Consensus Fluid/cc Sc 3

Front 1

Innate Immunity and Host Defense Peptides in Veterinary Medicine
What are the three main categories of host defense peptides

Back 1

a. Digestive enzymes targeting microbial structures (lysozyme)
b. Peptides that bind essential elements such as zinc or iron (calprotectin, lactoferrin)
c. Peptides that disrupt microbial membrane (defensins and cathelicidins)
102

Front 2

How do Host defense peptides (HDP) target organisms

Back 2

a. Look for anything with a cholesterol-free, negatively charged membrane but can also kill transformed or cancerous cells
103

Front 3

Alpha defensins are predominantly located in what cell

Back 3

a. Neutrophils, constitutively expressed
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Front 4

How are cathelicidins stored

Back 4

a. Inactive propeptides and processed upon stimulation resuling in release of active HDP in ECF, typically expressed in mylleoid precursor cells
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Front 5

How are defensins antimicrobial and cytotoxic

Back 5

a. Form pores in membrane
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Front 6

How do TLR and Nod proteins trigger the production of HDP

Back 6

a. Through NF-kB
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Front 7

What is the biological activity of HDP

Back 7

a. Abundant in circulating neutrophils and participate in inflammatory response by activing as chemoattractant s for immune cells (including neutrophil recruitment by induction of IL-8) production and mobilization of immunocompetent T-cells. Are encoded from peptides from an RNA template and there is no evidence of microbial resistance to them.
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Front 8

What is the role of HDP and antibiotics

Back 8

a. Can act synergistically with certain conventional antibiotics targeted at Gram negative as well as gram positive bacteria
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Front 9

Continuous Glucose Monitoring in Dogs and Cats 2008
How do continuous glucose monitoring devices work

Back 9

a. They measure subcutaneous interstitial fluid glucose concentrations, shown to correlate well with blood concentrations
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Front 10

What is necessary on a daily basis when using a continuous glucose monitoring device

Back 10

a. To calibrate the machine with 3 blood glucose samples
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Front 11

What are disadvantages to continuous glucose monitoring

Back 11

a. Sensor can become detached from the skin, can only measure a range between 40 and 400 mg/dL
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Front 12

What are the advantages of continuous glucose monitoring

Back 12

a. Measures BG every 5 minutes, does not necessitate the patient being in the hospital, alleviates multiple phlebotomies on patients that need aggressive monitoring such as patients with DKA, easily tolerated by patients (dogs and cats) and the monitor is small and can be wireless. The recording device is about the size of a deck of cards and can be worn as a backpack on the patient
113

Front 13

Illness Severity Scores in Veterinary Medicine: What Can we learn

Back 13

2010
What is an illness score

Hint 13

a. Number assigned to a patient that correlates with a probability that a specific outcome will follow. Can be diagnosis dependent or independent
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Front 14

What are limitations of illness scores

Back 14

a. That they are frequently outperformed by clinicians who are experienced and that they are not appropriate to score individual patients or prognosticate a single patient
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Front 15

What are some of the benefits of illness scores

Back 15

a. Assist prediction of requirement for ICU care and appropriate triage, used as a performance measure
116

Front 16

What are the diagnosis independent scoring systems used for humans vs. animals

Back 16

a. Humans: APACHE, MPM, SAPS, and ICNARC
b. Animals: SPI and SPI2
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Front 17

Cachexia and Sarcopenia: Emerging Syndromes of Importance in Dogs and Cats
What is the definition of cachexia

Back 17

a. Loss of lean body mass (causes in humans include CHF, cancer, chronic kidney disease, AIDS, chronic obstructive pulmonary disease, and rheumatoid arthritis
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Front 18

What is the difference between weight loss and healthy animals versus cachexia

Back 18

a. Healthy animals utilize fat for energy during states of negative energy balance whereas cachectic animals use muscle for energy and not fat during negative energy balance
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Front 19

