Reproductive disorders of the Dog Flashcards

1
Q

What is Cystic Endometrial Hyperplasia?

A
  • Degenerative, progressive, irreversible
  • Progesterone-mediated
    • repeated exposure of the estrogen-primed uterus to progesterone
      • proliferation and secretory activity of endometrial glands
      • Closure of cervix
      • Inhibits myometrial contractility
      • Dilation of the endometrial glands resulting in cysts and endometrial hyperplasia
    • Asymptomatic ⇢ subfertility
      • embryo distribution
      • placentation
    • Predispose to pyometra
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2
Q

What is the CEH-Pyometra Complex?

A
  • During Proestrus and Estrus the cervix opens and bacteria ascend
  • During diestrus progesterone
    • suppresses the immune system
    • stimulates endometrial gland secretion
    • uterine contractility decreases
    • stimulates closure of the cervix
    • RESULTS in:
      • bacterial growth
      • accumulation of inflammatory exudate
  • Bacteria colonize the pathologic endometrium
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3
Q

What are the different types of pyometra

A
  • Open-cervix pyometra
    • uterine drainage is established
    • mild systemic disease
  • Closed-cervix pyometra
    • uterus distends with purulent fluid
    • severe systemic disease due to endotoxemia and septicemia
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4
Q

What is the common signalment and history of patients with pyometra

A
  • 8+ years old
  • Nulliparous > multiparous
  • Commonly seen
    • receiving estrogen for pregnancy termination
    • Progesterone for estrus suppresion/prevention
    • hyperestrogenism: ovarian cysts, granulosa cell tumor
  • No breed predispositions
  • Occurs during diestrus or anestrus
    • 8 wks after estrus (1 wk to 4 months)
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5
Q

What are the clinical signs of Pyometra?

A
  • Anorexia
  • Depression
  • Vomiting
  • Diarrhea
  • PU/PD
  • Enlarged uterus
  • Abdominal enlargement
  • Vulvar discharge
    • malodorous
    • mucoid to watery, red-brown
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6
Q

What is the clinical pathology of pyometra?

A
  • Leukocytosis
  • Neutrophilia
  • Hyperproteinemia
  • Hypergloculinema
  • If endotoxemia/septicemia
    • leukopenia
    • neutropenia
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7
Q

How is pyometra diagnosed?

A
  • Recent history of estrus
  • Clinical signs
  • Vaginal cytology and aerobic culture
    • E. coli
    • Streptococcus spp. Staphylococcus spp, pasteruella multocida, pseudomonas aeurginosa
  • Diagnostic imaging
    • abdominal palpation, radiographs/US
  • Pyometra should be considered in any ill post-estrual intact female
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8
Q

What is the treatment for CEH-Pyometra complex?

A
  • OHE
    • CEH is irreversible
    • predisposed to recurrence
  • Medical therapy
    • young, genetically valuable
    • Open-cervix, no systemic illness
    • too compromised for surgery
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9
Q

What are the goals of medical management of pyometra?

A
  • Remove the effects of progesterone
  • Maintain and promote an open cervix
  • Promote uterine evacuation
  • Control bacterial growth
    • Antibiotics up to 4 weeks
    • Culture and sensitivity
    • Ampicillin 20 mg/kg PO TID
  • Promote endometrial regeneration
    • prolong anestrus
    • mibolerone for 2-3months following treatment of pyometra
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10
Q

What is the medical treatment for pyometra?

A
  • PGF2a
    • Luteolysis
    • uterine contractions and evacuation
    • Measure progesterone
      • >2ng/ml indicates functional luteal tissue
      • Progesterone inhibits uterine contractility
    • Dinoprost
      • 0.1-0.5 mg/kg SC BID-TID
      • 2-7 days or until uterine size returns to normal
  • Combo dinoprost and bromocriptine
    • faster luteolysis and resolution
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11
Q

What is the prognosis for pyometra

A
  • Good if improvement clinically w/in 48 hrs
    • vulvar discharge stops in 4-7days
    • leukogram w/in normal values 10-15 days
    • Survival rate with medical therapy 80%
    • Recurrence 10-77%
    • 40-68% conception rate on next estrus
      • failure to conceive
      • early embryonic death
      • abortion
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12
Q

How can pyometra be prevented from recurrence?

A
  • Vaginal culture at next proestrus
  • Breed at the next estrus
  • OHE
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13
Q

What is vaginitis

A
  • Inflammation of the mucosal lining of the vagina
  • Forms:
    • Juvenile (pre-pubertal) - self-limiting
      • immaturity of the vaginal canal and epithelium
      • immaturity of natural immune system defense mechanism
      • transient inflammation from bacterial colonization until natural defenses develop
      • Resolves with first estrus
    • Adult (post-pubertal)
      • Bacterial or viral infection
      • Urine pooling
      • UTI
      • anatomical abnormalities
      • Foreign body or neoplasia
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14
Q

What are the clinical signs of vaginitis

A
  • purulent or mucopurulent vulvar discharge
  • Excessive vulvar licking
    • vulvar hyperemia
    • clitoral hypertrophy
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15
Q

How is vaginitis diagnosed?

A
  • Vaginal cytology
    • large number of neutrophils
    • non-cornified epithelial cells
  • Vaginoscopy
    • hyperemia
    • +/- follicular hyperplasia
  • Vaginal culture
    • overgrowth of single isolate of normal flora
      • E. coli, B-hemolytic streps, S. aureus and intermedius
  • brucella canis and canine herpes virus
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16
Q

What is the treatment for vaginitis

A
  • juvenile form is self-limiting
  • ID and terating the predisposing cause
  • Systemic antibiotics for 4 weeks
  • SPayed females with no underlying cause:
    • oral estrogen to reinstate local defense mechanisms
    • Diethylstilbestrol: 1mg PO SID for 5 days followed by 1 mg PO twice weekly for 2-3wks. then decrease to once weekly unless sings recur
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17
Q

What is vaginal hyperplasia

A
  • Extrusion of the vaginal mucosal lining through the vulva
  • Estrogen-mediated
    • exacerbation of normal thickening of the vaginal squamous epithelium and edema
    • proestrus and estrus
  • Adult, intact females
  • occur during any estrous cycle
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17
Q

What are the clinical signs of vaginal hyperplasia

A
  • Solid tumor-like mass protruding from the vulva
  • Mucosal excoriation
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18
Q

What is the treatment for vaginal hyperplasia?

A
  • Self-limiting
  • Induce ovulation: GnRH or hCG
  • Keep tissue clean and prevent trauma
    • tissue regresses with the onset of diestrus
    • Does not affect fertility
    • Recurrence 66-100%
  • Purse-string suture
  • OHE or ovariectomy
19
Q

What are the causes of failure to cycle in the bitch

A
  • Previous OHE or ovariectomy
  • Husbandry
  • Silent Heat
  • Endocrine or systemic disease
    • Hypothyroidism
    • Hyperadrenocorticism
    • Diabetes mellitus
  • Exogenous steroids
  • Luteal cyst
  • Aging
20
Q

How can the presence of ovaries in a bitch be determined/?

A
  • Serum concentrations of gonadotropins LH and FSH are elevated because of lack of negative estrogen feedback from the ovary to the pituitary
    • Estrogen - negative feedback
      • occurs during follicular phases when estrogen levels are still low
      • Following Ovariectomy ⇢ loss of negative feedback resulting from an increase in FSH and LH
      • LH secretions increase w/in 10 days of Ovariectomy
  • Serum LH Test Kit:
    • Positive if LH >1ng/ml
    • Negative = intact
    • Sensitivity 98%
21
Q

What happens to progesterone and Anti-muellerian hormone (AMH) due to failure to cycle? How can these be used to judge whether or not ovaries are preset

A
  • Progesterone:
    • <0.2 ng.ml in dogs w/out ovaries
    • Rise following ovulatoin
  • Anti-Muellerian Hormone (AMH)
    • Produced solely by granulosa cells
    • Used at any point of estrous cycle in post-pubertal femal
    • Utilized to detect ORS
22
Q

What is Canine Brucellosis

A
  • Reportable disease in most states
  • Most common presentation is abortion in late gestation
    • 45-60 days
    • W/out signs of maternal illness
    • If pregnancy reaches term both live and dead puppies may be born
      • die w/in a few days
      • generalized lymphadenomagaly, hyperglobulinemia, recurrent fever, leukocytosis and seizures
  • Causes:
    • Brucella canis **
    • Brucella melitensis
    • Brucella suis
    • Brucella abortus
  • Phagocytosis by macrophages occurs at the site of bacterial exposure
  • Replicates in lymphatic and genital tissue
  • Prolonged bacteremia may be intermittent
23
Q

How is Canine Brucellosis transmitted?

