biliary u/s)
Post-hepatic = EHBDO or rupture (Chem, abn biliary u/s)

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Blood Supply to Liver and Biliary Tract

A

Liver:
Hepatic Artery – (20% of blood and 50% of O2)
Portal Vein – (80% of blood and 50% of O2)

Biliary:
Cystic artery is a branch of the hepatic artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

T/F: the gallbladder lies between the quadrate and the right medial lobes of the liver.

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Gall Bladder + Ducts Anatomy

A

Gall Bladder
Cystic Duct - gall bladder to first hepatic duct
Common bile duct - first hepatic duct to papilla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Feline megacolon

A
  • middle aged, M > F
  • a diagnosis of exclusion + radiographs
  • Tx: Diet (canned diet), stool softeners, pro-kinetics, hydration, increase activity
  • -> may require manual deopstipation under gen. anesthesia
  • -> exhaust medical options prior to subtotal colectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

T/F: the feline rectal exam should always be performed under sedation

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Dyschezia

A
  • difficult and painful defecation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Tenesmus

A
  • ineffectual straining to defecate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Constipation

A
  • infrequent, difficult evacuation of dry/ hard feces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Obstipation

A
  • severe constipation to the point of inability to defecate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Megacolon

A
  • irreversible colonic dilation ass/ w/ chronic constipation; usually based on radiograph
  • idiopathic is the most common form
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Underlying causes of constipation

A
  1. dehydration
  2. neurological
  3. obstruction (intra or extra luminal)
  4. Electrolyte disturbances
  5. idiopathic megacolon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Top 3 causes of obstipation

A
  1. Idiopathic megacolon (62%)
  2. ortho (23%)
  3. neuro (11%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

4 functions of the colon

A
  1. electrolyte and water absorption
  2. storage of feces
  3. fermentation of indigestible ingesta
  4. vitamin production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Diet modification for Feline Megacolon

A
  • canned diet to inc water content
    • increase digestibility to dec. stool volume
    • increase fiber concentration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Indications for subtotal colectomy

A
  • refractory idiopathic megacolon after exhausting all medical options ( ideally spare the ileocolic jxn)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Risk factors for Canine Pancreatitis

A
  • hypertriglyceridemia (DM, hypoT4, Cushings, obesity)
  • drugs (l-spar, diuretics, azathioprine)
  • trauma/ ischemia
  • diet?
  • hypercalcemia?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Diagnostic pathway for Canine Pancreatitis

A
  • CBC
  • Chem (high ALT, ALP)(hyperbili, hypercholest, triglyc, hypocalcemia, hyperglycemia, azotemia)
  • TLI is more for EPI
  • spec cPL is ideal
  • rads are insenstitve
  • U/S is great, but operator dependent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

T/F: there is no perfect test for canine pancreatitis

A

T, but spec cPL + U/S would is best

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Treatment of Canine Acute Pancreatitis

A
  • stabilize the patient first
  • nutrition: many, small meals (low fat, high digest.)
  • analgesia: partial and full u-agonists
  • anti-emetics: 5HT3 (ondansetron) or NK1 (cerenia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Pathobiology of Canine Acute Pancreatitis

A
  • fusion of lysosomes and zymogen granules (vacuolization):
  • -> premature activation of zymogens by proteases
  • -> further activation by trypsin
  • -> damage propagated by elastases and phospholipases
  • systemic inflammatory response (TNF-a and IL-6 resulting in mutlisystemic inflammation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Protective measures of the pancreas

A
  • pancreatic secretory trypsin inhibitor
  • pancreatic polypeptide
  • plasma protease inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What types of pancreatitis to cats get?

