ear Flashcards

(45 cards)

1
Q

portals of entry to the ear

A

 Extension from the
external environment** most common
 Hematogenous spread
 Extension from the middle ear

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2
Q

defense mechanisms of the external ear

A

Defense Mechanisms:
 Integumentary defenses
 Epithelial migration
 Cerumen barrier and acidity
 Commensal organisms
 Structural defenses

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3
Q

middle ear portals of entry

A

 Extension through TM
(perforation)**
 Ascending (auditory tube)
 Extension (temporohyoid joint degeneration)
 Extension (TB erosion)
 Migration – vascular/neural path

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4
Q

defense mechanisms of the middle ear

A

Defense Mechanisms:
 Mucociliary apparatus
 Surfactant
 Auditory tube lymphoid tissue
 Commensal organisms

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5
Q

internal ear portals of entry and defense mechanisms

A

 Main anatomical features:
 Petrous bone and cochlea
 Portals of entry:
 Extension from the middle ear
 Hematogenous spread
 Migration along vascular or neural pathways

Defense Mechanisms:
 Structural defense (bone)

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6
Q

aural hematoma

A

Dogs and Pigs&raquo_space; Cats
 sporadic occurrence
 Secondary to HEAD SHAKING
 Shearing forces damage auricular cartilage in the middle and rupture small vessels within the pinna leads to pooling of blood.

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7
Q

ear necrosis (vascular injury)

A

 Circulatory or Trauma

 Usually INFARCTION:
 Vascular injuries
 Thrombosis

 Bacterial septicemia
- Salmonelosis
- Erysipelas

 Frostbite
 Toxins: Ergot and fescue
 Biting injury: Other Trauma

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8
Q

frost bite in ears (vascular injruy)

A

 Young animals most susceptible outdoors
 Ischemia to keep blood warm in core body
 Leads to infarction and necrosis: Dry gangrene

 ERGOT vasoconstriction similar in appearance

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9
Q

blue ear disease in pigs

A

 Ears are dark red to purple-
black
caused from PRRS virus vasculitis (arteriovirus)
-ear tip necrosis due to vasculitis from immunesuppression

DDX: Salmonellosis:
- Thrombosis due to endotoxin
released by bacterium.
 May also include the tail and
sloughing of ear/tail

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10
Q

otitis externa

A

-prevelant in dogs

- Chronic and repeated:
-Permanent changes to structure and function with no chance of return to
normal.

 ODOR and COLOR of discharge can be indicative of pathogen present.

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11
Q

different exudate in otitis externa and what they cause?

A

ear mites: dry, dark and grangular (otodectes cynotis) usually in cats

bacteria: moist, yellow, odiferous

yeast: reddish brown, waxy (malassezia otis externa)

ceruminous or sebaceous: yellow, waxy to oily

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12
Q

otitis media (most common)

A

 Usually Suppurative +
bacteria
 Extension of Otitis Externa
 Dogs may be up to 80% of cases of OM
 Perforations reported >40%

 Large animals:
 Nasopharyngeal ascent of
bacteria through the auditory
tubes.

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13
Q

otitis media in pics bacterial causes

A

 Pasteurella multocida,
Trueperella pyogenes, and
Mycoplasma hyorhinis are most
commonly isolated from
suppurative otitis media.

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14
Q

otitis media in cattle bacterial causes

A

 Histophilus somni, Pasteurella
multocida, Trueperella pyogenes
(Arcanobacterium pyogenes),
and Mycoplasma bovis

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15
Q

pasturellosis in rabitts

A
  • May start as ‘snuffles’ (rhinitis
    caused by Pasteurella multocida)
  • Presented as torticollis (head tilt from in inner ear)
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16
Q

hearing loss

A

 Congenital or Acquired
 Conduction loss or
Neurosensory loss

 Genetic:
 Heterochromia
 Blue eyes (NOT 100% linked)

 Age related

 Ototoxicity:
 Noise trauma
 Aminoglycosides
 Asprins

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17
Q

pinnal alopecia

A

 Herefords (polled): congenital
disease**
 Ears and muzzle in newborns
 Epidermal maturation and
keratinization defects

 Acquired disease in Dogs and
Cats
Dachshunds
 (Chihuahuas, Boston terriers, Whippets and
Italian greyhounds)
 Progressive over time
 Anagen follicles are smaller in diameter and shorter
than normal areas
Siamese Cats

