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277 Cards in this Set
- Front
- Back
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What is the fungus that calls Aspergillosis?
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Aspergillus fumigatus
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Is Aspergillosis infectious? Contagious?
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Infectious, non-contagious
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Aspergillosis is a major cause of mortality in [captive or free-living] birds
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More commonly in captive birds
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What part of the body does Aspergillosis predominantly affect?
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It is predominantly a disease of the resp. tract, but all organs can be involved
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What are some important causative factors of Aspergillosis?
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Impaired immunity and the inhalation of a considerable amt. of spores
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Even though Aspergillosis is mostly caused by A. fumigatus, what are some other species that could cause Aspergillosis?
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A. flavus, A. niger, A. glaucus, A. nidulans, and others
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What is a possible reason for why A. fumigatus is the predominant species of airborne funfal infections?
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The spores are much smaller than the spores of other Aspergillus species
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What environmental factors could predispose a bird to aspergillosis?
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Increased concentration of spores in environment, a warm environment, humidity, poor ventilation, poor sanitation, and the long-term storage of feed may increase the amt. of spores in the air
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What are some factors impairing the bird's immunity that can also predispose them to mycosis?
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Tetracyclines, long-term steroids, vaccination, metabolic bone disease, an inadequate diet resulting in hypovitaminosis A, overcrowding, shipping, quarantine or capture of wild birds, starvation, thermal discomfort, migration, inbreeding, toxicosis, traumatic injuries, & repro. activity
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What is the main infection route in birds to Aspergillosis?
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Inhalation
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What's usually the primary infection site in Aspergillosis?
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Air sacs since inhaled air reaches the posterior thoracic and abdominal air sacs prior to contacting epithelial surfaces in the lungs
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How do the spores of Aspergillus affect the lung parenchyma? And how does the lung parenchyma react?
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They get embedded in the atria & parts of the infundibula in the parabronchus. They are then engulfed by (surface) phagocytic epithelial cells
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What happens if there are too many spores or the bird has an impaired immune response?
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The innate mechanisms do not succeed in getting rid of infection. This may lead to development of loosely attached plaques, which may or may not become overgrown by CT of host. These plaques can obstruct trachea or bronchi &/or fill up lungs & air sacs.
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Where does sporulation occasionally occur?
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In the lungs and air sacs
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What do hyphae do to the air sacs?
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Hyphae containing fruiting bodies can fill the lumen & may penetrate the air sacs, causing serositis and superficial necrosis in the adjacent organs
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Besides direct extension of the infection through the air sac wall, how else does disseminated mycosis occur?
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By hematogenous spread
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What plays a role in the spreading mechanism?
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Hyphae, which are known to be tissue and angio-invasive, as well as host cells play a role.
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How do host cells play a role in spreading mechanism?
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Macrophages in the resp. tract ingest spores and find their way thru the interstitium into the blood & lymphatic stream & thus to other organs
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What are the 2 types of tissue reactions recognized?
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The granulomatous or deep nodular form & the infiltrative or superficial diffuse form
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Which type of tissue reaction is encapsulated?
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Granulomatous or deep nodular form
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In which form does the fungus frequently invade the blood vessels?
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Infiltrative or superficial diffuse form
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Which type of tissue reaction occurs in both aerated and non-aerated organs?
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Granulomatous or deep nodular forms
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A mixed type composed of both tissue reactions in the same tissue section is also possible. T or F?
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True
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Is it true that the scarcity of free avian resp. macrophages results in an inadequate or incompetent avian resp. immune system & is therefore responsible for the high susceptibility of birds to resp. pathogens?
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That is an assumption and lacks scientific foundation. Instead, it may be attributed to diff. in anatomical, physiological and resp. immune system characteristics compared w/ mammals.
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What do clinical manifestations depend on?
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The infective dose, the spore distribution, pre-existing diseases, and the immune response of the host
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What is the diff. b/w acute aspergillosis and chronic aspergillosis?
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Acute aspergillosis is thought to be the result of inhaling an overwhelming # of spores. Chronic aspergillosis is generally a/w immune suppression.
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What are some clinical signs of Aspergillosis?
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Exudative rhinitis, malformation of beak & cere, periorbital swelling, turbid discharge, swollen eyelids, neuro signs, epidermal cysts on comb, right ventricular dilation, unilateral drooping of wing
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How can Aspergillosis be diagnosed?
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Dx. is difficult due to signs being non-specific. Dx. usually relies upon accumulation of evidence from hx., clinical presentation, hematology, & biochem., serology, rad. changes, endoscopy, and culture of fungus
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What evidence can be taken from the history?
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Hx. can reveal a stressful event &/or some underlying environmental factors &/or an immunosuppressive condition or tx. It may also reveal chronic debilitation, voice change, or exercise intolerance.
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What do clinical signs depend on?
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Depend on which form of aspergillosis the bird develops and which organs are involved.
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Are results of hematology and plasma biochem. considered indicative or diagnostic?
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Indicative
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What is usually seen on hematology and plasma biochem. of a bird with aspergillosis?
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Leukocytosis, heterophilia w/ left shift, monocytosis, lymphopenia, non-regen. anemia, increased TP, increased globulin fraction
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How will the increase in globulin fraction be different b/w acute & chronic infections?
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Acute infections often present an increase in beta-globulins. Chronic infections show an increase in beta-globulin and/or gamma-globulin fractions.
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What are the serological test methods that have been applied in birds?
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Counter-immunoelectrophoresis, agar gel immunodiffusion, and enzyme-linked immunosorbent assays
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In the acute stage, antibody production trails behind antigen exposure by _______ days
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10-14 days
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What could cause a false negative result in a serological test?
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If the bird is immunosuppressed, the low antibody production results in false negative results
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In acute infections or immunosuppressed birds, what would be most helpful in detecting?
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Serum antigen
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What would be more helpful in detecting in chronic cases?
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Antibodies (b/c antigen levels may be low)
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Although radiographs are not diagnostic, what radiographic changes can be seen?
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Radiographic changes of pneumonia and consolidating airsacculitis (non-specific)
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Although endoscopy is invasive & requires anesthesia, what can it be helpful in seeing?
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Allows the extent of the lesions to be seen as well as the progress of infection during tx. Useful for showing a single lesion, such as a plaque. Samples for cytology & culture can be taken.
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What can be used to best evaluate the lower resp. tract?
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Laparoscopy
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What gross lesions can be seen on a necropsy of a chronic infection of aspergillosis?
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Yellow, green, or white granulomatous foci can be noted in chronic aspergillosis patients
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What gross lesions can be seen on a necropsy of an acute infection of aspergillosis?
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Numerous miliary granulomatous foci
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How could a definitive diagnosis be made?
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Presence of organism by cytology or histopath. & its ID by culture. Aspergillus is ubiquitous & can be a contaminant so an ABUNDANT culture from any organ should be regarded as diagnostic.
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Why are histopathological lesions suggestive, but diagnostic, of aspergillosis?
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B/c in vivo hyphae of hyaline filamentous fungi are very similar and their in situ manifestations are not pathognomonic
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What makes treating aspergillosis difficult?
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Ltd knowledge on pharmacokinetics of antifungal agents in diff. bird species, granulomatous infection makes if difficult for drug to reach fungus, presence of concurrent dz &/or immunosuppression, and the late stage at which birds are usually presented
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What is the best way to overcome the disease?
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Topical therapy after removing the granulomatous tracheal lesions by suction. This can be used in combo with an early, aggressive systemic antifungal therapy.
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Why are granulomatous lesions difficult to remove in most birds?
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B/c of their location within the resp. system and b/c of the risk of surgical trauma & anesthesia
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How is topical therapy administered?
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By nebulization, nasal or air sac flushing, or surgical irrigation of the abdominal cavities, while systemic therapy can be administered intravenously and orally
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How can Aspergillosis be prevented?
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Vaccinations have been attempted. Questionable in immunosuppressed birds that would need passive immunization w/ Ig. Immune stimulants have been suggested, incl. Levamisole for chronic infections.
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Characteristics of fungi?
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Eukaryotic, multicellular, non-motile, aerobic, cell wall mde of chitin & glucans, ergosterol
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What is mycosis?
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Disease caused by multiplication of fungi in the body or by the immune response to these organisms
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What are some fungi of medical importance?
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Aspergillus sp., Candida sp., Macrorhabdus ornithogaster, Cryptococcus sp., Histoplasma sp., Dermatophytes, and Zygophycetes
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What organs are affected by acute aspergillosis?
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Lungs and air sacs
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What are the 3 chronic forms of aspergillosis?
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Focal, generalized, disseminated
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What is affected by the focal chronic form?
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Nasal, sinuses, and trachea
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What's affected by the generalized chronic form?
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Lungs and air sacs
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What's affected by the disseminated chronic form?
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Multiple organs, including eyes, liver, gonads, bone marrow, kidney, etc.
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What are the wet mounts used for Aspergillus?
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KOH with Parker Ink, India ink, lactophenol cotton blue, calcofluor white w/ 10% KOH, Grocott's Methenamine Silver (GMS) stain
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What are the cultures that can be used for Aspergillus?
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Sabouraud's dextrose agar, potato dextrose agar, bird seed agar, and Czapek Dox Agar for Aspergillus & Penicillium
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Why is Sabouraud's dextrose agar preferred?
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B/c it has antibiotics to get rid of bacteria so that only fungus will show up
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What do Sabouraud's dextrose agar and potato dextrose agar have in common?
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Carbs and protein
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What is PCR? What does it do?
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Polymerase Chain Reaction takes few copies of DNA and amplifies. Used to confirm presence of microorganism.
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What is the etiology of Candidiasis?
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Candida albicans
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What body system is Candidiasis a/w?
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Gastrointestinal
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Candida albicans is a saprophyte. What is a saprophyte?
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Fungi that obtains its nutrients from dead or decaying matter. Inhabits parts of the body and do not cause any disease.
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What are the predisposing factors to Candidiasis?
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Crop paralysis, hypovitaminosis A, concurrent disease, immunosuppresion, and PROLONGED ANTIBIOTIC THERAPY
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What is Macrorhabdus ornithogaster?
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Megabacteria
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What are the innate immune responses to infection?
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Physical barrier, commensal flora, inflammation, complements, cytokines, chemokines, heterophils, dendritic cells, macrophages, and other antigen-presenting cells
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What is commensal flora?
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Located in resp. tract & GI tract. When in equilibrium, they keep bad bacteria from overgrowing.
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What are the complements used?
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C3a, C3b, C5a
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What is the most infective form of aspergillus?
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Conidia spores
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What is the first line of cellular defense against fungal infection?
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Macrophages
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Where are the macrophages present?
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Upper resp. tract
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How do macrophages play a role in which birds are more susceptible to aspergillosis?
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Some birds are more susceptible to aspergillosis than others. It could be due to the # of macrophages present - differs by species.
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What are the birds' neutrophils called?
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Heterophils
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What are the fungal mechanisms aimed to avoid host defenses?
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Thermal tolerance, morph type hyphae, toxins, enzymes, number of microorganisms
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Explain morph type hyphae
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Morph type hyphae > TLR2 > Il-10 pathway >> switch to Th2 profile
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What are the toxins used by the fungus to avoid host defenses?
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Funagillin, Helvolic acid, and Gliotoxin
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What are the enzymes used by the fungus to avoid host defenses?
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Elastase, hyaluronidase, collagenase, etc.
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What do they enzymes do?
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Help to break down elastic, collagen, CT, and invade the bloodstream. In acute form, the enzymes will be on overload.
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What is the potent toxin produced by Aspergillus fumigatus?
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Gliotoxin
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What does gliotoxin do?
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Capable of suppressing T cell response and inducing apoptosis in monocytes
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What are some problems with humoral diagnosis of fungal infections?
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Commensals, cross-reactivity, # of species, lack of reagents, and immunosuppression
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Cellular and humoral immune response to influenza virus?
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CD8T cells and Atb anti H and anti N
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Where does B cell production occur in birds?
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Bursa of Fabricius
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When does B cell production and diversification occur?
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Over only a few weeks early in life
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Where do B cells mature?
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Within the bursa of fabricius
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B cell receptor diversity increases by which mechanism?
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Gene conversion
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Which B cells are eliminated?
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Self-reactive B cells
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Which cells produce antibodies?
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Plasma cells
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What are antibodies?
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Gamma globulins; soluble glycoproteins
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Which antibodies are in plasma? And which are in mucosal surfaces?
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IgG & IgM are in plasma. IgA is in mucosal surfaces.
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What are the antibodies in avians?
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IgM, IgA, IgY
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What are metallothioneins (MT)?
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Cysteine- & metal-rich proteins containing sulfur-based metal clusters formed with zinc, cadmium, and copper ions
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How many isoforms of MTs are there in mammals?
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4 (MT-1 thru MT-4)
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Which MT's are inducible?
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MT-1 & 2
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How can MT's 1 & 2 be induced?
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Wide range of stimuli, incl. metals, drugs, and inflammatory mediators
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Which MT is expressed in the CNS?
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MT-3
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Which MT is expressed in cornified and stratified squamous epithelium?
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MT-4
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Which MT's have been reported to be secreted?
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MT-1, MT-2, & MT3
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What are some function of MT's?
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Involvement in zinc & copper homeostasis, protection against heavy metal toxicity, and oxidative damage
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Which MT's are expressed in almost all tissues?
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MT-1 & 2
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What can induce MT-1 & 2?
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Stress conditions and compounds, incl. glucocorticoids, cytokines, reactive oxygen species (ROS), and metal ions
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Which metal toxicity is MT resistant to? (a characteristic of MT, not its evolutionary function)
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Cadmium
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What are the major zinc-binding proteins in the cell?
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MTs
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MTs are efficient scavengers of free ______ radicals formed during various forms of ________________
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Hydroxyl
Oxidative stress |
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The primary targets of the free-radical attack in MTs are _________ groups of the metal-thiolate clusters, which may be repaired in the cell by reduced _________
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Thiolate
Glutathione |
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What is the most distinctive biological property of MT-3?
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Its extracellular growth inhibitory activity in neuronal primary cultures
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Which MT can be toxic?
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MT-3
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Which is the main cell type expressing MT-1 & 2?
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Astrocytes
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Where is MT-3 localized?
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Neurons & astrocytes
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What does MT-3 do in the CNS?
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Plays an important role in the homeostasis of copper & zinc
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Which MT's have been reported to be secreted?
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1,2,3
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Where is MT-3 particularly concentrated?
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In presynaptic terminals of zinc-enriched neurons of cerebral cortex & hippocampus
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In some neurodegenerative diseases, which MT has been shown to be downregulated or altered?
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MT-3
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Where are MT's localized?
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To the membrane of golgi apparatus
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What do MT's bind?
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Heavy metal, incl. zinc, copper, selenium, cadmium, mercury
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What do MT's regulate?
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Zinc & copper
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What do MT's protect against?
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Oxidative stress & metal toxicity
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Which 3 metals are able to induce MT-1 & 2?
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Cadmium, copper, and zinc
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Which MT is found in hypoxic tumors?
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MT-3
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How did cats react to receiving only fomepizole?
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Experienced mild sedation
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Cats receiving fomepizole for EG intoxication survived if therapy was initiated within ____ hrs. of EG ingestion
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3
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Which tx. is more effective at treating EG ingestion: fomepizole or EtOH?
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Fomepizole (in high doses)
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Which species has a more grave prognosis for successful outcome w/ EG intoxication: dogs or cats?
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Cats
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How does the case fatality rates differ b/w dogs & cats?
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Dogs: 59-70%
Cats: 96-100% |
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What is the lethal dose of EG in dogs & cats?
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Cats: 1.4 ml/kg
Dogs: 4.4-6.6 ml/kg |
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Is EG toxic?
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No, but it's metabolic byproducts are.
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What are the primary therapeutic goals for EG intox.?
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Inhibition of EG metabolism and promoting renal excretion of the unchanged molecule
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How are the therapeutic goals accomplished?
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By inhibiting EG oxidation by liver alcohol dehydrogenase (ADH), the enzyme responsible for catalyzing the first step in the EG metabolic pathway, and facilitating diuresis, respectively
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How does EtOH treat EG intox.?
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It has a higher affinity for ADH & competes effectively for the EG binding sites on ADH
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What are the disadvantages of treating with EtOH?
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Exacerbates CNS depressive effects of EG, enhances EG-induced serum hyperosmolarity, and worsens the osmotic diuresis. Also long & labor-intensive.
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What are the advantages of fomepizole (4-methypyrazole)?
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Does not compound CNS depression, diuresis, or hyperosmolarity a/w EG intox. It is a reversible competitive inhibitor of ADH. Effects are longer lasting & more potent.
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What is fomepizole's MOA?
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Directly inhibits the ADH enzyme by forming a ternary complex with ADH and its coenzyme nicotinamide adenine dinucleotide, thereby inhibiting oxidation of EG by blocking its binding site.
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Why is diuresis indicated with EG tox.?