A
  • chronic suppurative pancreatitis (CP)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Etiology of Feline Pancreatitis

A
  • IBD
  • Cholangitis
  • idiopathic
  • -> all three would be a triaditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Diagnosis of feline pancreatitis

A
  • same as the dog
  • use spec fPL and a good U/S
  • histopath is gold standard (cats get the chronic mononuclear, firbosis and atrophy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Therapeutics for feline pancreatitis

A
  • hydration
  • nutrition
  • analgeisa
  • treat underlying disease first if applicable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Canine vs feline pancreatitis (similarities)

A
  • clinical signs
  • clinpath evaluation
  • diagnosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Canine vs feline pancreatitis (differences)

A
  • Nutrition (cats – hydrolyzed diet d/t IBD, dog – get them food)
  • Chronicity (dogs are acute, cats are chronic)
  • Clinical consequences (dogs can die, cats get hepatic lipidsosi and EPI)
    Etiology (cats are triaditis and dogs are usually singular)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

T/F; it is important to distinguish between a hepatopathy and liver dysfunction when it comes to anesthesia

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How to distinguish between a hepatopathy and liver dysfunction

A

hepatopathy: AST, ALT, GGT,

Liver Dysfunction: BUN, Cholesterol, Albumin, bilirubin, glucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

T/F: the goal of anesthesia for liver disease is to maintain adequate blood supply to the liver

A

T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What are some drugs to avoid during anesthesia for liver disease/ dysfunction?

A
  • acepromazine, alpha-2 agonists, benzodiazepines (if hepatic encephalopathies), ketamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What are some drugs that are OK to use in anesthesia for liver disease/ dysfunction?

A
  • opioids (no morphine or meperidine), propofol, etomidate, inhalents, and alfaxalone are fine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Functional parameters of the liver

A
  • BUN (high w/ disease)
  • cholesterol (low w/ disease)
  • bilirubin (high w/ disease)
  • glucose (low w/ disease)
  • albumin (low w/ disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

T/F: liver enzyme values (AST, ALT) tell us nothing about liver function

A

T

55
Q

T/F: ALT and AST are leakage enzymes while ALP and GGT represent cholestasis

A

T

56
Q

ALT

A
  • more liver specific than AST
  • also present in heart, kidneys, and muscle
  • longer half life in dogs (60hrs) than cats (6hrs)
  • any damage to the liver will cause leakage
57
Q

AST

A
  • less liver specific than ALT
  • high concentrations in skeletal muscle
  • necrosis and inflammation can increase AST
  • most AST is bound to mitochondria so more damage is required vs ALT
58
Q

ALP

A
  • high sens., low spec in dogs
  • membrane bound in liver, renal, bone, intestinal mucosa
  • 3 causes of increase:
    1. cholestasis
    2. increased osteoblastic activity (growing)
    3. admin. of corticosteroids
  • elevation in cats is of significant concern and we must find cause
59
Q

T/F: GGT is more sensitive than ALP for inflammatory bile duct disease in cats than dogs. GGT&raquo_space; ALP in most cholestatic disorders, except for hepatic lipisosis

A

T

60
Q

T/F: Cats commonly develop marked hepatic fibrosis, cirrhosis, and acquired PSS compared to dogs

A

F; cats rarely develop these conditions

61
Q

T/F: Bilirubinuria is rarely a concern in cats compared to dog

A

F; cats have roughly 7x higher renal threshold than dogs so bilirubinuria in cats is a huge concern

62
Q

T/F: increased ALP is always important in cats

A

T

63
Q

T/F: triaditis is more common in dogs than cats

A

F; triaditis (enteritis, pancreatitis, cholecystitis) is common in cats

64
Q

How to run Bile Acids?

A
  1. fast dog for 12-18 hours
  2. take blood test (preprandial)
  3. feed small meal (CCK will trigger bile release)
  4. blood test post-prandially
65
Q

How to read a bile acids

A
  • hepatic disease will cause difficulty re-uptaking bile acids from blood causing increased [bile acids]
  • PSS = normal pre and markedly elevated post
66
Q

Feline hepatic diseases

A
  1. Hepatic Lipidosis (25-50%)
  2. Cholangitis (25%)
  3. Neoplasia (20%)
  4. 2nd* reactive hepatopathies (16%)
  5. Vascular - PSS (6%)
  6. Toxic (5%)
  7. FIP (<2%)
67
Q

