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61 Cards in this Set

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

a. 5 days
2
What CBC parameters would indicate that the bone marrow is not able to keep up with increased demand

a. Band neutrophils with normal to low numbers of mature neutrophils= degenerative left shift
3
Dogs with a degenerative left shift were found to have 2 fold greater risk of what

a. Death or euthanasia
4
Which disease processes seemed to affect outcome regardless of the presence of DLS

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

a. Base excess was correlated with survival in dogs with diabetic ketoacidosis and bicarbonate concentration has been inversely correlated with mortality in cats.
6
What are causes of a metabolic alkalosis

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
What causes a metabolic acidosis

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
What was the most common abnormality found in this experimental group

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
9
What electrolyte changes were most common in animals with a metabolic alkalosis

a. Hypokalemia and hypochloridemia
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

a. Upper airway resistance because of narrowed nostrils, elongated and thickened soft palate, everted laryngeal saccules and a hypoplastic trachea; possibly prominent nasopharyngeal turbinates.
11
What is sleep apnea/hypopnea syndrome (SAHS)

a. Complete upper airway collapse during sleep that can result in intermittent nocturnal hypoxemia and systemic hypertension
12
How did brachycephalic dogs compare to non-brachycephalic dogs with respect to PaO2, PCV, PaCO2, and arterial blood pressure

a. Brachycephalic dogs had lower PaO2, higher PCV, higher PaCO2, and higher BP when compared to the control group.
13
How are the peripheral chemoreflex stimulated in situations of chronic hypoxemia

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
14
What was noted with older dogs in this study

a. Age was correlated with having a higher PaCO2
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

a. Systolic and diastolic blood pressure were higher when measured by the veterinarian alone as well as heart rate
16
What was noted about blood pressure among the breeds

a. Labs had lower diastolic BP compared to the Dachshunds; Labs also had lower HR and catecholamine concentrations compared to the other dog breeds
17
What was found to be significant in regards to the catecholamines

a. Both epinephrine/creatinine and norepinephrine/creatinine ratios increased after the exam and the ELISA assay was validated for canine urine
18
Association of Dietary Copper and Zinc Levels with Hepatic Copper and Zinc Concentrations in Labrador Retrievers
What is copper-associated hepatitis

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
How does zinc work in regards to copper storage disorders

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

a. 75%
21
What was found to be true of dietary amounts of zinc and copper

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
What role did zinc play

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

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
24
What was found in dogs that received lipopolysaccharide in this study

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

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

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

a. They were more likely to have increased levels of IL-10 compared to dogs with sepsis but not when compared to noninfectious SIRS.
28
Were the biomarkers sensitive or specific in predicting survival to discharge or differentiating sepsis from noninfectious SIRS

a. No
29
What kind of cytokine is IL-10

a. Anti-inflammatory cytokine
30
The immunopathology of sepsis: pathogen recognition, systemic inflammation, the compensatory anti-inflammatory response, and regulatory T-cells
What is SIRS

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

a. SIRS in association with bacteria, viral, protozoal, or fungal infection
32
What is severe sepsis

a. Sepsis together with evidence of organ dysfunction, hypoperfusion, or hypotension
33
What is Septic shock

a. Sepsis with hypotension despite adequate fluid recusitation
34
What is MODS

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

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
36
What are the 2 major classes for bactericidal AMPs

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
37
What are pattern recognition receptors (PRR)

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)
38
What are PAMPS

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
39
What are DAMPS

a. Danger-associated molecular patterns which are signals from the host cell that signals endogenous cell damage -> “alarmins”
40
What are the three families of pattern recognition receptors

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
What cells express TLR’s

a. Dendritic cells, macrophages, b cells, natural killer cells, endothelial cells, epithelial cells, and fibroblasts
42
Which TLR’s are expressed on external plasma membranes

a. TLRs 1,2,4,5,6, and 11
43
Which TLR’s are expressed on endosomes

a. TLR 3,7,8,9
44
Which TLR recognizes PAMPs associated with gram+ bacteria, peptidoglycan, hemagglutin, clostridium, chlamydophila, and herpes simplex

a. TLR-2
45
Which TLR recognizes PAMPs from lipopolysaccharide, viral protein envelopes

a. TLR4
46
Which TLR is expressed by epithelial cells of the respiratory and intestinal tract an is a PRR for flagellin

a. TLR5
47
Where are NLRs typically located in the cell

a. Cytoplasm
48
What do NLR’s activate when they encounter a PAMP

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

a. Caspase-1
50
What cells activate Tumor necrosis factor alpha

a. Macrophages and T cells (also mast cells, b cells, NK cells, neutrophils, endothelial cells, myocytes, osteoblasts, and fibroblasts.
51
What are the two types of TNF

a. TNFR1: Proinflammatory and apoptotic
b. TNFR2: promotion of tissue repair and angiogenesis
52
What are the effects of TNFalpha

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

a. NF-kB
54
What is the function of IL-10

a. Inhibits release of TNF-alpha, IL1B, and IL-6. Produces IL-1 receptor antagonist protein and soluble TNFR
55
What does the anterior pituitary gland produce that is increased in SIRS and sepsis

a. Macrophage migratory inhibitory factor
56
How are coagulation and SEPSIS linked

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
What has been shown to inhibit coagulation in sepsis

a. Activated protein C
58
What is ADAMTS-13

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
59
What is CARS

a. Compensatory anti-inflammatory response syndrome thoguth to be an adaptive response to the excessive Proinflammatory process in SIRS
60
What is responsible for a majority of the immune cell death in sepsis

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
What is the role of T-regulatory cells

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