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Increasing renal blood volume, thus increasing renal blood flow & glomerular filtration rate, one would be able to more rapidly eliminate these toxicants via diuresis
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What kind of clinical pathology changes occured?
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Phosphorus concentrations increased w/onset of renal failure as glomerular filtration decreased.
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What may be the major anion contributing to acidosis?
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Glycolic acid
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Why is EG tox. more difficult to treat after 3 hours?
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EG half-life increases if treated hrs. after ingestion. Tx. increases amt. of unmetabolized EG that cannot be excreted thru kidney due to renal tox.
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Measured osmolarity & osmole gap were higher in cats treated with what?
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EtOH
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The higher concentration of glycolic acid in the EtOH-treated cats would suggest what?
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These cats had higher circulating levels of EG metabolites in general
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Why do animals with EG tox. have a severe anion gap metabolic acidosis early in the course of dz?
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Due to presence of EG metabolites, which are unmeasured anions
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Serum _______ concentrations were higher in the ethanol treated group
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Glycolate
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Why is there a decrease in total calcium over time?
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Secondary to chelation by oxalate
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Main reason why fomepizole is superior to EtOH?
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Serum glycolate concentrations are lower in fomepizole-treated animals
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What are the 2 effects of luminal [NaCl] at the macula densa?
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Regulation of glomerular arteriolar resistance through tubuloglomerular feedback and control of renin secretion
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Tubuloglomerular filtration (TGF) acts as a minute-to-minute stabilizer of distal _____ delivery
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salt
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The site of the macula densa is particularly suited for the location of a chemoreceptor b/w [NaCl] at this site is _______, _______, & determined almost exclusively by _______________________
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Hypotonic, variable
Loop of Henle flow rate |
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Glomerular filtration rate is inversely related to:
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[NaCl] at the macula densa
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How does the macula densa [NaCl] affect renin secretion?
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A decrease in MD [NaCl] stimulates and an increase inhibits renin secretion
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The mechanism of resetting is presumably multifactorial, but what is the most important single factor?
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Extracellular Ang II
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What happens when [NaCl] at the macula densa is increased for a prolonged time?
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Decrease in GFR predicted from acute TGF function does not occur
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What is the primary purpose of TGF?
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To regulate amt. of NaCl leaving distal portion of nephron
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What is caused by macula densa getting large amt's of NaCl?
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Decrease in GFR and afferent arteriole constriction
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Chronic changes in delivery affects what?
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Renin secretion
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What is the driver of GFR?
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Hydrostatic pressure w/in glomerulus compared to within bowman's capsule?
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What causes renin release?
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Decreased blood flow into afferent arteriole.
Decreased NaCl concentration to MD. |
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What does Angiotensin II do?
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Causes vasoconstriction, aldosterone release from adrenal gland, release of ADH, stimulates thirst center of medulla
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Are there more angiotensin II receptors in the efferent arteriole or the afferent arteriole?
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Efferent arteriole
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What causes the exact opposite effect of Ang II?
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Ang 1-7
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What were the 4 tx. protocols in the study on dogs with calcium oxalate urolithiasis?
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A low calcium, low protein diet designed to prevent calcium oxalate uroliths w/ & w/o HCTZ and a maintenance diet w/ higher protein & calcium w/ & w/o HCTZ
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What did HCTZ decrease?
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Decreased urine calcium & potassium concentration & excretion. Also decreased serum potassium concentration.
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What did the urolith prevention diet decrease?
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Decreased urine calcium & oxalic acid concentration & excretion. Also decreased serum concentrations of albumin & urea nitrogen.
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Which protocol had the greatest reduction in urine calcium concentration & excretion?
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Dogs receiving HCTZ and urolith prevention diet
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What is the hypothesis of thiazide diuretics' MOA?
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Promotes mild extracellular volume contraction, which in turn promotes proximal tubular reabsorption of sodium & calcium
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How do thiazides promote natriuresis?
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They inhibit NaCl cotransport @ luminal surface of distal tubules, which decreases intracellular [Na+], which stimulates calcium-sodium exchange @ basolateral tubular membrane resulting in Ca2+ reabsorption from tubular fluid
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What would be expected to happen if dietary calcium were reduced w/o a concomitant reduction in oxalate acid?
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Intestinal absorption and subsequent urinary excretion of oxalic acid would be expected to increase
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There is a greater propensity for precipitation of calcium oxalate in urine a/w increases in ___________ concentration than with increases in _________ concentration.