Feline Hepatic Lipidosis

A
  • accumulation of excess triglycerides in hepatocytes

- obesity, stress, and anorexia

68
Q

Feline Hepatic Lipidosis ( Pathogenesis)

A
  • excessive fatty acid uptake
  • inability to oxidize fa
  • excessive lipogenesis
  • inhibition of VLDL synthesis or secretion
69
Q

Feline Hepatic Lipidosis ( Diagnosis)

A
  • mod increased in ALT, ALP
  • mod increase in serum bili
  • n to mildly increase GGT
  • enlarged hyperechoic liver on U/S
70
Q

Feline Hepatic Lipidosis (Management)

A
  • do not force feed the cat
  • appetite stim. are not effective and may worsen a hepatopathy
  • aggressive nutritional and fluid support
  • do not restrict dietary fat or protein in cats w/ HL
  • feed based on RER ( RER= 70*BW^0.75 / day)
71
Q

Feline Hepatic Lipidosis (Prognosis)

A
  • good w/ 80% survival w/ aggressive nutritional support
72
Q

Cholangitis (3 forms)

A
  1. Neutrophilic (80%) (presents more sick than 2)
  2. Lymphocytic (20%)
  3. Chronic cholangitis d/t flukes
  • can only differentiate via histopath
73
Q

Cholangitis (Clinical signs)

A
  • nothing specific (anorexia, weight loss, lethargy, vomiting, diarrhea)
  • jaundice
  • fever (lipidotic cats are not febrile)
74
Q

T/F: a good way to differentiate between cholangitis and hepatic lipidosis in the cat is to take a rectal temp. Lipidotic cats will not have an elevated temperature

A

T

75
Q

Neutrophilic Cholangitis

A
  • think bacterial infection (E. coli, clostridia, bacteroides) (go to bile for culture)
  • underlying cause unknown
76
Q

Lymphocytic cholangitisi

A
  • small lymphocytes mainly restricted to portal areas, variable portal fibrosis, biliary proliferation
77
Q

Cholangitis (surgery)

A
  • on indicated if discrete choleliths or complete biliary obstruction observed
78
Q

Cholangitis (medical therapy)

A
  • Ursodeoxycholic Acid (Actigall) (anti-inflammatory, immunomodulatory, and antifibrotic properties)
  • Denamarin (antioxidant)
  • Neutrophilic –> treat underlying dz
  • lymphocytic –> pred or chlorambucil
79
Q

Cholangitis (prognosis)

A
  • extremely variable
80
Q

What are the two components of Denamarin

A
  • SAMe

- Silybin

81
Q

Hepatic Disorders in the Dog

A
  1. Reactive Hepatopathy
  2. Chronic Hepatitis
  3. Copper Hepatotoxicity
  4. PSS
  5. Neoplasia
  6. Superficial Necrolytic Dermatitis
82
Q

Copper Associated Hepatotoxicosis

A
  • abnormal accumulation of copper in hepatic lysosomes

- up to 10k ppm (n <400ppm)

83
Q

Cu-Ass Hepatotoxicosis (Bedlington terrier)

A
  • autosomal recessive inherited gene

- deletion of commD1gene - inability to excrete Cu in bile ducts

84
Q

Cu-Ass Hepatotoxicosis (Diagnosis)

A
  • high ALT, ALP, bilirubin
  • Quantification of hepatic copper from biopsy
  • stain for copper (rhodanine)
  • -> 1* metabolic disorders - centrilobular
  • -> cholestasis - accumulation in the portal tracts (periportal region)
85
Q

Cu-Ass Hepatotoxicosis (Treatment)

A
  • dietary copper restriction
  • Zinc Gluconate = decreased absorption via induction of metallothionein
  • Cu chelating agent (d-penicillamine, trientine) (use when Cu >1000ppm)
  • Anti-oxidants (denamarin)
  • Ursodeoxycholic acid
86
Q

Why is it inappropriate to give Zn-gluconate with d-penicillamine and denamarin?