How does the loss of lean body mass affect the body

Back 19

a. Deleterious effects on strength, immune function, wound healing, and survival; cachexia is an independent predictor of survival in people
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Front 20

How can one measure lean body mass

Back 20

a. Body weight is insensitive and weight loss can be masked by accumulation of fat or water. Identification of cachexia is extremely difficult in the earlier stages when it is subtle. Muscle condition score is proposed as it specifically evaluates muscle mass via visual inspection and palpation
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Front 21

What is sarcopenia

Back 21

a. Syndrome characterized by progressive and generalized loss of skeletal muscle mass and strength with a risk of adverse clinical outcomes such as physical disability, poor quality of life, and death. These patients do not have disease unlike cachexia. Loss of LBM is also accompanied with increase in fat mass so total weight may not change
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Front 22

Have causes for sarcopenia been identified

Back 22

a. No, CRP, TNF alpha, and IGF-1 have been studied and not statistically different among groups
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Front 23

Dogs with what kind of heart disease have more advanced muscle loss

Back 23

a. Dogs with right sided CHF
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Front 24

What is the obesity paradox

Back 24

a. Obesity is a risk factor for development of heart disease and other inflammatory conditions but dogs and cats that are obese when they develop cardiac or renal disease tend to have improved survival compared to those who are normal or underweight
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Front 25

What are the proposed mechanisms behind cachexia in various types of disease

Back 25

a. Increased caloric requirements, decreased nutrient absorption, decreased energy intake, metabolic alterations, and increased inflammatory cytokines
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Front 26

How does ghrelin play a role in cachexia

Back 26

a. Ghrelin is an endogenous ligand for growth hormone secretagogue receptor and is secreted by gastric endocrine cells in response to fasting. It modulates growth hormone secretion and IGF-1 secretion, stimulates neuropeptide Y and AgRP (agouti-related protein), decreases pro-opiomelanocortin, attenuates cardiac and renal sympathetic tone, stimulates gastric motility, and has anti-inflammatory effects. Ghrelin has been shown to be increased in patients with CHF and CKD so it is theorized that there can be some degree of ghrelin resistance as patients that were supplemented with ghrelin had improvement in their appetites
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Front 27

Which signals decrease appetite

Back 27

a. Leptin, adiponectin, pro-opiomelanocortin, serotonin, insulin, cholecystokinin, glucagon like peptide, alpha melanocyte stimulating hormone
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Front 28

Which signals increase appetite

Back 28

a. Ghrelin, endocannabinoids, agouti-related protein, neuropeptide y
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Front 29

Which inflammatory cytokines are known to cause cachexia

Back 29

a. TNF, interleukin 1B (IL-1), interleukin-6
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Front 30

Which drugs have been theorized to help ameliorate inflammatory cytokine production

Back 30

a. Omega-3 fatty acids, ACE inhibitors (primarily through inhibition of RAAS system which is catabolic), beta blockers, Amiodarone, levosimendan
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Front 31

Which proteolytic pathway has been shown to be the most important pathway in cachexia

Back 31

a. Ubiquitin-proteosome pathway mediated by NF-kB
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Front 32

What is myostatin

Back 32

a. Member of TGF beta super family that negatively impacts skeletal muscle mass, can be decreased by exercise training
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Front 33

How are adipokines related in cachexia

Back 33

a. Research in humans and animals is ongoing and variable. Studies in people showed that those with cacheix and CHF had higher levels of adiponectin
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Front 34

How have omega-3 fatty acids been used in cachexia

Back 34

a. They have been shown to decrease TNF and IL-1 and decrease muscle loss in dogs with CHF and improve appetite in some animals. Flax seed should be avoided because of inefficient conversion to EPA and DHA
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Front 35

Potential adverse effects of omega-3 fatty acids in dogs and cats 2013
How are omega-3 fatty acids considered anti-inflammatory

Back 35

a. EPA and DHA in plasma membranes result in production of different eicosanoids that are less Proinflammatory compared to those derived from Arachadonic acid
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Front 36

