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From Flashcardlet > GI, GDV, Exocrine Pancreas > Flashcards

GI, GDV, Exocrine Pancreas Flashcards

1
Q

Green, JVECC, 2011, Eval initial lactate and gastric necrosis and subsequent lactate survival. What were main findings?

A
  1. NO * sig relationship b/t survival and presence of macroscopic gastric necrosis with initial lacate > 6
    • sig relationship b/t initial lactate > 2.9 mmol/L for predicting necrosis and 50% reduction in lactate 12h after tx (of the 40 that had repeat lactate)
  3. The other 3/40 that had repeat lactates that were not more than 50% lower, all died
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2
Q

Beal, JVECC, 2011. Regarding fluoroscopically placed NJT, which of the following is true?

a) Most common primary diagnosis was adenocarcinoma
b) Ability to achieve transpyloric passage was 92.3%
c) Ability to achieve jejunal access was 58.2%
d) Median duration of feeding was 6.5 days

A

b

panc most common primary dz, jejunal access in 78.2%, medial duration feeding 3.3 d

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3
Q

What is stress related injury?

A

Diffuse, superficial mucosal erosions that are unlikely to result in GI bleeding associated with hemodynamic compromise.

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4
Q

What is stress related mucosal disease?

A

Stress ulcers extend deeper into submucosa and are more focal. Increased risk for bleeding necessitating pRBC transfusion and intervention to control bleeding

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5
Q

Difference in mortality in humans with SRMD?

A

48.5% with bleeding vs. 9.1% w/o bleeding

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6
Q

Alaskan sled dogs SRMD incidence?

A

48.5%

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7
Q

Pathogenesis for SRMD involves…

A

Splanchnic ischemia
Loss of host defenses
Assault by gastric acid

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8
Q

What is the GMDS?

A

gastric mucosal defense system that protects against gastric acid, pepsin, and bile acids

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9
Q

What makes up the GMDS?

A
  1. Extracellular mucus barrier
  2. Cellular membrane properties
  3. Rapid epithelial cell restitution
  4. Mucosal HCO3 secretion
  5. High mucosal blood flow rate
  6. Neurohormonal factors
  7. Prostaglandins
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10
Q

What is the extracellular mucus barrier?

A

unstirred layer of mucus gel, bicarb, and surfactant phospholipids

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11
Q

What is fxn of extracellular mucus barrier?

A
  1. maintain surface pH 7
  2. prevent pepsin infiltration and proteolytic degredation
  3. hydrophopic properties of surfactant phospholipids to repel water soluble agents
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12
Q

Mucus gel is…

A

95% water, 5% mucin glycoproteins

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13
Q

What are trefoil factor family proteins?

A

peptides co-secreted with mucus gel - fxn in intracellular assembly and packing of mucins and increase mucus viscosity

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14
Q

What influences gastric mucus secretion?

A

ACTH, corticosteroids, NSAIDS

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15
Q

What prevents back diffusion of acid and pepsin in stomach?

A

cellular tight jxns and correct functioning of membrane pumps and exchanges

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16
Q

What do gastric epithelial cells secrete?

A

prostaglandins, TFFs, heat shock proteins, cathelicidins, defensins

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17
Q

What do cathelicidin and defensins do?

A

participate in innate immunity, preventing bacterial colonization

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18
Q

What is epithelial restitution?

A

rapidly sealing epithelial compromise

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19
Q

pH requirement for epithelial restitution?

A

> 3.0

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20
Q

What is survivin?

A

protein expressed by progenitor cells that prevents apoptosis and promotes mitosis. Takes 3-7 days for epithelial restitution.

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21
Q

What do parietal cells do?

A

secrete acid from apical membrane and bicarb from basolateral membrane (alkaline tide). The interstitial bicarb transported paracellularly to GI epithelial surface to be trapped in mucus.

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22
Q

What vasodilators do endothelial cells produce?

A

NO, prostacyclin (PGI2)

protects from vasoconstrictors

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23
Q

What are vasoconstrictors?