A

D-penicillamine (a chelating agent) will chelate the Zn rather than the Cu

87
Q

Chronic (Active) Hepatitis

A
  • a canine disease
  • active = neutrophils on biopsy
  • idiopathic inflammatory condition ass. w/ Cu toxicity, infectious disease (lepto), drugs (tetracycline), idiopathic
88
Q

Chronic (Active) Hepatitis (pathogenesis)

A
  • immune mediated disease 2* to hepatocyte injury and release of hepatic antigens
89
Q

Chronic (Active) Hepatitis (Signalment, Clinical Signs, types)

A
  • female, middle-aged (dobermans)
  • non-specific + icterus, jaundice, seizures, bleeding
    3 types:
  • short fulminant = death
  • progressive waxing and waning
  • asymptomatic
90
Q

Chronic (Active) Hepatitis (Lab findings)

A
  • high ALT, ALP, bilirubin
  • hypoalbuminemia
  • abn bile acids
91
Q

Chronic (Active) Hepatitis (Histo features)

A
  • initial lympho-plasma infiltration
  • bile duct hyperplasia
  • bile stasis fibrosis, necrosis
92
Q

Chronic (Active) Hepatitis (Treatment)

A
  • manage excess copper if present
  • arrest inflammation (cyclosporine)
  • resolve fibrosis
  • Zn gluconate
  • antioxidants
93
Q

PSS (3 classifications)

A
  • congential vs acquired
  • intra vs extra hepatic
  • single vs multiple
94
Q

T/F: toy breeds are predisposed to congenital, extrahepatic, single PSS while large breeds are predisposed to acquired, intrahepatic, single PSS

A

T

95
Q

PSS (Diagnosis)

A
  • signalment
  • min. database (microcytosis, fx liver abn)
  • serum bile acids
  • abd rads, ultrasound
  • hepatic scintigraphy (great y/n test)
  • exploratory laparotomy
96
Q

PSS (therapy)

A

Medical (for hepatic encephalopathy)

  • decreased urease producing bacteria w/ an antibiotic (ampicillin, neomycin)
  • avoid metro d/t neurotoxicity
  • lactulose
  • Diet (do not restrict protein unless encephalopathic)

Surgical
- Ameroid Ring Constrictor (ARC)

97
Q

Why does administering lactulose help w/ hepatic encephalopathy?

A
  • acidify the colon to converts NH3 –> NH4 which prevents re-absorption in the colon
98
Q

Portal venous Hypoplasia

A
  • type of microscopic PSS
  • congenital in Cairn ter. Yorkies, toy breeds
  • result of hypoplastic small intrahepatic portal veins
  • high serum bile acids w/ no visible shunt
  • biopsy –> similar to that of shunt dog
  • do not need therapy and have great prognosis
99
Q

Primary Survey of the Acute Abdomen

A

A- airways
B- breathing
C- circulation
D- disability/ dysfunction

100
Q

Perfusion Parameters

A
  • mentation
  • mm color
  • CRT
  • heart rate
  • pulse quality
  • extremity temp
101
Q

4 broad causes of abdominal pain

A
  1. distension
  2. traction
  3. ischemia
  4. inflammation
102
Q

Hemoabdomen

A
  • free blood in the abdomen that does not clot and pCV > circulating PCV
  • causes: trauma, coagulopathy, ruptured viscera, torn blood vessel
103
Q

Fluid Analysis (uroabdomen)

A

requires either:

  • [creatinine] x 2 > serum
  • [potassium] x 1.4 > serum
104
Q

Fluid Analysis (bile peritonitis)

A

requires:

- [bilirubin] x 2 > serum

105
Q

Fluid Analysis (septic peritonitis)

A

requires both:

  • glc @ 20mg/dl < blood
  • lactate @ 2mmol/L > blood
106
Q

Because an elevation in AST can also come from a severe myositis, it is important to check this other chem panel value whenever we see that elevation?

A

CK

107
Q

Why is an elevation of ALP in the cat more significant than in the dog?

