Jvim Fluid/cc Sc

Front 1

The prognostic utility of degenerative left shifts in dogs
How many day’s worth of neutrophils does the bone marrow store

Back 1

a. 5 days
2

Front 2

What CBC parameters would indicate that the bone marrow is not able to keep up with increased demand

Back 2

a. Band neutrophils with normal to low numbers of mature neutrophils= degenerative left shift
3

Front 3

Dogs with a degenerative left shift were found to have 2 fold greater risk of what

Back 3

a. Death or euthanasia
4

Front 4

Which disease processes seemed to affect outcome regardless of the presence of DLS

Back 4

a. Septic peritonitis, patients had greater risk for adverse outcome and those with gastrointestinal disease had reduced adverse outcome
5

Front 5

Incidence, nature, and etiology of metabolic alkalosis in dogs and cats
What was found in previous studies evaluating acid base status and patient outcome

Back 5

a. Base excess was correlated with survival in dogs with diabetic ketoacidosis and bicarbonate concentration has been inversely correlated with mortality in cats.
6

Front 6

What are causes of a metabolic alkalosis

Back 6

a. Compensation for respiratory acidosis
b. Excessive loss of acid (HCL) from foreign body obstruction and or vomiting
c. Renal overproduction of bicarbonate in either contraction alkalosis or Cushing’s disease
7

Front 7

What causes a metabolic acidosis

Back 7

a. Diabetic ketoacidosis due to high number of ketone bodies
b. Lactic acidosis due to anaerobic metabolism during heavy exercise or hypoxia
c. Chronic renal failure preventing excretion of acid and absorption of bicarbonate
d. Diarrhea in which a large amount of bicarb is excreted
e. Ingestion of methanol, ethylene glycol, or excessive aspirin
8

Front 8

What was the most common abnormality found in this experimental group

Back 8

a. Metabolic alkalosis with mixed respiratory acidosis (was suspected to be compensation for Hypercapnea in this study)(also a large amount of dogs in this study had received lasix
b. 49% of animals had pure metabolic acidosis and 19% had pure metabolic alkalosis
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Front 9

What electrolyte changes were most common in animals with a metabolic alkalosis

Back 9

a. Hypokalemia and hypochloridemia
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Front 10

Evaluation of Arterial Blood Gases and Arterial Blood Pressures in Brachycephalic Dogs
What are the characteristics of disease seen in brachycephalic dogs that make up brachycephalic syndrome

Back 10

a. Upper airway resistance because of narrowed nostrils, elongated and thickened soft palate, everted laryngeal saccules and a hypoplastic trachea; possibly prominent nasopharyngeal turbinates.
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Front 11

What is sleep apnea/hypopnea syndrome (SAHS)

Back 11

a. Complete upper airway collapse during sleep that can result in intermittent nocturnal hypoxemia and systemic hypertension
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Front 12

How did brachycephalic dogs compare to non-brachycephalic dogs with respect to PaO2, PCV, PaCO2, and arterial blood pressure

Back 12

a. Brachycephalic dogs had lower PaO2, higher PCV, higher PaCO2, and higher BP when compared to the control group.
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Front 13

How are the peripheral chemoreflex stimulated in situations of chronic hypoxemia

Back 13

a. Hypoxemia and to a less extent, hypercapnia stimulate the peripheral chemoreceptors in the carotid and aortic arch which then stimulate peripheral chemoreflex. The cranial nerves X and XI are then stimulated to conduct impulses to the respiratory center in the medulla oblongata in the brainstem
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Front 14

What was noted with older dogs in this study

Back 14

a. Age was correlated with having a higher PaCO2
15

Front 15

Blood pressure, heart rate, and urinary catecholamines in healthy dogs subjected to different clinical settings
What was the effect observed on blood pressure in this study

Back 15

a. Systolic and diastolic blood pressure were higher when measured by the veterinarian alone as well as heart rate
16

Front 16

What was noted about blood pressure among the breeds

Back 16

a. Labs had lower diastolic BP compared to the Dachshunds; Labs also had lower HR and catecholamine concentrations compared to the other dog breeds
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Front 17

What was found to be significant in regards to the catecholamines

Back 17

a. Both epinephrine/creatinine and norepinephrine/creatinine ratios increased after the exam and the ELISA assay was validated for canine urine
18

Front 18

Association of Dietary Copper and Zinc Levels with Hepatic Copper and Zinc Concentrations in Labrador Retrievers
What is copper-associated hepatitis

Back 18

a. Disease seen in Dutch and American Labrador Retrievers where copper accumulates in the canine liver and progresses over several years without signs-> resulting in chronic hepatitis and cirrhosis
19