How do omega-3 fatty acids affect platelet function

Back 36

a. Result in production of thromboxane A3 which is less potent than thromboxane A2 so have less platelet aggregation (this is not suspected to be clinically relevant however)
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Front 37

How can omega-3 fatty acids result in diarrhea

Back 37

a. If they are undigested, can act as a substrate for bacteria in the upper GI tract and predispose to secretory diarrhea
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Front 38

Is there a known risk of pancreatitis with omega-3 fatty acids

Back 38

a. No, may be even reduced since omega-3 fatty acids reduce hypertriglyceridemia
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Front 39

What is lipid peroxidation and how is it prevented

Back 39

a. Free radical attack on unsaturated fatty acid that can occur in presence of oxygen. Prevent by having sufficient vitamin E as vitamin E is a hydrogen donor to free radicals
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Front 40

Is there any evidence of toxin exposure or nutrient excess or weight gain with omega-3 fatty acid supplementation or hyperglycemia

Back 40

a. No
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Front 41

A Review of the Studies Using Buprenorphine in Cats 2014
Are plasma concentrations of buprenorphine correlated with analgesia

Back 41

a. No
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Front 42

Is there a ceiling effect with buprenorphine

Back 42

a. No
143

Front 43

What is the MOA for buprenorphine

Back 43

a. Partial agonist at mu opioid receptors
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Front 44

What behavioral effects can buprenorphine have

Back 44

a. Euphoria, purring, rolling, rubbing, and kneading with forepaws
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Front 45

What are some adverse effects with buprenorphine

Back 45

a. Vomiting, nausea, dysphoria, hyperthermia (rare), mydriasis
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Front 46

What route is not recommended at clinical doses by the author

Back 46

a. Subcutaneous administration; optimal pain relief is when given IV or IM and when combined with an NSAID
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Front 47

Multiple Organ Dysfunction Syndrome in Humans and Animals 2014
MODS is a Sequelae of what processes

Back 47

a. Sepsis, septic shock, trauma, neoplasia, and SIRS
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Front 48

What is the definition of MODS

Back 48

a. Presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention
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Front 49

What are the proposed mechanisms behind MODS

Back 49

a. Cell or tissue hypoxia; induction of cellular apoptosis, translocation of microbes or compenents of microbes from the gastrointestinal tract, immune system Dysregulation, mitochondrial dysfunction
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Front 50

Unchecked CARS (compensatory anti-inflammatory response syndrome)can result in what

Back 50

a. Immunoparalysis which leaves the host vulnerable to further injury and infection
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Front 51

Describe mitochondrial dysfunction

Back 51

a. Oxidative stress and Proinflammatory cytokine signaling lead to uncoupling of oxidative phosphorylation via mitochondrial permeability transition (a pore is opened in the innter mitochondrial membrane allowing inappropriate proton gradient within the mitochondria and uncoupling of oxidation from phosphorylation-> cytopathic hypoxia
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Front 52

What are the two stages of hepatic dysfunction

Back 52

a. Primary stage, septic shock results in hepatic hypoperfusion leading to decreaed protein production, lactate clearance, gluconeogenesis, and glycogenolysis
b. Second stage, kuppfer cell activation and production of Proinflammatory cytokines, reactive oxygen species, and NO leading to further liver damage.
c. See hyperbilirubinemia with no preexisting liver disease
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Front 53

What are the two ways in which ARDS can occur

Back 53

a. Direct pulmonary causes or indirect causes from sepsis, pancreatitis, burns, trauma, transfusions
b. Characterized by neutrophil infiltration, alveolar-capillary barrier damage, pulmonary vascular leakage, and release of Proinflammatory cytokines
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Front 54

What complement mediator is theorized to play a role in myocardial dysfunction

Back 54

a. C5a
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Front 55

What is the most common form of AKI specific to MODS

Back 55

a. Apoptosis caused by inflammatory cytokines and endotoxin appears to be a predominant form of AKI from sepsis