A
  • no steroid induced iso-enzyme
  • a lot less ALP per gram of hepatocyte
  • shorter half-life (6hrs)
108
Q

T/F: ALP is made by bile caniliculi epithelium, GGT by bile duct epithelium

A

T

109
Q

Classic PSS U/S findings

A
  • microhepatica
  • actual shunt
  • possibly stones in the bladder
  • slight renomegaly
110
Q

Gold Standard for PSS diagnostics

A
  • nuclear scintigraphy (tells us yes/ no for shunt)
111
Q

Classical signs of SIBO

A
  • low B12, high folate

- not necessarily required for diagnosis

112
Q

2 breeds predisposed to BOTH canine chronic and acute pancreatitis

A

yorkies

schnauzers

113
Q

pancreatitis ultrasound findings

A
  • enlarged, hypoechoic pancreas

- hyperechoic mesentery surrounding it

114
Q

What is the gold standard test for diagnosing a septic peritonitits

A
  • intracellular bacteria present on cytology of the effusion
115
Q

What is the gold standard test for diagnosing a uroabdomen

A
  • positive contract cystourethrogram
116
Q

Surgical treatment for hilar splenectomy (2 important arteries)

A
  • ligation of the splenic and short gastric arteries
117
Q

Adv./ Dis of Active Drain - Closed Suction for Septic Peritonitis

A 
Adv. 
- closed system = dec nosocomials
- relatively cheap
- fluid samples for cytology
Dis.
- no opportunity to re-debride
118
Q

Adv./ Dis of Open Abdominal Drainage for Septic Peritonitis

A 
Adv.
- improved drainage
- inability to re-explore
- discourages anaerobic growth
Dis 
- cost
- monitoring
- hypoproteinemia
- nosocomial infections common
119
Q

5 factors that predispose to GDV

A
  • large breed
  • deep chest
  • previous splenectomy
  • fed once per day
  • increasing age
120
Q

Acute Hemorrhagic Diarrhea Syndrome

A
  • acutely ill dog w/ bloody diarrhea
  • often present in shock w/ normal to mild dehydration
  • PCV = 10 x TP
121
Q

AHDS (Signalment)

A
  • younger to middle age small breeds
122
Q

AHDS ( History)

A
  • most commonly starts w/ vomiting

- progresses to hemorrhagic diarrhea w/in hrs - days

123
Q

AHDS (Physical Exam)

A
  • dehydration

- poor perfusion parameters

124
Q

AHDS (pathogenesis)

A
  • idiopathic
  • disruption of intestinal permeability d/t inflammation –> acute transolcation of plsama like fluid –> hypovolemia and dehydration
125
Q

AHDS (Treatment)

A
  • resolve shock (often 1.5 - 3x blood volume in isotonic crystalloids)
  • antimicrobials: concurrent sepsis or neutropenia
  • GI protectants: consider ondansetron/ maropitant for first two day. Antacids not indicated
126
Q

Parvovirus (signalment)

A
  • a puppy w/ hemorrhagic diarrhea
127
Q

Parvovirus (Diagnosis)

A
  • ELISA snap test
  • vaccines can induce weak positives
  • PCR the feces if unsure
128
Q

Parvovirus (2 major forms)

A
  1. myocarditis (almost nonexistent)

2. enteritis (v common)

129
Q

Parvovirus (Clinical Signs)

A
  • vomiting w/ or w/out diarrhea
130
Q

Parvovirus (treatment)

A
  • large volume IV fluids
  • offer food daily (NG tube if truly anorexic)
  • pain control?
131
Q

Parvovirus (Prognosis)

A
  • good w/ aggressive therapy
132
Q

Parvovirus ( Outpatient treatment)

A
  • give estimated deficit SQ
  • daily calculate maintenance per TID SQ
  • Antimicrobial once (cefovicin) SQ
  • Antinausea/ antiemetic
133
Q

Parvovirus ( post-infection immunity)

A
  • immunity for rest of life

- some will never recover from bone marrow insult

VET 433a - Small Animal Stream 1 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions