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129 Cards in this Set
- Front
- Back
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3 epidermal layers
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stratum basale - proliferative with melanocytes and Langerhan's cells (macrophages)
stratum spinosum - keratinocytes to produce keratin and immunological functions stratum corneum - cornified barrier layer |
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3 phases of hair follicles
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anagen - growing and producing
catagen - receding, "flame follicles telogen - end stage |
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types of adnexal glands in skin
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apocrine - watery secretion into follicle lumen
sebaceous - oily secretions into follicle lumen eccrine - of foot and nose |
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components of the dermis
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connective tissue
collagen and elastic fibers blood and lymphatic vessels nerves collagen muscle fibers |
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cardinal signs of inflammation
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heat
swelling pain redness |
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gross lesions of inflamed skin
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crust
erosions pustules ulcers |
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pyoderma
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pus in the skin
can be deep or superficial focal or diffuse often involves hair follicles |
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folliculitis
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around and within follicle
follicle lumen can be filled with neutrophils increased sebum can lead to infection if treated, infection can be eliminated before hair loss and loss of of follicles common causes: bacteria dermatophytes demodex |
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perifolliculitis
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inflammation around hair follicles
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furunculosis
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destruction of follicles
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atopy
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skin immediate hypersensitivity due to inhaled or food allergens or transdermal absorption of allergen
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pigmentary incontinence
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melanophages in dermis
damaged melanocytes drop their pigments down into the dermis where macrophages engulf them |
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acantholytic cells
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keratinocytes separated from each other
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dyskeratosis
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necrosis of individual cells
leads to eosinophilia |
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pemphigus foliaceous
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most common dermatologic autoimmune disease
acantholytic cells in pustules cells attack intracellular processes in stratum spinosum forms pustule covered with stratum corneum can break open cell don’t die, just aren’t attached any more |
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discoid and systemic lupus erythemathosis
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dermatologic autoimmune disease
basal layer damage lichenoid lymphocytes and plasma cells pigment incontinence can be related to other disease sunshine +/- elevation makes it common in CO |
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dermatomyositis
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dermatologic autoimmune disease
cleft formation attack on the basal cell layer suprabasalar cleft |
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sebaceous adenitis
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dermatologic autoimmune disease
attacks sebaceous glands lymphocytic inflammation with plasma cells sebum will not be produced dry flaking skin seen |
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alopecia areata
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dermatologic autoimmune disease
attacks growing hair follicles hair recedes immunosuppression to treat |
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erosion
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partial loss of layer of epithelium
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ulceration
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full thickness loss of epithelium
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vescicle
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circumscribed accumulation of fluid within the epithelium
"blister" |
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acanthosis
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thickening of stratum spinosum in healing epidermis
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hyperkeratosis
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thickening of stratum corneum in healing epidermis
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Hyperpigmentation
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increased melanin granules
can be seen during healing of epidermis |
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HERDA
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hereditary equine regional dermal asthenia
horses genetic defect causing derangement of collagen fibers in the deep dermis skin separates from underlying CT seen in performance Quarter horses presents as a lot of skin wounds back is most affected because the skin is so detachable, will tear |
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Mucinosis
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Sharpeis
degenerative condition, but normal for this breed excess production of mucin by the dermis fibroblasts not behaving properly skin is puffy and swollen because of the mucin makes their skin “oozy” steroids can decrease mucin production |
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Calcinosis cutis
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mineralization occurs in Cushing’s disease
thick crusted lesions lots of calcium is laid down on the collagen in the dermis body recognizes it as abnormal iatrogenic with high levels of steroids |
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UV light affects on epidermis
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decreased immunologic functions
stimulates melanocytes acute - causes epidermal cells in stratum spinosum and endothelial cell damage in dermis chronic - solar elastosis - excessive laying down of elastic fibers irregularly - sagging and wrinkling |
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congenital alopecia
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hereditary lack of hair follicles because of hypoplasia of the follicles
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dermatological atropy
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normal and has regressed
associated with endocrine diseases and aging effects epidermis and follicles most notable affected follicles were present but later atrophied hypothyroidism hair follicle with go into telogen stay there due to a change in hormones with hyperkeratosis/orthokeratosis |
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color dilution alopecia
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dysplasia
clumped pigments in hair shafts make hair weak lack of survival, not lack of production |
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folliculopathy
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hair grown in an abnormal way
distorted hair follicle on histopath |
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trichoepithelioma
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neoplasia of epidermis
common benign ulcerated surface of hair follicle |
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Carcinoma in situ
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neoplasia of epidermis
proliferative mitotic figures lack of orderly differentiation |
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Invasive squamous cell carcinoma
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proliferation invading outward into the dermis
common with pale skinned dogs and horses |
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Fibrosarcoma
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dermis neoplasia of connective tissue
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Equine sarcoid
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neoplasia of the epithelium and connective tissues
proliferating spindle cells |
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Hemangioma
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neoplasia in the dermis
can often appear black and be mistaken for a melanoma |
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Pruitis
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itch/scratching
usually indicates allergy or ectoparasites |
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Alopecia
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loss of hair
Endocrine diseases Secondary to inflammatory diseases Folliculopathy - weak distorted hair shaft, poor production, color dilution alopecia Post-clipping idiopathic alopecia Pruritis |
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upper airway defenses
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mucus and cilia
particles trapped in mucus removed by beating cilia, coughing, sneezing pushed to pharynx to be swallowed exposure to tonsils to trigger immune system humoral immunity based on IgA neutralizes viruses opsonize bacteria |
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Lower airway defenses
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bronchial associated lymphoid tissue (BALT)
Normal bacterial flora competes with pathogenic flora phagocytosis of material by alveolar macrophages - main defense defenses weaker than upper airways |
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Pneumonia
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inflammation of the lungs
changes are described by location, type of exudate, duration and cause lesions can affect bronchi, bronchioles, alveoli severe inflammation leads necrosis of bronchiole and alveolar walls leads to abscessation |
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catarrhal inflammation
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mucoid exudate due to increased goblet cell secretions and serous exudate
Damaged ciliated epithelial cells |
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Membranous (type I) pneumocytes
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form a thin layer in alveolus
act as the site of gas exchange fragile cells with no regenerative capacity |
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Granular or secretory (type II) pneumocytes
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cuboidal cells that make surfactant
source of cell renewal to produce more membranous cells |
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Injury to alveoli
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necrosis and sloughing of Type I cells first
type II cells survival and an intact basement membrane enables type II cells proliferate and recover the surface "epithelialization" |
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Bronchopneumonia
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lesions are centered around bronchioles in a lobular pattern
Aerogenous insult by particles leads to cranioventral distribution Lobular pattern progresses to uniform consolidation eventually may spread to whole lobe and pleura Macrophages phagocytize debris and lyse fibrin. Coughing and collateral ventilation remove exudates Stress, decreased immunology defense, crowding can increase risk Later stages have necrosis and hemorrhage |
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Chronic bronchopneumonia
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due to incomplete resolution
basement membranes destroyed abscesses or granulation suppuration, fibrosis, bronchiectasis death due to hypoxia and toxemia |
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Lobar pneumonia
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type of bronchopneumonia
Inflammation begins at bronchiole-alveolar junction but spreads quickly entire lobe consolidated hemorrhage and necrosis due to extremely virulent organisms and compromised defenses e.g. Mannheimia haemolytica, |
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Interstitial pneumonia
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alveolar walls and capillaries
stays in alveoli acute or chronic, and have a patchy or diffuse distribution NOT anterior-ventral Often hematogenous route - septicemia, salmonella, distemper damage to type I pneumocytes and endothelium exudate and fibrin as a result of increased vascular permeability appear mottled, heavy, rubbery proteinaceous fluid, foamy on cross section congestion and hemorrhage formation of hyaline membranes fibroplasia can occur early |
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bronchointerstitial pneumonia
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injury to alveoli and small bronchioles
e.g. BRSV infection |
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Pleuropneumonia
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travels into the connective tissue on the lung surface
typically of a very virulent agent a lot of fibrinous exudate |
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Thrombosis
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states of hyper coagulability
systemic illnesses stasis of blood endothelial damage Look granular compared to postmortem clot pulmonary can form due to HW irritation |
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high altitude disease
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pulmonary hypertension
vasoconstriction in response to low oxygen content in inspired air can lead to arteriosclerosis and more hypertension |
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atelectasis
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Incomplete expansion of a lung or part of a lung
lungs don't float sunken areas of dark consistency |
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congenital atelectasis
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Lungs were never aerated or lungs expanded initially but did not refill
Ex: stillbirth |
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Acquired atelectasis
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Obstructive - Blockage of airway prevents air from filling alveoli
Compressive - pressure from mass, hydro/hemo/pyo-thorax, abdominal distention Hypostatic - recumbent |
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emphysema
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excess air in lungs
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alveolar emphysema aka vesicular
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Abnormal enlargement of alveoli
destruction of alveolar walls Irreversible change pale, puffy lungs may see small vesicles or bullae formed by coalescence of alveoli wall destruction and larges spaces on histo overexertion on inspiration |
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interstitial emphysema
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Air is present in connective tissues, interlobular septa.
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Chronic bronchiolitis
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emphysema in horses aka "heaves"
chronic obstructive pulmonary disease recurrent airway obstruction (RAO) difficult respiration mucoid exudate in broncioles, bronchi variable emphysema and bullae goblet cell hyperplasia squamous metaplasia, peribronchioloar lymphocytic and plasmacytic infiltrates and fibrosis |
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Rhinitis - serous
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watery exudate
some degeneration of epithelial cells Shiny appearance distruption of ciliary clearance Usually viral Some fluid accumulates in tissues as well |
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Rhinitis - mucoid or catarrhal
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high level of mucus secretion
Bacteria have become involved Increased levels of damage can be lethal: Cats with upper respiratory disease become depressed rapidly |
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Rhinitis - purulent
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Increasing numbers of PMN's in mucoid exudate
Neutrophils in the exudate Increasing amount of damage to epithelium - Erosions and ulcers. Bacteria involved Fibrino-necrotic exudates = extensive damage Fibrin leaking out as well with purulent exudate |
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Rhinitis - eosinophilic
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serous or mucoid with many eosinophilic
Hypersensitivity inhaled allergens |
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rhinitis - granulomatous
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Chronic condition characterized by accumulations of macrophages
Fungal elements Can appear like a tumor |
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Nasal polyps
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raised nodules formed in chronic inflammation
Not neoplastic One or more Varying degrees of epithelium degeneration or loss Hyperplasia possible Thickening possible Fibroplasia |
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Sinusitis
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similar to rhinitis but drain with difficulty
Cases usually advanced by the time they are seen clinically |
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Empyema
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pus in sinus cavity
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laryngitis/tracheitis
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Usually an extension of rhinitis, similar changes
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Purulent bronchitis, bronchiolitis
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Usually caused by bacteria
thick yellow exudate in lumens mucus, sluffed epithelial cells, and degenerate PMN's in lumens damaged epithelial cells |
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Fibrinous or fibrinonecrotic bronchitis
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thick yellow exudate attached to surface
similar material to purulent but loss of epithelial cells and seeming merger of wall and exudate |
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Bronchiolitis fibrosa obliterans
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Fibrin stimulates fibroplasia, like any wound healing
nodules plug airways Fibrous connective tissue of variable density e.g. BRSV |
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Bronchiectasis
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Dilation of bronchi following necrotizing inflammation
Often in cows Walls have been weakened and dilated damage from eosinophils and bacterial enzymes all the way to cartilage Fibrous scars occur as a result of repair |
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bronchiogenic tumors
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primary neoplasia, rare
originate near the hilus of the lung. classification includes: squamous cell carcinoma-can be related to chronic irritation, I.e. cigarette smoke adenocarcinoma adenosquamous carcinoma |
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Bronchioalveolar tumors
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primary neoplasia, rare
originate from secretory cells of bronchioles or alveor type II pneumocytes often located at periphery of lobules |
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Continuous circulation of blood
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adequate cardiac output
adequate blood volume normal pressure intact vessels Pressure needed to maintain flow. Resistance regulated by the amount of tone |
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vessel permeability
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For proper exchange of oxygen, nutrients, and hormones
Depends on balance of arteriole and venous hydrostatic pressures and blood and tissue osmotic pressures |
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Arteriosclerosis
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hardening of vessels
constricts the vessel lumen reduces compliancy leads to hypertension muscle constriction feedback can make it worse Heart has to overwork to meet the resistance |
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Atherosclerois
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form of arteriosclerosis with lipid deposits in the intima
Smooth muscle cells and fibroblasts migrate into the intima making a firm lesion |
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hypertension
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uncommon in animals
causes arteriolosclerosis, with a positive feed-back loop can lead to heart failure can cause thrombosis |
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causes of hypertension
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high altitude with low inspired O2
emphysema with loss of alveolar capillaries left to right shunt of blood left heart failure idiopathic (more common in people related to diet) |