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Oxalate acid
Calcium |
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What are struvite uroliths made of?
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Mostly MgNH4, PO4, 6H2O
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What are struvite stones called?
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Fever or infection stones
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How are struvite stones treated?
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Antibiotics, dissolution, prevention
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How are calcium oxalate stones treated?
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Reduce dietary intake of calcium and oxalate. Increase water intake.
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What is renal clearance?
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The volume of plasma freed of a substance by only renal mechanisms, per unit time
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How is small intestine a/w calcium?
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SI is the site where dietary calcium is absorbed.
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How is bone a/w calcium?
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Bone serves as a vast reservoir of calcium
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Why is kidney a/w calcium?
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Kidney is critically important in calcium homeostasis
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How does PTH play a role in calcium homeostasis?
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It serves to increase blood concentrations of calcium. Maximizes tubular reabsorption of calcium w/in kidney. This activity results in minimal losses of calcium in urine.
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How does Vitamin D play a role in calcium homeostasis?
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Acts to increase blood concentrations of Ca2+
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How does calcitonin play a role in calcium homeostasis?
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It is a hormone that functions to reduce blood calcium levels.
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How did the urolith prevention diet affect composition of glycosaminoglycans, Tamm-Horsfall glycoprotein, and nephrocalcin in cats with calcium oxalate uroliths?
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No effect on quantity of Tamm-Horsfall glycoprotein and nephrocalcin in urine. Concentration of glycosaminoglycans was sig. higher.
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What are glycosaminoglycans?
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Glycoprotein inhibitors of growth and aggregation of calcium oxalate crystals
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What was the focus of the study from 2001?
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Urolith prevention diet & its effect on reducing calcium concentration
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What was the focus of the study from 2012?
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The focus is on potential organic matrices that inhibit urolith formation
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What are some factors of urolithiasis?
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Sex hormones, osteopontin, pH, obesity, genetics
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What artificial sweetener has been removed from hazardous substances list?
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Saccharin
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What are the primary cardiac biomarkers that have become a mainstay for both diagnosis and patient monitoring in human heart dz?
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Cardiac troponin and natriuretic peptides
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What is a biomarker?
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Defined as a substance elaborated by a specific tissue that can be detected in circulation
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What are some biomarkers used in vet patients?
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BUN, creatinine, ALT
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What is the function of natriuretic peptides?
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They stimulate natriuresis, renal blood flow, diuresis, and vasodilation as well as enhancing diastolic heart function
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Which natriuretic peptides are increased primarily in response to increased myocardial wall stress?
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Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP)
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Where do ANP and BNP originate from?
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ANP originates from the atria while BNP comes from both atrial and ventricular myocytes.
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Both ANP & BNP are released as precursor molecules then cleaved by serum proteases to form equal amts of:
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The active C-terminal fragments (C-ANP & C-BNP) and an inactive N-terminal fragment (NT-proANP & NT-proBNP)
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Which of those fragments have ultrashort half-lives, making it difficult to measure circulating concentrations?
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C-ANP & C-BNP
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Which of those fragments have longer half-lives and are more stable for collection & sampling?
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NT-proANP & NT-proBNP
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In conjunction with other diagnostic tools, what can pro-BNP used to diagnose in dogs?
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Heart dz
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NT-proBNP can be falsely elevated in which cases?
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In cases of severe pulmonary dz and concurrent pulmonary hypertension
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Which 3 cardiac markers were found to be helpful in diagnosing occult cardiomyopathy?
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NT-proANP, C-BNP, and cardiac troponin
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Which of the 3 biomarkers had the best sensitivity and specificity for detection of occult dz?
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BNP
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What organ dysfunction may falsely elevate NT-proBNP concentration?
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Renal dysfunction
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Theoretically, what can influence NT-proBNP concentrations in both healthy & diseased dogs?
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Diet, water intake, and exercise
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Heart dz is unlikely in dogs if the NT-proBNP level is:
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<566 pmol/L
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In patients with resp. signs, an NT-proBNP level >__________ is likely associated with CHF
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1200 pmol/L
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What are the 3 subunits of the troponin complex?
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cTnI, cTnT, and cTnC
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What does the troponin complex do?