Front 19

How does zinc work in regards to copper storage disorders

Back 19

a. Zinc is not a copper-chelator but rather works by blocking copper uptake in the enterocytes and it also incudes the endogenous copper chelator metallothionein when it is absorbed in the enterocytes. Copper enters the enterocyte, zinc becomes displaced by copper from the metallothionein binding site forming a copper-metallothionein binding complex (remains in the enterocyte and is shed in the feces)(metallothionein normally complexes with zinc when zinc is consumed)
20

Front 20

What percentage of Labradors in this study had abnormally high levels of copper despite being relatively asyptomatic

Back 20

a. 75%
21

Front 21

What was found to be true of dietary amounts of zinc and copper

Back 21

a. Level of copper in pet food as well as its relative zinc content compared to copper may be a factor in the accumulation of hepatic copper in Labrador Retrievers with a family history of copper-associated hepatitis
22

Front 22

What role did zinc play

Back 22

a. Despite higher levels of zinc or sinc supplementation, copper levels were not lowered unless the diet already contained lower levels
23

Front 23

Hypocalcemia and hypovitaminosis D in dogs with induced endotoxemia
What has been shown previously in dogs and cats regarding low calcium levels in critical settings

Back 23

a. Patients with sepsis that also have the lowest ionized calcium levels stay in hospital longer, dogs that die in hospital also have more severe ionized hypocalcemia, and cats that do not have normalization of their hypocalcemia in hospital are less likely to survive
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Front 24

What was found in dogs that received lipopolysaccharide in this study

Back 24

a. They had fever, tachycardia, tachypnea, hypotension, vomiting, diarrhea, lower ionized and total calcium concentrations-> most likely from hypovitaminosis D (not likely related to alkalosis, increased calciuresis, or hypoparathyroidism); magnesium concentrations were not very different and so not likely influence the calcium levels
25

Front 25

Incidence, Nature, and Etiology of Metabolic Acidosis in Dogs and Cats
What was the conclusion of this study

Back 25

a. Metabolic acidosis was found commonly in a group of patients and was associated with a wide variety of disease processes. Mixed acid base disorders were also frequent so categorizing metabolic acidosis on presence of high AG or hyperchloremia can be misleading
26

Front 26

Plasma inflammatory mediator concentrations at ICU Admission in dogs with naturally developing sepsis
What was found in dogs that had sepsis and noninfectious SIRS

Back 26

a. They were more likely to have measurable TNF activity, and IL-6 concentrations compared to healthy dogs.
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Front 27

What was found about healthy dogs

Back 27

a. They were more likely to have increased levels of IL-10 compared to dogs with sepsis but not when compared to noninfectious SIRS.
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Front 28

Were the biomarkers sensitive or specific in predicting survival to discharge or differentiating sepsis from noninfectious SIRS

Back 28

a. No
29

Front 29

What kind of cytokine is IL-10

Back 29

a. Anti-inflammatory cytokine
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Front 30

The immunopathology of sepsis: pathogen recognition, systemic inflammation, the compensatory anti-inflammatory response, and regulatory T-cells
What is SIRS

Back 30

a. Systemic inflammatory response syndrome which is the clinical manifestation of the systemic response to injury
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Front 31

What is Sepsis

Back 31

a. SIRS in association with bacteria, viral, protozoal, or fungal infection
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Front 32

What is severe sepsis

Back 32

a. Sepsis together with evidence of organ dysfunction, hypoperfusion, or hypotension
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Front 33

What is Septic shock

Back 33

a. Sepsis with hypotension despite adequate fluid recusitation
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Front 34

What is MODS

Back 34

a. Multiple organ dysfunction syndrome which is altered organ function in acutely ill patients such that homeostasis cannot be maintained
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Front 35

What are AMPs

Back 35

a. Antimicrobial peptides (host-defense peptides) on mucosal surfaces. Made of 3 groups: digestive enzymes and peptides that bind the microbial cell membrane, peptides that bind essential elements, and peptides that act as decoys for microbial attachment
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Front 36

What are the 2 major classes for bactericidal AMPs

Back 36

a. Defensins and cathelicidins – secreted onto epithelial surfaces of the GIT, respiratory, and urinary tract –secreted by immune cells and atypical defese cells such as type II pneumocytes
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Front 37

What are pattern recognition receptors (PRR)

Back 37

a. Receptors expressed on effector cells of the immune system and also epithelial cells, endothelial cells, and myocytes that recognize pathogen-associated molecular patterns (PAMPS)
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Front 38

What are PAMPS

Back 38

a. Produced only by the microbial pathogen, are generally invariant molecules shared by the entire class of microorganisms, and are usually structures vital to the survival of the microorganism
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Front 39