A

leukotriene C4, thromboxane A2, endothelin-1

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24
Q

How does H2S help maintain mucosal blood flow?

A

mucosal protectant, modulates inflammation via inhibiting leukocyte adherence to vascular endotheliam

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25
Q

Vagal stimulation does what in GMDS?

A

increases mucus secretion and intracellular bicarb concentration

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26
Q

When vagal afferents detect noxious stimulus or acid at gastric epitheliam, nerve endings release..

A

calcitonin gene-related peptide
substance P

Result: NO mediated vasodilation

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27
Q

What other peptides enhance mucosal blood flow?

A 
gastrin
cholecystokinin
thyrotropin-releasing hormone
corticotropin releasing factor
epidermal growth factor
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28
Q

What does ghrelin do?

A

stimulates appetite and increases acid secretion

Maybe: enhance mucosal blood flow thru NO and CGRP, and inhibit IL-1B, IL-6, TNF-alpha

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29
Q

What prostaglandins are cytoprotective in the gastric mucosa?

A

PGE2 and PGI2

Fxn: stimulation of mucus, bicarb, and phospholipid secretion AND inhibit acid secretion, tissue mast cell degranulation, leukocyte and plt adhesion

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30
Q

ROS

A

superoxide anion, hydrogen peroxide, hydroxyl radical

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31
Q

Where are parietal cells found?

A

oxyntic glands

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32
Q

What happens in parietal cells?

A

carbonic anhydrase converts water and CO2 to H and HCO3. H secreted thru apical H-K-ATPase pump and HCO3 secreted thru basolateral membrane in exchange for Cl-

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33
Q

Secretion of gastric acid is mediated by…

A

gastrin (paracrine)
acetylcholine (neurocrine)
histamine (endocrine)

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34
Q

What is the most potent secretogogue?

A

histamine

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35
Q

How do gastrin, ACh, and histamine increase acid secretion?

A

Bind their receptors, activates second messenger that increases intracellular calcium (gastrin, ACh) of increases cAMP (histamine). The second messengers then activate protein kinase, increasing cytosolic phosphoproteins, which ultimately activate proton pump

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36
Q

Risk factors for SRMD

A

PPV and coagulopathy (HIGHEST)

sepsis
shock/hypotension
renal failure
hepatic failure
neuro trauma and sx
MOF
trauma
aspiration pneumonia
ileus
major sx
burns >35% BSA
organ transplant
high dose corticosteroid
prolonged ICU stay
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37
Q

Where are SRMD lesions found?

A

stomach with oxyntic glands - fundus, body

contrast peptic ulcer dz is antrum and pylorus

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38
Q

Pepsin inhibited and fibrinogen halted at pH over…

A

> 4

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39
Q

pH over ___ required for plt aggregation and fibrin clot formation

A

> 6

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40
Q

Histamine released from…

A

tissue mast cells and enterochromaffin cells

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41
Q

Where is the H2 receptor?

A

basolateral membrane of parietal cells

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42
Q

List H2 receptor antagonists

A

cimetidine
nizatidine
ranitidine
famotidine

metabolized in liver
secreted in kidneys

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43
Q

Which H2 receptor antagonists have prokinetic actions?

A

ranitidine

nizatidine

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44
Q

Which H2 receptor antagonist impairs P450 liver?

A

cimetidine

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45
Q

Adverse effects of H2RAs

A

diarrhea, headache, drowsiness, fatigue, muscle pain, constipation, leukopenia, thrombocytopenia, anemia

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46
Q

What reaction has IV famotidine caused in cats? Speculated reason?

A

hemolysis, maybe due to benzyl alcohol preservative

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47
Q

How do PPIs work?

A

Substituted benzimidazoles that bind to the proton pump, inhibiting the final step in gastric acid secretion in a dose dependent manner

weak base, accumulates in canaliculi where converted to sulfenamide form which irreversibly binds to proton pump

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48
Q

List PPIs

A 
omeprazole
lansoprazole
pantoprazole
esomeprazole
rabeprazole
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49
Q

Bases behind why PPIs provide more potent acid suppression than H2RAs?

A

Irreversible proton pump inhibition, progressive intracellular acidification, drug accumulation

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50
Q

What drug has decreased bioactivation via CYP 450 when administered with omeprazole?

A

clopidogrel

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51
Q

What drugs have prolonged eliminates when administered with PPIs?

A 
cyclosporine
diazepam
phenytoin
warfarin
theophylline
propanolol

P450 pathway

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52
Q

Reported adverse effects of PPIs in people?

A

Abd pain, nausea, vomiting, diarrhea, pancreatitis, hepatic necrosis/failure, pancytopenia, agranulocytosis, hypergastrinemia with chronic use

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53
Q

What is sucralfate?

A

Complex salt of sucrose sulfate and aluminum hydroxide

Aluminum negative and will bind everything

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54
Q

What are benefits of sucralfate?

A
  1. Coat mucosa
  2. Inhibit pepsin molecules
  3. Stimulate prostaglandin release
  4. Increase mucosal blood flow
  5. Increase HCO3 and mucus secretion
  6. Stimulates epidermal growth factor for cell renewal
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55
Q

What are potential benefits of EN?

A
  1. Acid buffering
  2. Mucosal energy source
  3. Enhance mucosal immunity
  4. Induction of prostaglandin secretion
  5. Improve mucosal blood flow
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56
Q

Gastric layers.

A

Serosa, longitudinal SM, circular SM, submucosa, mucosa

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57
Q

When myenteric plexus is stimulated, what happens?

A
  1. Increased tonic contraction
  2. Increase intensity of rhythmical contractions
  3. Increase rate of rhythm of contraction
  4. Increase velocity of conduction of excitatory waves along the gut wall
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58
Q

Some of the neurons of the myenteric plexus secrete what inhibitory NT?

A

vasoactive intestinal polypeptide

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59
Q

Where is gastrin released from?

A

G cells of antrum, duodenum, and jejenum

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60
Q

What stimulates release of gastrin?

A

protein, distension, vagal stimulation (ACh)

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61
Q

What inhibits release of gastrin?

A

acid

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62
Q

What does gastrin do?

A

stimulates gastric acid secretion and mucosal growth

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63
Q

Where is cholecystokinin released from?

A

I cells of dudenum, jejunum, and ileum

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64
Q

What stimulates release of CCK?

A

protein, fat, acid

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65
Q

What does CCK do?

A

Stimulates pancreatic enzyme and bicarb secretion, stimulate GB contraction and growth of exocrine panc

Inhibits gastric emptying

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66
Q

Where is secretin released from?

A

S cells of duodenum, jejunum, ileum

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67
Q

What stimulates release of secretin?

A

acid!!!!!! and fat

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68
Q

What are the actions of secretin?

A

Stimulates: pepsin secretion, pancreatic bicarb secretion!!!!, biliary bicarb secretion, growth of exocrine panc

Inhibits: gastric acid secretion

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69
Q

Where is gastric inhibitory peptide (GIP) released from?

A

K cells of duodenum and jejunum

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70
Q

What stimulates release of GIP?

A

protein, fat, carbs

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71
Q

Fxns of GIP

A

Stimulates insulin release and inhibits gastric acid secretion

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72
Q

GIP also known as

A

glucose-dependent insulinotropic peptide

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73
Q

Where is motilin secreted from

A

M cells of duodenum and jejunum

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74
Q

Motilin secretion stimulated by?

A

fat, acid, nerve

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75
Q

What does motilin do?

A

Stimulates gastric and intestinal motility

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76
Q

Oxyntic glands (acid forming) secrete…

A

hydrochloric acid and intrinsic factor (from parietal cells), pepsinogen (from chief or peptic cells)
mucus (from mucous neck cells)

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77
Q

Pyloric glands secrete…

A

mucus and gastrin

78
Q

Ach stimulates what in the stomach

A

pepsinogen by peptic/chief cells, HCl by oxyntic/parietal cells, and mucus by mucous cells

79
Q

Gastrin and histamine stimulate what…

A

strongly stimulate acid by parietal/oxyntic cells

80
Q

Pyloric glands secrete…

A

mucus and gastrin

81
Q

What activates pepsinogen to pepsin?