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aneurism
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weakening and outpocketing of a vessel wall
most common aneurism in vet med caused by parasite damage in horses rupture possible |
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vasculitis
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Inflammation of vessel wall
“fibrinoid necrosis” entails fibrin deposits in the wall Amorphous, homogenous, eosinophilic material, wall effaced Causes: certain infectious agents, immune mediated injury, uremia, parasites, i.e. HW, idiopathic, drug reactions |
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Thrombosis
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clotted blood that is attached to the vessel wall
procoagulant conditions Abnormal intimal surface changes in flow: stasis or turbulence shock, lower CO can lead to occlusion of vessels |
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Hemangioma
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common skin smashes
if removed typically don’t reform Localized |
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Hemangiosarcoma
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malignant endothelial cells
proliferate in bazaar methods Large basophilic cells, hyperchromatic nuclei, frequent mitotic figures very common in dogs often start in right atria easy to break off and form metastises, i.e. lungs |
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coronary vessels
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supply oxygen continuously.
muscles normally take 75% of oxygen out of blood so there isn’t much reserve if flow is decreased - can lead to myocardial infarction |
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Primary Cardiomyopathy
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idiopathic degeneration of heart muscle
can cause chronic disease or sudden death Classified anatomically as hypertrophic, dilated, or restrictive |
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Secondary cardiomyopathy
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hereditary
nutritional (taurine deficiency in cats) infectious agents some toxins |
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Myocarditis
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can follow valvular endocarditis
occasionally follows septicemia few infectious agents (Toxoplasma, C. chauvoei) |
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Pericarditis
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usually follows septicemia
can be caused by mechanical introduction of bacteria to pericardial space example: hard-ware disease in cattle |
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Heart Necrosis
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Infarction in humans
toxins in plants rattlesnake venon vitamin E/Selenium deficiency rumensin toxicity |
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Dilation of the heart
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increased CO
usual compensation for an increased workload caused by volume overload sarcomeres-actin/myosin stretched - if too far become dissociated and don't interact at all |
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Hypertrophy of the heart
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compensation for increased workload due to increased pressures
has limitation can lead to failure |
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Concentric cardiac hypertrophy
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ventricle wall is bigger but the lumen is not bigger
wall hasn't stretched typically due to increased pressure load pulmonary disease, systemic hypertension, valve stenosis |
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Eccentric cardiac hypertrophy
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Lumen is bigger
wall is stretched variable increase in ventricle mass increased blood volume to pump valve insufficiency or septal lesions |
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Right sided cardiac hypertrophy
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pulmonary resistance:
heartworm high altitude emphysema |
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Left-sided cardiac hypertrophy
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increased peripheral resistance
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Left to right cardiac shunts
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overload on the right heart
atrial septal defects - patent foramen ovale ventricular septal defects patent ductus arteriosis |
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Right to left cardiac shunts
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cyanosis
tetralogy of Fallot Persistent truncus |
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Rhabdosarcoma
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primary tumor of myofibers
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Congestive heart failure
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inadequate cardiac output
primary heart problem, pressure/volume overload beyond compensation body response: renin-aldosterone to retain fluid, baroreptors, ADH release, sympathetic increase of HR and vascular tone |
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SHock
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inadequate perfusion of body tissues
results in widespread metabolic disorders |
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Cardiogenic shock
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variety of mechanisms
myocardial ischemia/infarction heart failure myocarditis drug toxicites Response: catecholamine release, increased HR and BP Renin-aldosterone and ADH increase blood volume Signs: low BP, depressed metabolism, dyspnea, oliguria, cyanosis |
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Hypovolemic shock
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loss of blood, plasma, or interstitial fluid