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Help regulate excitation-contraction coupling in the cardiac myocyte
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_____ component that prevents interaction b/w actin & myosin until ______ binds to calcium ions
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cTnI
cTnC |
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Injury to the sarcomere causes detachment of _____ from actin & subsequent disruption of cellular membrane allows leakage of _____ into general circulation
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cTnI
cTnI |
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What does a high level of cTnI in serum or plasma indicate?
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Myocardial cell damage and necrosis
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Elevated cTnI is a/w adverse long-term outcome and is an independent predictor of _________
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mortality
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In dogs, what can cause dramatic increases in cTnI?
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Pyometra, gastric dilation-volvulus (GDC), pericardial effusion, trauma, sepsis, myocarditis (as in babesiosis & chagas)
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What heart diseases in dogs showed increased cTnI?
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Cardiomyopathy, mitral valve dz, and subaortic stenosis
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Combination of which 2 biomarkers would provide a better diagnostic tool for asymptomatic patients?
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cTnI and NT-proBNP
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What is the myocardial injury marker?
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Troponins
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What is the myocardial stress marker?
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NT-proBNP
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A useful biomarker should fulfill these 3 criteria:
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It can be easily measured.
It should add new info. It should assist in managing the case. |
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What are the causes of myocyte injury?
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Tissue ischemia, neurohumoral overstimulation, inflammation, and necrosis/apoptosis
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What are the conditions a/w high troponin I levels?
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Myocardial trauma, feline hypertrophic cardiomyopathy, canine DCM, canine mitral valve dz, pericardial effusion, severe skeletal muscle injury
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Troponins are highly sensitive & specific for what kind of injury?
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Cardiac muscle injury, esp. acute injury
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Levels of troponin assess severity of injury. T or F?
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True
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When can there be a false negative with troponin levels?
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Chronic progressive dz's may not cause massive release of cTnI
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ANP is mainly secreted by atria, but is secreted by ventricles in which condition?
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Cardiovascular dz
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Where is BNP stored?
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Granules
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Where is BNP synthesized & secreted from?
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Synthesized in ventricles and secreted from both atria & ventricles
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Where is CNP found?
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Predominantly in brain and also synthesized by vascular endothelial cells
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What are the 3 receptors for natriuretic peptides?
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NPR-A or NPR1
NPR-B or NPR2 NPR-C or NPR3 |
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WHere are NPR-A receptors found?
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Kidneys, lungs, adipocytes
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Where are NPR-B receptors found?
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Predominantly in brain
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Where are NPR-C receptors found?
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Most abundant in tissues: vasculature, kidneys, adrenal, brain, etc.
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Which of the 3 receptors is involved in removing natriuretic peptides from circulation?
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NPR-C
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ANP & BNP have been shown to be physiological antagonists of the effects of:
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Ang II on vascular tone, aldosterone secretion, renal-tubule sodium reabsorption, and vascular remodeling
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What type of hormone is vasopressin?
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Antidiuretic
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Vasopressin was most efficient when administed when?
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Before crystalloid resuscitation
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What is one of the common causes of severe hypoperfusion in animals?
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Hemorrhage
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Which vasopressors are used when the last phase of hemorrhagic shock is uncontrolled by fluid resuscitation?
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Dopamine, epinephrine, and norepinephrine.
Used to support blood flow and increase blood pressure. |
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What is vasopressin?
|
An endogenous neurohypophysial hormone which acts on V1 receptors
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What is the diff. b/w vasopressin & other vasodilators?
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Vasopressin preferentially constricts arterioles in extracerebral tissues, with relatively less constriction in renal & coronary blood vessels, and may actually dilate the cerebral & pulmonary vasculature, thereby improving cerebral & pulmonary perfusion
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Why is fluid therapy a prerequisite for vasopressin administration in decompensatory hypovolemic shock?
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Since vasopressors can reduce blood flow to some tissues, esp. the kidney & gut, while transiently increasing CO in hypovolemic states, circulating blood volume must be adequate
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What were the 3 groups in the study?
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Crystalloid b4 vasopressin, vasopressin b4 crystalloid, and only vasopressin
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What group showed better hemodynamic and oxygen delivery effects for controlled hemorrhagic shock?
|
Vasopressin prior to crystalloid resuscitation
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What are the goals of anesthesia?
|
Analgesia, muscle relaxation, and unconsciousness
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Sympathetic nervous system receptors & neurotransmitter? location?
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Thoracolumbar
Norepinephrine Alpha 1 & 2 Beta 1 & 2 |
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Parasympathetic nervous system receptors & neurotransmitter? location?