A

hydrochloric acid

82
Q

Fxn of pepsin.

A

proteolytic enzyme, optimal pH 1.8-3.5

83
Q

What are the 3 phases of gastric secretion?

A

cephalic, gastric, intestinal

84
Q

Basic stimuli that cause pancreatic secretion.

A

ACh, CCK, secretin

85
Q

Young GSDs with EPI predisposed to what severe cause of acute abdominal pain?

A

mesenteric torsion

86
Q

Severe vomiting and GI FBs have what typically on blood gas?

A

hypochloremia metabolic alkalosis with hypokalemia and hyponatremia

87
Q

Where is free peritoneal gas usually seen on radiographs?

A

B/t stomach or liver and diaphragm on lateral view

Or, can increase sensitivity with pet in LEFT lateral recumbency and horizontal beam focused on least dependent area

88
Q

Most common causes of pure transudate in abdomen?

A

hypoalbuminemia

portal vein obstruction

89
Q

Most common causes of modified transudate in abdomen?

A

R-CHF, HWD, cancer, liver dz

90
Q

What is a poor prognostic indicator in cats with acute panc?

A

ionized hypocalcemia

91
Q

Radiographic signs of acute panc?

A

increased density and loss of detail right cranial abdomen
widening of angle b/t prox duodenum and pylorus
displacement of descending duodenum to right
caudal displacement of transverse colon

92
Q

What is the rational for using FFP for pancreatitis?

A

provide a source of alpha-2 macroglobulins (protease inhibitors to help clear activated circulating proteases)

93
Q

In experiimental feline panc, what pressor has shown ability to reduce panc inflammation by decreasing microvascular permeability?

A

dopamine

94
Q

What is feline triaditis?

A

pancreatitis, cholangitis, IBD

95
Q

Obstructive biliary dz in dogs most commonly…

A

pancreatitis

96
Q

What makes up bile?

A

water, conjugated bile acids, bile pigments, cholesterol, inorganic salts

97
Q

Obstructive biliary dz in cats most commonly d/t…

A

cancer

98
Q

Sensitivity of US to detect GB rupture with mucocele?

A

86%

99
Q

What percent of dogs with GB mucocele had rupture intraop?

A

50%

100
Q

Liver fluke in cats?

A

Platynosomum fastosum

101
Q

What is Caroli’s syndrome?

A

congenital malformation of the bile ducts

102
Q

What are the most common causes of bile peritonitis?

A

necrotizing cholecytitis, trauma, cholelithiasis

103
Q

MOA of ursodeoxycholic acid

A

Hydrophilic bile acid that increases water content of biliary secretions, encourages choleresis, decreases inflammation and immune-mediated reactions, and lessens hepatotoxic nature of bile acis

104
Q

Mortality with biliary surgery if…

A

septic bile peritonitis, prolonged PTT, post op hypotension

105
Q

MOA chlorpromazine

A

alpha-2 adrenergic antagonist
D2 dopaminergic antagonist
H1 histaminergic antagonist
M1 muscarinic cholinergic antagonist

106
Q

MOA cisapride

A

5-HT4 serotinergic agonist

107
Q

MOA dimenhydrinate

A

H1 histaminergic antagonist

108
Q

MOA diphenhydramine

A

H1 histaminergic antagonist

109
Q

MOA dolasetron

A

5-HT3 serotonergic antagonist

110
Q

MOA domperidone

A

D2 dopaminergic antagoist

increased gastroesophageal sphincter tone and antiemetic

111
Q

MOA erythromycin

A

motilin agonist

112
Q

MOA famotidine

A

H2R antagonist

113
Q

MOA maropitant

A

NK1 receptor antagonist

114
Q

MOA metoclopramide

A

D2 dopaminergic antagonist
5HT3 serotinergic antagonist
5HT4 serotonergic agonist

