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55 Cards in this Set

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

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
How do Host defense peptides (HDP) target organisms

a. Look for anything with a cholesterol-free, negatively charged membrane but can also kill transformed or cancerous cells
103
Alpha defensins are predominantly located in what cell

a. Neutrophils, constitutively expressed
104
How are cathelicidins stored

a. Inactive propeptides and processed upon stimulation resuling in release of active HDP in ECF, typically expressed in mylleoid precursor cells
105
How are defensins antimicrobial and cytotoxic

a. Form pores in membrane
106
How do TLR and Nod proteins trigger the production of HDP

a. Through NF-kB
107
What is the biological activity of HDP

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.
108
What is the role of HDP and antibiotics

a. Can act synergistically with certain conventional antibiotics targeted at Gram negative as well as gram positive bacteria
109
Continuous Glucose Monitoring in Dogs and Cats 2008
How do continuous glucose monitoring devices work

a. They measure subcutaneous interstitial fluid glucose concentrations, shown to correlate well with blood concentrations
110
What is necessary on a daily basis when using a continuous glucose monitoring device

a. To calibrate the machine with 3 blood glucose samples
111
What are disadvantages to continuous glucose monitoring

a. Sensor can become detached from the skin, can only measure a range between 40 and 400 mg/dL
112
What are the advantages of continuous glucose monitoring

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
Illness Severity Scores in Veterinary Medicine: What Can we learn
2010
What is an illness score

a. Number assigned to a patient that correlates with a probability that a specific outcome will follow. Can be diagnosis dependent or independent
114
What are limitations of illness scores

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
115
What are some of the benefits of illness scores

a. Assist prediction of requirement for ICU care and appropriate triage, used as a performance measure
116
What are the diagnosis independent scoring systems used for humans vs. animals

a. Humans: APACHE, MPM, SAPS, and ICNARC
b. Animals: SPI and SPI2
117
Cachexia and Sarcopenia: Emerging Syndromes of Importance in Dogs and Cats
What is the definition of cachexia

a. Loss of lean body mass (causes in humans include CHF, cancer, chronic kidney disease, AIDS, chronic obstructive pulmonary disease, and rheumatoid arthritis
118
What is the difference between weight loss and healthy animals versus cachexia

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
119
How does the loss of lean body mass affect the body

a. Deleterious effects on strength, immune function, wound healing, and survival; cachexia is an independent predictor of survival in people
120
How can one measure lean body mass

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
121
What is sarcopenia

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
122
Have causes for sarcopenia been identified

a. No, CRP, TNF alpha, and IGF-1 have been studied and not statistically different among groups
123
Dogs with what kind of heart disease have more advanced muscle loss

a. Dogs with right sided CHF
124
What is the obesity paradox

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
125
What are the proposed mechanisms behind cachexia in various types of disease

a. Increased caloric requirements, decreased nutrient absorption, decreased energy intake, metabolic alterations, and increased inflammatory cytokines
126
How does ghrelin play a role in cachexia

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
127
Which signals decrease appetite

a. Leptin, adiponectin, pro-opiomelanocortin, serotonin, insulin, cholecystokinin, glucagon like peptide, alpha melanocyte stimulating hormone
128
Which signals increase appetite

a. Ghrelin, endocannabinoids, agouti-related protein, neuropeptide y
129
Which inflammatory cytokines are known to cause cachexia

a. TNF, interleukin 1B (IL-1), interleukin-6
130
Which drugs have been theorized to help ameliorate inflammatory cytokine production

a. Omega-3 fatty acids, ACE inhibitors (primarily through inhibition of RAAS system which is catabolic), beta blockers, Amiodarone, levosimendan
131
Which proteolytic pathway has been shown to be the most important pathway in cachexia

a. Ubiquitin-proteosome pathway mediated by NF-kB
132
What is myostatin

a. Member of TGF beta super family that negatively impacts skeletal muscle mass, can be decreased by exercise training
133
How are adipokines related in cachexia

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
134
How have omega-3 fatty acids been used in cachexia

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
135
Potential adverse effects of omega-3 fatty acids in dogs and cats 2013
How are omega-3 fatty acids considered anti-inflammatory

a. EPA and DHA in plasma membranes result in production of different eicosanoids that are less Proinflammatory compared to those derived from Arachadonic acid
136
How do omega-3 fatty acids affect platelet function

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)
137
How can omega-3 fatty acids result in diarrhea

a. If they are undigested, can act as a substrate for bacteria in the upper GI tract and predispose to secretory diarrhea
138
Is there a known risk of pancreatitis with omega-3 fatty acids

a. No, may be even reduced since omega-3 fatty acids reduce hypertriglyceridemia
139
What is lipid peroxidation and how is it prevented

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
140
Is there any evidence of toxin exposure or nutrient excess or weight gain with omega-3 fatty acid supplementation or hyperglycemia

a. No
141
A Review of the Studies Using Buprenorphine in Cats 2014
Are plasma concentrations of buprenorphine correlated with analgesia

a. No
142
Is there a ceiling effect with buprenorphine

a. No
143
What is the MOA for buprenorphine

a. Partial agonist at mu opioid receptors
144
What behavioral effects can buprenorphine have

a. Euphoria, purring, rolling, rubbing, and kneading with forepaws
145
What are some adverse effects with buprenorphine

a. Vomiting, nausea, dysphoria, hyperthermia (rare), mydriasis
146
What route is not recommended at clinical doses by the author

a. Subcutaneous administration; optimal pain relief is when given IV or IM and when combined with an NSAID
147
Multiple Organ Dysfunction Syndrome in Humans and Animals 2014
MODS is a Sequelae of what processes

a. Sepsis, septic shock, trauma, neoplasia, and SIRS
149
What is the definition of MODS

a. Presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention
150
What are the proposed mechanisms behind MODS

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
151
Unchecked CARS (compensatory anti-inflammatory response syndrome)can result in what

a. Immunoparalysis which leaves the host vulnerable to further injury and infection
152
Describe mitochondrial dysfunction

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
153
What are the two stages of hepatic dysfunction

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
154
What are the two ways in which ARDS can occur

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
155
What complement mediator is theorized to play a role in myocardial dysfunction

a. C5a
156
What is the most common form of AKI specific to MODS

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