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18
Q

non congenital causes of pinnal alopecia

A

 Atopy
 Food allergy
 Canine hypothyroidism
 Hyperadrenocorticism
 Demodicosis
 Dermatophytosis

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19
Q

neoplasia of the skin and pinnae

A

 Melanoma
 Squamous cell Carcinoma (actinic dermatitis)
 Dentigerous cysts

20
Q

nasopharyngeal polyps in cats

A

Non-neoplastic, inflammatory
masses affecting cats often under 2 years of age

 They may be confined to the
middle ear
 protrude through the auditory tube
into the nasopharynx
 penetrate through a ruptured
tympanic membrane

 Symptoms may be Otitis externa
or media, or Respiratory Stridor

21
Q

feline ceruminous cytomatosis

A

 Cause unknown
 Hyperplasia of ceruminous
glands
 Symptoms may be Otitis
externa or media

22
Q

otitis externa predisposing factors

A
  • Conformation or obstructive ear diseases
  • Auricular phenotype or Breed (Chinese Shar Pei)
  • External ear moisture (swimmer’s ear)**
  • Excessive cerumen production**
  • Systemic diseases (immune suppression, etc.)
23
Q

otitis externa primary causes

A

-Parasites (Otodectes cynotis “ear mites” and skin parasites)

  • Hypersensitivity reactions (ATOPY, food and contact hypersensitivity)**
  • Keratinization disorders (ENDOCRINE DISEASE)**
  • Foreign bodies
24
Q

cattle lactation

A

 dairy Around 23,000 lbs or 2674 gal per
305 days of lactation

Beef:
IgG receptors are present for about 1
week before parturition and disappear
during lactation
-glands and ducts with fibrovascular stroma

25
failure of passive transfer lesions
-not enough colostrum in first 24 hours. -mild fibrinous polyserositis, polyarthritis, meningitis, -all from endothelial damage and leakage of fibrinogen -diffuse pulmonary edema and congestion: from vasodialation, endothelial leakage and cardio compromise. -skin: generalized petechiation from endo damage-> DIC -spleenomegaly MEATY spleen and lymphomegaly from activation of macrophages.
26
mammary anatomy
 Epithelial remodeling can lead to unchecked hyperplasia and cell transformation  The normal check for this is the stimulus of chronic and solid stress  hyperplasia within the lumen should trigger removal of these cells  If not -- the pre-neoplastic ductal mass may invade surrounding tissue and migrate further
27
portals of entry to mammary
 Ascending infections**: can be forced up ducts by an automated milker (DAIRY). -Bacteria, fungi, parasites - Teat lesions  Direct penetration: Penetrating injury  Systemic infection and localization -Systemic fungi, viruses, mycoplasmas, mycobacteria
28
defense mechanisms of the mammary glands
 Drainage of secretions  NORMAL CONFORMATION of ducts and sphincter  Neutrophils/ macriophages  Lactoferrin:  Increases with MASTITIS and involution, Withholds iron from bacteria  Lysozyme: Cell wall Lysis  Complement  Cytokines  Microbial recognition molecules
29
clinical manifestations of mastitis (types)
1. Severe mastitis (± necrosis) Severe with necrosis = gangrenous mastitis 2. Suppurative mastitis 3. Subclinical mastitis 4. Granulomatous mastitis
30
etiology of mastitis
Contagious:  Streptococcus agalactiae**  Staphylococcus aureus**  Mycoplasma bovis Skin or environmental contaminants:  Escherichia coli  Klebsiella pneumonia
31
streptococcus agalatactia
 Suppurative to Severe (±Necrotizing) mastitis due to endotoxin release  NOT FATAL  Milk quality is altered, and strands or clumps of debris or pus are present in the milk  Associations:  Older cattle, inadequate hygiene and antibacterial treatments -large $$ loss
32
pathogenesis of strep. agalactiae
 Pathogenesis:  Edema + neutrophils -> brief epithelial hyperplasia -> Macrophages and fibrosis in lumen of alveoli -> spreads outward to adjacent alveoli -> INVOLUTION and periductal fibrosis and granulation** -> squamous metaplasia with regeneration of the ducts
33
staphylococcus aureus pracute form
PERACUTE form: most severe, necrosis and infarction (gangrenous)**  Occurs shortly after parturition.  Classic heat, redness, swelling, and pain (inflammation)  progresses to coldness, blue-black color and edema (necrosis)  Can be fatal  Pathogenesis:  Interalveolar edema -> epithelial swelling, vacuolation, and focal erosion (ductal junctions) -> epithelial attachment of bacteria -> focal damage, necrosis and neutrophils -> luminal pus accumulation
34
staph aureus acute form
 ACUTE form: less severe form  Fever, anorexia, toxemia  May be fatal
35
staph aurues chronic form
 Chronic is MOST COMMON FORM  Decreased milk yield  watery with clots  Inflammation and abscessation  can lead to Botryomycosis: granular bacterial and necrotic debris surrounded by granuloma**  Pathogenesis: (<48h post infection)  CHRONIC: similar to S. agalactiae ± lymphocytes
36
mycoplasma bovis
 Sporadic individual cases and outbreaks -> culling ($$$)  Infection by hematogeous and ascending routes  Quarters are enlarged and firm with nodular abscesses  Dramatic drop in milk production  Systemic disease limited  mycoplasmal arthritis or pneumonia
37
coliform mastitis
 Milder forms in herds with good control of contagious mastitis  Environmenatl Bacteria -> ascending infection  Milk quality is altered,  strands or clumps of debris or pus***  Gram negative bacteria with endotoxins (LPS) -> vascular damage  Endotoxemia -> Death  septicemia ~1/3 of clinical cases -in well maintanted healthy herd, enviro basteria: E.coli, klebsiella pneymoniae
38
coliform mastitis acute form
 ACUTE form (Gram negative):  Older cattle, inadequate hygiene and antibacterial treatments  Hyperemia, edema, hemorrhage, necrosis and inflammation centered on the lactiferous ducts  Sequestration:** necrotic mammary tissue separates from the viable tissue (can be a large portion of a quarter)
39
Suppurative mastitis causes
Suppurative mastitis: * Trueperella pyogenes * Mycoplasma bovis * Streptococcus dysgalactia
40
mastitis of sheep
-blue bag:  There are two main bacterial agents recovered from mastitis of sheep:  Mannheimia haemolytica and Staphylococcus aureus  ACUTE, unexpected death:  bacteria cause an acute necrotizing/gangrenous mastitis  "blue bag"  Maedi-visna virus (multisystemic)  chronic inflammation  mammary glands = “hard udder”
41
mastitis of goats
 Staphylococcal and streptococcal mastitis in goats are similar to cattle  Mycoplasma agalactiae:  Inflammation in mammary gland is followed by progressive fibrosis and glandular atrophy, hence dramatic decrease in milk production (agalactia).  This disease is initially septicemic and often fatal.  Caprine arthritis encephalitis virus: Chronic mastitis = hard udder
42
mastitis in dogs
 Mastitis occurs early in lactation or pseudopregnancy**  Staphylococcus sp., Streptococcus sp., and Escherichia coli  May be superimposed on top of mammary hyperplasia or neoplasia
43
mammary tumors dogs and cats
 Cat vs. Dog  Mammary tumors are most common in dogs and uncommon in cats  ~80% are benign in dogs vs. ~80% are malignant in cats -Epithelial and combined epithelial and myoepithelial tumors  Fibrosarcoma and osteosarcoma are particularly aggressive and metastatic  Ovariohysterectomy after the second estrus** dramatically increases the prevalence of this disease.  A high-protein diet decreases susceptibility
44
fibroadenomatous hyperplasia
 Highly prevalent and is the most common disease of the gland  It occurs in young, intact queens (<2y) and most often in SPRING  The lesion is proliferation of mammary ducts and adjacent stroma  Progesterone -> Overstimulation/dysregulation of tissue growth  Hemorrhages, coagulative necrosis, and/or ulceration can occur  Resolution is spontaneous or with ovariohysterectom
45
feline mammary tumors
 Most often carcinomas with relatively wide range of post- excisional survival  Metastasis common  Ovariohysterectomy before the second estrus dramatically decreases the prevalence of mammary tumors in cats**  Cats with neoplasms that are greater than 3 cm in diameter have shorter survival -**graded based on: invasion, mitotic rate, and nuclear shape