115
Q

MOA nizatidine

A

cholinesterase inhibitor

H2RA antagonist

116
Q

MOA omeprazole

A

PPI

117
Q

MOA ondansetron

A

5HT3 serotonergic antagonist

118
Q

MOA pantoprazole

A

PPI

119
Q

MOA prochlorperazine

A

alpha2 adrenergic antagonist
D2 dopaminergic antagonist
H1 histaminergic antagonist
M1 muscarinic cholinergic antagonist

120
Q

MOA ranitidine

A

H2R antagonist

121
Q

MOA scopolamine

A

M1 muscarinic cholinergic antagonist

122
Q

MOA sucralfate

A

sucrose sulfate aluminum complex cytoprotective

123
Q

MOA yohimine

A

alpha-2 adrenergic antagonist

124
Q

Enterocyte life span

A

2-5 days

125
Q

Rotavirus and coronovirus affect the intestinal crypts. T/F

A

F - affect the tips of villi (parvo affects crypts)

126
Q

Bacterial causes of gastrointeritis.

A

Clostridium (perfringens and difficle), Campylobacter, Escherichia, Salmonella, Heliocobacter

127
Q

Where does serotonin come from in GI tract?

A

Enterochromaffin cells (95% of body’s serotonin in GI tract) - released and secreted into lamina propria in high concentrations which overflows into portal circulation and intestinal lumen

128
Q

5HT^1P

A

Initiates perstaltic and secretory reflexes (no drugs for this receptor)

129
Q

5HT3

A

activates extrinsic sensory nerves and is responsible for the feeling of nausea and induction of vomiting from visceral hypersensitivity
5HT3 antagonist = ondansetron, dolasetron, granisetron, metoclopramide

130
Q

5HT4

A

Increases presynaptic release of AcH and calcitonin gene-related peptide, enhancing neurotransmission
5HT4 agonist = cisapride, tegaserod, metoclopramide

131
Q

Why does metoclopramide cause extrapyramidal signs?

A

It crosses the BBB to antagonize D2 receptors in CRTZ

Extrapyramidal signs: involuntary muscle spasms, motor restlessness, inappropriate aggression (can reverse with diphenhydramine)

132
Q

How do ranitidine and nizatidine increase GI motility?

A

Acetylcholinesterase inhibition - so increase amt of acetylcholine available to bind smooth muscle muscarinic cholinergic receptors

133
Q

If severe GI bleed and underlying cause not found on diagnostics, not responding to medical mgmt, options are:

A
  1. Exploratory sx
  2. Scintigraphy with technetium-labeled red blood cells
  3. arteriography
134
Q

Causes of secondary megaesophagus.

A

MG, NM dz, hypoadrenocorticism, lead toxicity, hypothyroidism

135
Q

What is odynophagia?

A

pain on swallowing

136
Q

What drug may stimulate esophageal contractions in some dogs?

A

bethanechol - parasympathomimetc that stimulates muscarinic receptors, not nicotinic

137
Q

Where is the chemoreceptor trigger zone?

A

floor of 4th ventricle, lacks complete BBB

138
Q

What receptors make up the CRTZ?

A

D2, H1, alpha2, 5HT3, M1, NK1, ENKudelta

139
Q

What receptors make up the vestibular system?

A

H1, M1, NMDA

140
Q

What receptors are in teh vomiting center?

A

alpha2, 5HT^1a

141
Q

What receptor does apomorphine work on?

A

D2 - CRTZ

142
Q

What increases risk of post op peritonitis?

A

preop peritonitis, intestinal FB, alb < 2.5 g/dL

143
Q

Single paracentesis (blind) successful in ….

A

20% patients with low volume (10 ml/kg)

144
Q

DPL technique

A

Clip, scrub, use peritoneal dialysis catheter or 14/16 g cath, insert caudal to umbilicus, influse 22 ml/kg warm isotonic crystalloid and remove

145
Q

Uroperitoneum if fluid:serum creatinine and K>

A

> 2:1 (creat) or >1.4.1 (K)

146
Q

Presence of bicavitary effusion increases mortaliy by…

A

3.3 fold

147
Q

What are gastropexy options?