What are DAMPS

Back 39

a. Danger-associated molecular patterns which are signals from the host cell that signals endogenous cell damage -> “alarmins”
40

Front 40

What are the three families of pattern recognition receptors

Back 40

a. Toll-like receptors
b. Nucleotide-binding domain, Leucine-rich repeat containing proteins (NLR’s, previously NOD)
c. Retinoic acid-inducible gene-1 like receptors (RLR’s)
41

Front 41

What cells express TLR’s

Back 41

a. Dendritic cells, macrophages, b cells, natural killer cells, endothelial cells, epithelial cells, and fibroblasts
42

Front 42

Which TLR’s are expressed on external plasma membranes

Back 42

a. TLRs 1,2,4,5,6, and 11
43

Front 43

Which TLR’s are expressed on endosomes

Back 43

a. TLR 3,7,8,9
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Front 44

Which TLR recognizes PAMPs associated with gram+ bacteria, peptidoglycan, hemagglutin, clostridium, chlamydophila, and herpes simplex

Back 44

a. TLR-2
45

Front 45

Which TLR recognizes PAMPs from lipopolysaccharide, viral protein envelopes

Back 45

a. TLR4
46

Front 46

Which TLR is expressed by epithelial cells of the respiratory and intestinal tract an is a PRR for flagellin

Back 46

a. TLR5
47

Front 47

Where are NLRs typically located in the cell

Back 47

a. Cytoplasm
48

Front 48

What do NLR’s activate when they encounter a PAMP

Back 48

a. Activation of a series of kinases leading to phosphorylation which in turn leads to transcription of inflammatory cytokine genes via mobilization of NF-kB and AP-1. It also activates inflammasome, macromolecule that forms caspase-1 which is important in making IL-1B, IL-18 and induces programmed cell death pyroptosis
49

Front 49

Excessive amounts of what compound has been shown to be implicated in endotoxic shock

Back 49

a. Caspase-1
50

Front 50

What cells activate Tumor necrosis factor alpha

Back 50

a. Macrophages and T cells (also mast cells, b cells, NK cells, neutrophils, endothelial cells, myocytes, osteoblasts, and fibroblasts.
51

Front 51

What are the two types of TNF

Back 51

a. TNFR1: Proinflammatory and apoptotic
b. TNFR2: promotion of tissue repair and angiogenesis
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Front 52

What are the effects of TNFalpha

Back 52

a. Increased production of inducible nitric oxide synthase, and cyclooxygenase leading to vasodilation, stimulates expression of endothelial adhesion molecules such as E-electin, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1
53

Front 53

Which moleculte results in activation of Proinflammatory interleukins such as IL-1, IL-6, CXCL-8, and IL-12

Back 53

a. NF-kB
54

Front 54

What is the function of IL-10

Back 54

a. Inhibits release of TNF-alpha, IL1B, and IL-6. Produces IL-1 receptor antagonist protein and soluble TNFR
55

Front 55

What does the anterior pituitary gland produce that is increased in SIRS and sepsis

Back 55

a. Macrophage migratory inhibitory factor
56

Front 56

How are coagulation and SEPSIS linked

Back 56

a. Increased activation of coagulation, as well as downregulation of anticoagulant mechanisms and reduced fibrinolysis in human SIRS and sepsis patients. Large numbers of tisse factor expessing microparticles have been identified in blood samples from septic human patients and may correlate with mortality, stimulating extrinsic pathway
57

Front 57

What has been shown to inhibit coagulation in sepsis

Back 57

a. Activated protein C
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Front 58

What is ADAMTS-13

Back 58

a. Disintegrin-like and metalloproteinase with thrombospondin-1 motifs-13 is produced by stellate Ito cells in liver an acts to cleave ultra large von Willebrand’s factor into smaller multimers. Decreased ADAMTS-13 has been shown to be associated with a poor prognosis in human sepsis patients
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Front 59

What is CARS

Back 59

a. Compensatory anti-inflammatory response syndrome thoguth to be an adaptive response to the excessive Proinflammatory process in SIRS
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Front 60

What is responsible for a majority of the immune cell death in sepsis

Back 60

a. Apoptosis or type 1 programmed cell death. Other lesser frequent potentials include autophagy (cellular clean up process) and pyroptosis (caspase-1 mediated apoptosis)
61

Front 61

What is the role of T-regulatory cells

Back 61

a. Plays role in peripheral tolerance, complementing the intrinsic mechanisms. They interact with cells of the innate and adaptive immune system mediating a suppressive function to prevent the development of autoaggressive responses and maintain the population of peripheral CD4+ T cells. They also express a variety of TLR’s, also secrete immunosuppressive cytokines including IL-10 and TGF-B