A
  • Routes:
    • Oral
    • vaginal
    • Conjunctival
    • Transplacental
  • Infectious:
    • Vulvar discharge
    • Milk
    • Urine
    • Semen
    • Aborted tissue
    • fetal membranes
  • 1-4 week incubation
  • 6-64 months of shedding
24
Q

What are the clinical signs of Canine Brucellosis?

A
  • Systemically Asymptomatic
  • Reproductive:
    • Embryonic death
    • Abortion
      • 7-9 wks gestation
      • prolonged vaginal discharge following
    • Still birth
    • Vulvar discharge
    • Testicular atrophy
    • Epididymitis
    • Scrotal dermatitis
25
Q

How is Canine Brucellosis diagnosed

A
  • SUspect if a healhty female aborts approximately 2 wks before term or if she fails to whelp following an apparently successful mating
  • Definitive:
    • Culture
      • blood
      • lymphnode aspirates
      • aborted material
      • vulvar discharge urine
    • PCR
    • AGID
26
Q

What is the treatment for Canine Bruceloosis

A
  • Intracellular location of organisms makes achieving effictive antibiotic levels difficult
  • Antibiotic therapy is unreleable and often unsuccessful at eliminating the organism from tissues
    • dog may relapse afer stopping treatment
    • Combo tetracycline (4wk) w/ gentamicin for first 2wk
    • combo tetracyclein (4wk) w/ streptomycin for first 2wk
  • Sterilization
    • Proestrus, estrus, pregnancy and abortion
    • shed in urine
    • tissue persistence
  • Euthanasia
27
Q

How is canine brucellosis controlled

A
  • Quarantine and test new dogs 2x at 30 day intervals
  • Remove proven positive dogs form breeding program
  • Use only Brucella negative males
  • Test all animals at 3-6 month intervals
  • Positive dogs on property ⇢ quarantine and test all dogs monthly
    • require 3 consecutive negative tests
  • Prognosis for cure without recrudescence is guardd
28
Q

What is Canine herpes virus 1

A
  • Mild respiratory disease in adults
  • Severe viral infection of puppies worldwide
    • often 100% mortality rate
    • Focal necrosis and hemorrhage
  • Seroprevalence 20-98%
  • Lifelong llatent infection
    • persists in tonsils and parotid salivary gland
29
Q

What are the clinical signs of canine herpes virus 1

A
  • classic presentation of the infected female
    • loss of previously confirmed pregnancy
    • Birth of abnormal, nonviable pups
      • stillborn
      • low birth weight
      • weak
  • Abortion
  • Maceration
  • Mummification
  • Stillbirth
  • neonatal death < 1wk
30
Q

How is Canine herpes virus 1 transmitted?

A
  • Transplacentally
  • Passage through the birth canal (Vulvar discharge)
  • Oronasal secretions
  • Venereal
  • Aborted tissues
31
Q

How is canine herpes virus 1 diagnosed?

A
  • Poorly immunogenic
    • short lived antibody response
    • paired serum samples
  • Virus isolation or immuno fluorescence
    • nasal or vaginal swabs
    • aborted tissues
  • Histopathology
    • necrosis and viral inclusion bodies in placenta and fetal tissues
32
Q

What is the treatment for Cnine herpes virus 1

A
  • Unnecessary in adults
    • self-limiting in immune competent
  • Neonates
    • supportive care and antiviral therapy
    • persistent neurological and myocardial damage
    • shed large amounts of virus for 2-3wks
33
Q

How ic canine herpes virus 1 controlled

A
  • No vaccine
  • Expose naive female prior to breeding
    • high titer have protective immunity
    • less likely to develop reproductive or neonatl problems
  • Isolate during the last 3 wks of testation & first 3 wks after parturition
  • Good biosecurity
  • Neonatal prophylaxis
    • ensure adequate colostrum
    • immunized serum from preciously infected animal
    • maintain adequate ambient temperature
34
Q

How should a post-partum bitch be monitored? what for?