A 
tube
incisional
muscular flap
circumcostal 
belt loop
148
Q

Post op GDV arrhythmia source?

A 
poor myocardial perfusion
electrolyte disturbance
acidosis
DIC
pain
myocardial depressant factor
149
Q

Perioperative risk factors significantly associated with death before suture removal GDV.

A

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

150
Q

In the cat, mean serum:abd fluid creatinine and K for diagnosis of uroabd.

A

creat 1:2

K 1:1.9

151
Q

In the dog, serum:abd fluid creatinine and K for diagnosis of uroabd.

A

creat 1:2 (86% sensitive, 100% specific)

K 1:1.4 (100% sensitive and specific)

152
Q

Bilirubin serum:abd fluid for diagnosis of bile peritonitis?

A

> 1:2

153
Q

What is hypotensive resuscitaiton?

A

Mean 60, SBP 80 are goals to prevent excessive bleeding or diruption of clot fxn or formation

154
Q

Most common cause of uroperitoneum in cat?

A

blunt trauma (60%) due to ruptured bladder (85%)

155
Q

What is most common cause of bile peritonitis after blunt trauma?

A

Ductal rupture just distal to the last hepatic duct

156
Q

Blind needle paracentesis may yield peritoneal fluid when _____ fluid present.

A

5.2-6.6 ml/kg

157
Q

A peritoneal dialysis catheter used for abdominocentesis may detect presence of _____ abd fluid.

A

1-4.4 ml/kg

158
Q

Indications for abdominocentesis.

A
  1. loss of serosal detail on rads
  2. abd injury w/o obvious peritoneal entry wound
  3. shock, multiple injuries, signs of abd injury blunt trauma
  4. head or spinal injury precluding abd exam
  5. persistent abd pain or fluid distension of unknown cause
  6. postop complications
159
Q

What is a Cullen sign?

A

periumbilical ecchymosis (abd or retroperit bleeding)

160
Q

Significant hemorrhage is present if the PCV of peritoneal fluid exceeds _____ from a DPL.

A

5%

161
Q

Indications for peritoneal drainage.

A 
Septic peritonitis
Bile peritonitis
Uroperitoneum
Pancreatitis-associated peritonitis
Peritoneal dialysis
Increased IAH
Abdominal pressure compromising ventilation or causing pain
162
Q

What two H2RAs have gastric prokinetic effects?

A

ranitidine and nizatidine

MOA: anticholinesterase activity

163
Q

What’s special about cimetidine?

A

Inhibits hepatic P450 so can be used therapeutically (acetaminophen tox) or can delay metabolism of drugs

164
Q

H2RA MOA

A

block H1 receptor on parietal cells

competitive inhibitors

165
Q

Rank potentcy of nizatidine, famotidine, ranitidine, cimetidine

A

famotidine > nizatidine > cimetidine = ranitidine

166
Q

Which H2RA absorption is delayed by food?

A

cimetidine

167
Q

Which H2RA has longest duration of action?

A

famotidine

168
Q

Which H2RA does NOT undergo substantial first pass metabolism in liver?

A

nizatidine

169
Q

Which H2RA is most bioavailable? least bioavailable?

A

MOST - nizatidine

LEAST - famotidine

170
Q

Which two H2RAs undergo extensive liver metabolism? Which two excreted unchanged in urine?

A

extensive metabolism: cimetidine, ranitidine

excreted unchanged in pee: famotidine, nizatidine

171
Q

In what toxicity should cimetidine be considered for?

A

acetominophen - b/c cimetidine inhibits P450 markedly can lessen severity of acetominophen toxicity

Also decreases metabolism of other drugs (theophylline, lidocaine, metronidazole) - potentiating toxic effects of these meds

172
Q

Cimetidine decreases hepatic blood flow by 40%. T/F

A

F - 20%

173
Q

Side effects of H2RAs

A

CNS and cytopenias (only reported in humans)

hemolytic anemia with famotidine (CATS)

174
Q

PPI MOA

A

irreversibly inhibit H-K-ATPase on luminal side of parietal cell, thus stopping secretion of hydrogen ions into the gastric lumen

175
Q

Why should omeprazole be given 1 h before feeding?