GI loss, diabetes, third-spacing, some compensation by shifting fluid from interstitium to blood, concentrating urine increased HR and SV |
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Neurogenic shock
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massive vasodilation leading to relative hypovolemia
imbalance of sympathetic/parasympathetic stimuli to smooth muscle of vessels spinal cord injury, depressive/anesthetic drugs low HR fainting due to low pressure in brain |
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Anaphylactic shock
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vasodilation leading to relative hypovolemia
hypersensitivity reaction products of antigen and IgE release cause vasodilation and increased vascular permeability bronchospasm dyspnea, edema, hives, low BP, low mentation, increased HR, oliguria, edema treat with epinephrine (vasoconstriction/bronchodilation), LRS, steroids |
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Septic shock
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infectious agents
mediators of inflammation cause vasodilation and increased vascular permeability fever procoagulant - thrombi in small vessels hypotension, inadequate perfusion, tissue hypoxia, acidosis, multiple organ failure |
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Caries
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demineralization and enzymatic degradation of dental stroma
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Megaesophagus
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congenital
myastenia gravis - autoantibody to acetylcholine receptors obstruction - vascular ring anomalies or others |
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Forestomachs
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function as fermentation vats
stratified squamous epithelium |
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Glandular stomach
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Includes stomach, abomasum, and third compartment of the stomach in llamas
Glands secrete digestive enzymes and HCl Goblet cells make a protective layer of mucus |
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Gastric Dilation/volvulus
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large, deep chested dogs
cause unknown fills with gas and twists on its mesentery spleen may twist puts pressure one diaphragm and vessels to caudal body stomach wall becomes necrotic "cardiac depressent factor" released severe acid-base and electrolyte imbalances reperfusion injury can occur after repair |
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Abomasal displacement
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associated with high production and stress
left is common right is more serious - causes circulatory compromise |
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gastric dilation in horses
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obstruction
grain overload unknown factors |
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Ruminal tympany /Froathy bloat
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inability to eruct ate gas because of rumen function (vagas nerve defect) or obstruction (choke)
puts pressure on diaphragm and vessels to caudal part of body |
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Grain overload
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highly fermentable carbohydrates produce volatile fatty acids
cascade of reactions that lower the pH of the rumen acidic pH causes direct damage to the mucosa leads to possible infection of Fusobacterium dehydration - osmotic movement of water into the rumen acidosis - lactic acid circulation |
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Rotavirus in pigs and calves
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lesions confined to tips of villi of intestines
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transmissible gastroenteritis
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Pigs
corona virus destroys absorptive epithelial cells of entire villus |
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cryptosporidia
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colonize stomach to colon
become enmeshed in microvilli can cross species barrier |
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Giardia
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colonize duodenum
inhibit absorption of sugars leading to osmotic changes |
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Feline panleukopenia virus and Canine corona virus
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replicate in and destroy fast proliferating cells
specifically cryptal epithelial cells of small intestine hemorrhagic enteritis surviving crypt cells try to heal defect outcome based on balance between destruction and renewal affect other dividing cells often related to decline of maternal antibody |
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Clostridium perfringens
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necrotizing enteritis
colonize intestinal surface produce toxins enterotoxemia called "overeating disease" |
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Salmonellosis
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found in many vertebrates
200+ serotypes identified some are species specific/some not colonize intestinal surface invade and destroy epithelial cells cause erosions/ulcerations infection of lymph nodes/Peyer's patches start of septicemia/carrier state |
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endocardiosis
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common aging change, older dogs
valves shrunken and nodular surface intact endothelial cells still present still smooth and shiny contour bumpy |
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endocarditis
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inflammation of heart vales(less common)
inflammatory exudate on surface endothelial cells often absent making it less smooth bacteria can stick easily - high mechanical force appears granular, rounded contour makes valves incompetent streptococcus common |