A
  • Rectal temperatures daily for 2 weeks
    • metritis
    • mastitis
    • eclampsia
  • Vulvar discharge
    • greenish black to tan for 3wks
    • non-odorous
  • Mammary glands
    • secretions white to yellowish
    • no heat, non-painful
35
Q

What is subinvolution o placental sites?

A
  • Failure of fetal trophoblastic cells to degenerate
  • abnormal involution/repair endometrial placental sites
    • continued invasion of the uterus by trophoblastic cells
      • endometrium
      • myometrium
    • Systemic signs normally not present
  • May result in
    • damage to blood cessels
    • endometrial ulceration
    • uterine perforation
36
Q

What are the signs of subinvolution of placental sights? differentials?

A
  • Uncomplicated gestation and parturition
  • Present with vulvar hemorrhage
    • >3wks post-partum
    • intermittent or persistent
  • DDx:
    • metritis
    • vaginitis
    • cystitis
    • trauma
    • vaginal neoplasia
    • brucellosis
    • coagulopathy
37
Q

How is subinvolution of placental sites diagnosed

A
  • Presumptive dx
    • persistent hemorrhagic discharge
    • otherwise healthy
  • Radiographs or US
    • placental sites are 2x size of normal
  • Vaginal cytology
    • trophoblast-like cells
    • Pathognomonic >4 days post-partum
38
Q

What is the treatment for subinvolution of placental sites? Prognosis

A
  • Spontaneous resolution
  • Severe cases:
    • blood transfusion
    • OHE
  • Prognosis:
    • reproductive potential is not compromised
    • Not predisposed to SIPS in subsequent pregnancies
39
Q

What is Post-partum metritis

A
  • Inflammation of the endometrium and myometrium
  • Develops within the 1st wk post-partum
  • prolonged delivery
  • Dystocia
  • retained fetus or fetal membranes
  • Dilated post-partum cervix leave the uterus vulnerable to ascending infection
    • retained tisue or lochia serve as ideal grouth medium
40
Q

Clinical signs of Post-partum metritis

A
  • Depression
  • anorexia
  • fever
  • vomiting
  • neglect of puppies
  • Malodorous, red-brown, purulent vulvar discharge
  • endotoxemia
  • septicemia
41
Q

how is post-partum metritis diagnosed

A
  • Clinical signs
  • vaginal cytology - degenerate neutrophils
  • Bactreial Culture - aerobic and anaerobic
  • US and Radiographs
42
Q

What is the treatment for post-partum metritis

A
  • Stabilize patient
  • Broad-spectrum antibiotics
  • Ecbolics - cautiously
    • devitalized uterus could be prone to rupture
  • Surgical evacuation of uterine contents
    • fetal membranes
    • pups
  • OHE
  • Prognosis for future fertility - normal
43
Q

What is Eclampsia?

A
  • Depletion of ionized calcium increases membrane permeability and results in spontaneous muscle depoolarization when demand for milk is high
  • Most cases present 1-4eks post-partum
44
Q

What are the signs of eclampsia

A
  • Restlessness
  • nervousness
  • whining
  • panting
  • muscle tremors
  • dilated pupils
  • hypertherma (>105
  • Can progress to recumbency, extensor rigidity, convulsions and death
45
Q

HOw is eclampsia diagnosed

A
  • Hx
  • Clinical signs
  • Ionized hypocalcemia
    • some may have normal total calcium conentraiotn
      • <7mg/dl indicates hypocalcemia
  • +/- hypoglycemia
46
Q

Treatment for exlampsia

A
  • immediate calcium supplementation
  • Correct hypoglycemia
  • lower body temperature
  • remove puppies for at least 24 hrs ow wean
  • Hypocalcemia may recur during corrent lactation and subsequent litters
  • Prevent w/ balanced diet with Ca:P ratio of 1:1 or 1.2:1