A

undergoes 1st pass metabolism and remainder sequestered in acidic environment of parietal cells, so if give after feeding, maximize acidity of parietal cell and therefore increasing amt omeprazole sequestered in cell

176
Q

Side effects of PPIs

A

diarrhea (dogs), inhibits P450, elevations in liver enzymes, increased gastric pH can affect absorption of other meds (ketozonazole and digoxin)

177
Q

Sulcralfate MOA

A

octasulfate of sucrose combined with Al-OH; in acidic environment binds to epithelial cells for 6 h, stimulates local production of prostaglandins and pinding to epidermal growth factor

178
Q

Misoprostal MOA

A

PGE1 analog; antacid and mucosal protective properties (stimulates bicarb and mucus and increases gastric mucosal blood flow)

Acts directly on parietal cells to inhibit both nocturnal acid secretion and secretions in response to food, histamine, pentagastrin

food delays absorption, short half life

179
Q

Misoprostal side effects

A

diarrhea, uterine contractions

180
Q

What are 3 promazine derivatives used for antiemetics?

A

chlorpromazine, prochlorpromazine, acepromazine

may cause hypotension d/t alpha1 adrenergic antagonism

181
Q

Maropitant MOA

A

NK1 antagonist that blocks action of substance P in CNS and peripheral NK1 receptors in GI tract

182
Q

What is aminopentamide? Who should not take this?

A

anticholinergic antiemetic, not very good, maybe acts on muscarinic receptors

Contraindications with glaucoma, cardiomyopathy, tachycardia, hypertenion, MG, gastroesophageal reflux

183
Q

Consequences of IAH

A

increased CVP, PAP, RAP, PCWP, MAP, SVR
Decreased CO and urine output
Increased lactate
Decreased pulmonary compliance
Increased ICP
Decreased hepatic, portal, intestinal and gastric blood flow
Increased ADH, renin, aldosterone (reverse when reduce pressure)

184
Q

Renal effects of IAH

A

10-20 cm H20 decreases GFR

oliguria and anuria at > 25 cm H20

185
Q

Bacterial translocation to mesenteric LN reported with ACS pressures at…

A

34 cm H20

186
Q

IAH assessment

A 
0-10 = normal
10-20 = mild increase, ensure p normovolemic and press on
20-30 = moderate to severe IAH, volume resuscitation, diagnostics, consider decompression
>35 = severe IAH, decompression necessary to reverse organ damage and prevent further deterioration, explore or tap
187
Q

Enteropeptidase synthesized by…

A

duodenal enterocytes

188
Q

Where do salmonella organisms colonize?

A

ileum, invade M cells w/i Peyer’s patches

189
Q

What was always associated with failure to tolerate complete surgical attentuation of a CPSS, JAVMA, 2011, Lamb?

A

Ductular reaction w/o identifiable intrahepatic portal veins

190
Q

Breeds with benign familiarl hyperphosphatemia

A

Siberian husky

Scottish terrier

191
Q

McCord, JVIM, 2012. Spec cPLI vs. SNAP cPL in dogs suspected of having acute panc. Findings?

A 
SNAP:  SN 90%, SP 70%
Spec (>200):  SN 90%, SP 75%
Spec (>400): SN 75%, SP 85%
Amylase: SN 55%, SP 75%
Lipase:  SN 50%, SP: 90%

Negative result very likely to be accurate. Used to rule out panc.

192
Q

Israeli, JVIM, 2012. Serum pepsinogen-A, canine PLI, CRP as prognostic markers in dogs with GDV. Findings:

A

cPG-A * higher in GDV dogs compared to controls. Median cPB-A higher in nonsurvivors, compared to survivors. cPG-A increased with gastric wall damage.

cPG-A as predictor of death: AUC 0.75 (lactate AUC 0.66), SN 53%, SP 88%

CRP increased 75%, cPLI 40%, but no assc’n with outcome

From Flashcardlet (19 decks)

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