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Craniosacral
AcH Nicotinic & muscarinic |
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What do anti-hypotensive medications do?
|
Correct low arterial pressure, increase tissue circulation, increase oxygen supply, and decrease hypo-perfusion injury
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What is phenylephrine? And what does it do?
|
Direct alpha-1 agonist
Vasoconstriction Splenic contraction |
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What is more effective in improving overall O2 content: increasing hemoglobin level or increasing O2 fracgion of breathed gas?
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Increasing hemoglobin level
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What reflects tissue perfusion more accurately: BP or CO?
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CO
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What is the main determinant of oxygen delivery?
|
CO
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What predisposes animals to M. haemolytica infection?
|
Transportation, viral infections with bovine rhinotracheitis virus, parainfluenza-3 virus or bovine resp. syncytial virus, overcrowding, & other stressful conditions
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What gram stain is M. haemolytica? Where does it reside?
|
Gram-neg.
Polysaccharide capsule In mucus & secretions from ventral nasal meatus, sinuses, & tonsil |
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What plays a role in the attachment of M. haemolytica in the alveolus?
|
The capsular polysaccharide may be involved in an adhesin-receptor interaction, with surfactant mediating the attachment of M. haemolytica in the alveolus
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What binds to the carb. on the surface of the alveolar epithelial cells?
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Lectin in the pulmonary sulfactact
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What is lectin?
|
A calcium-dependent, mannose-binding protein
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Glycoconjugate/receptor binding may change, affecting the lectin affinity. What further enhances the binding?
|
Enzymatic activity of neuraminidase
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When is neuraminidase produced by M. haemolytica in increased amt's?
|
During times of stress in the host
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What accompanies the increased neuraminidase?
|
Increased replication of M. haemolytica
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What is released from M. haemolytica into the intraalveolar exudate during infection?
|
LPS, polysaccharide, and LKT
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What is taken up by neutrophils?
|
LPS
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|
|
Where does polysaccharide localize?
|
In the alveolus and alveolar macrophages
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|
M. haemolytica infection induces release of what 3 inflammatory mediators by lung tissue? This initiates a profound procoagulant state resulting in what?
|
IL-1, TNF-alpha, & IL-8
Extensive fibrin polymerization |
|
|
What are some other inflammatory mediators released by bovine lung in response to M. haemolytica products?
|
Leukotriene B4, histamine, and prostaglandin E2
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|
|
____ can be toxic to ruminant leukocytes
|
LKT
|
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|
LKT binds to _________ receptors or ruminant leukocytes and platelets.
|
Beta-2 integrin
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|
|
What does the binding of LKT to beta-2 integrins induce?
|
Induces apoptosis, formation of pore-like structures in the plasma membrane, activation of phospholipase A2 in calcium-dependent manner, and increased LTB4 prod. in neutrophils
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|
|
How does M. haemolytica LPS enhance LKT activity?
|
Thru the formation of LPS-LKT complex
|
|
|
What do M. haemolytica LPS & IL-1 induce?
|
Tissue factor formation & procoagulant activity by endothelial cells
|
|
|
What leads to increased leukocyte adherence & infiltration?
|
Endothelial cell activation
|
|
|
What is neutrophil infiltration during M. haemolytica pneumonia a/w?
|
Alveolar epithelial cell damage and necrosis
|
|
|
L-selectin is expressed on __________ & mediates __________ binding to _______________
|
Neutrophils
Neutrophil Endothelial cells |
|
|
Where are E- & P-selectins expressed?
|
Mainly on endothelial cells
|
|
|
What do E- & P-selectins mediate?
|
Binding to neutrophil selectin receptors
|
|
|
What is the exotoxin of M. haemolytica?
|
Leukotoxin
|
|
|
What does leukotoxin kill?
|
Neutrophils & macrophages
|
|
|
What are the 2 different classes of adhesion molecules?
|
Integrins & selectins
|
|
|
Which of the 2 needs to be activated?
|
Integrins (firm attachment)
|
|
|
What do integrins bind?
|
Leukocytes, endothelia, and extracellular matrix
|
|
|
What do beta-1 integrins bind?
|
VCAM-1
|
|
|
What do beta-2 integrins bind?
|
ICAM-1
|
|
|
Inflammation serves to:
|
Destroy, dilute, wall-off, and initiates healing thru repair
|
