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VET410 Endocrine/Reproduction > V410 Exam II > Flashcards

V410 Exam II Flashcards

1
Q

(L32) Unlike cows and dogs, horses are what kind of breeders?

A

Horses are long day seasonal breeders. They begin cycling in the spring.

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2
Q

(L32) Dogs exhibit a lot of variation in the length of anestrus. Horses exhibit variation in the length of which phase?

A

Horses exhibit huge variation in the length of estrus as they transition into the breeding season. With the beginning of spring, estrus can last for weeks and it’s not until cycles are predictable that horses are considered fertile.

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3
Q

(L32) Describe how the equine estrus cycle is different from the canine. How can you tell which phase they are in?

A

Horses do not exhibit proestrus and metestrus; they only undergo estrus and diestrus. They’re considered in estrus when they are receptive to a male and in diestrus after ovulation and when they’re no longer receptive.

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4
Q

(L32) Equine receptivity during estrus is most associated with which hormone?

A

The behavioral changes during estrus are thought to be primarily caused by decreasing progesterone (as opposed to increasing estradiol).

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5
Q

(L32) In which phase do mares ovulate? How is this different from the cow?

A

Mares ovulate before estrus ends. Cattle ovulate ~12 hours after estrus.

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6
Q

(L32) Like cows, horses have luteolytic mechanisms. Describe how they’re different.

A

In cows, a positive-positive feedback loop between endometrial PGF2-a and luteal oxytocin causes luteolysis.

In horses, however, the origin of the oxytocin is unknown (it could be from the endometrium or the posterior pituitary). Luteolysis is also systemic in horses; both uterine horns secrete PGF2-a which can circulate through the entire body. Though some of it gets metabolized in the lungs, enough comes back to the ovaries to induce luteolysis.

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7
Q

(L32) What kind of oocyte do mares ovulate? How does this compare to a dog or cattle?

A

Like cattle, mares ovulate a secondary oocyte that can be fertilized. Dogs ovulate a primary oocyte which hasn’t extruded its first polar body yet and, thus, cannot be fertilized.

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8
Q

(L32, 34) How does the equine embryo reach the uterine horn?

A

Around day 6, the equine embryo will reach the junction between the oviduct and the uterine horn. To enter, it releases prostaglandins (PGE2 mostly), to relax the smooth muscle, gaining passage. Unfertilized oocytes cannot signal and remain trapped in the oviduct.

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9
Q

(L32) What embryological structure facilitates trans-uterine migration in the horse? How does the uterus facilitate migration?

A

Horse embryos develop an embryonic capsule around day 6 which maintains its shape and protects it during migration. The embryo then migrates extensively between days 11 and 16, moved by endometrial contractions driven by PGE2 release.

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10
Q

(L32) What is different about the equine ovarian artery and uterine vein from the cow?

A

In cows, these two vessels are closely associated, which facilitates local circulation of PGF2-a.

In horses, there is not anatomic association between these two vessels, so PGF2-a is released systemically before reaching the ovary. There is less metabolism of PGF2-a in the equine lungs and horses appear to be more susceptible to PGF2-a, meaning that even the relatively small amount that returns can still induce luteolysis.

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11
Q

(L32) Say you have a mare with uterine unicornis or you unilaterally remove one of her uterine horns. How will she cycle?

A

Mares with one uterine horn will continue to cycle normally. No matter which side she ovulates on, the systemic path of PGF2-a ensures that there is luteolysis to either ovary.

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12
Q

(L32) How is maternal recognition of pregnancy established in the horse? How is this different than in cattle?

A

The equine embryo migrates throughout the uterus between days 11-16. However, the signal blocking endometrial release of PGF2-a in horses is not known.

In contrast, bovine embryos implant locally ipsilateral to the side they ovulate on and secrete interferon tau.

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13
Q

(L32) Over the course of development, horse fetuses have two types of placenta. What are they?

A

Initially, the horse fetus is nourished by the chorio-vitelline/yolk sac placenta until days 35-40. Then, it’s replaced by the more effective chorio-allantoic placenta.

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14
Q

(L33) Describe how endometrial cups and allantoic pouches form.

A

Trophoblasts from the chorionic girdle migrate and implant onto the endometrium, forming endometrial cups. By day 35-40, these structures start secreting eCG. Eventually, these trophoblast aggregates are rejected by the endometrium and taken up by the placental membranes, forming allantoic pouches.

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15
Q

(L33) What is eCG’s function?

A

eCG is morphologically identical to and acts like eLH. Thus, it can increase progesterone secretion by luteinizing other follicles and forming secondary corpora lutea.

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16
Q

(L28, 30, 33) How do dogs, cows, and horses differ in their sources of progesterone over the course of gestation?

A

Dogs entirely rely on luteal progesterone in order to maintain pregnancy.

The CL of cows secretes enough progesterone in order to maintain the pregnancy until day 150, after which the placenta supports itself with its own progesterone. However, the CL takes over progesterone support after day 240.

Horses are the least reliant on luteal progesterone - the equine placenta takes over progestogenic support of pregnancy after day 180-200.

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17
Q

(L33) How is 5-alpha-reductase involved in the maintenance of pregnancy in horses?

A

5-alpha-reductase expressed in the placenta converts progesterone into DHP, which is functionally similar and is responsible for maintaining progesterone support for the pregnancy.

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18
Q

(L33) What is the luteo-placental shift in horses?

A

In horses, there is a shift between luteal progesterone and placental progesterone in the maintenance of pregnancy. Around day 105 of gestation, increasing amounts of placental DHP replaces falling concentrations of luteal progesterone in supporting the fetus.

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19
Q

(L33) Why and how does regumate protect against luteal insufficiency?

A

Around the luteo-placental shift, if the manager is worried about a possible luteal progesterone deficiency, they can give regumate as a progestin therapy to supplement luteal progesterone. This treatment would continue until placental DHP takes over. This ensures that there is always enough progesterone to support the fetus.

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20
Q

(L33) The fetal equine gonads are hormonally active. What do they secrete?

A

The fetal gonads secrete DHEA, a weak androgen that is converted into estrone sulphate.

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21
Q

(L33) What is the feto-placental unit?

A

The feto-placental unit describes how androgens secreted by the fetal equine gonads are converted into estrogens, namely estrone sulphate. An assay for estrone sulphate in the maternal serum can be used to diagnose pregnancy.

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22
Q

(L30, 33) Cows and horses both exhibit progesterone withdrawal right before parturition. How is it different between the two species?

A

In cows, progesterone withdrawal is facilitated by cortisol and luteolysis. This removes progesterone support for the fetus. In horses, the progesterone withdrawal is caused by decreased fetal expression of 5-alpha-reductase, ending DHP support.

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23
Q

(L33) Describe three functions of cortisol before birth in the horse.

A

Activation of the fetal H-P axis and the subsequent release of cortisol does three things:

  1. increases surfactant secretion in the lungs
  2. prepares the gut for colostrum
  3. increases glycogenesis in the fetal liver
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24
Q

(L33) Around what time of day do most equine births occur?

A

At night

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25
Q

(L33) Oxytocin and PGF-a can be used to induce parturition in horses. However, the pregnancy is not maintained by a CL. How do these therapeutics work?

A

PGF2-a and oxytocin directly stimulate uterine contractions.

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26
Q

(L34) What egg layers do sperm cells need to cross in order to fertilize an egg? How is this accomplished?

A

A sperm cell needs to penetrate the cumulus cells of the corona radiata and the zona pellucida. This is accomplished via an acrosome reaction, where the sperm cell releases collagenases and proteases stored within the acrosome.

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27
Q

(L34) A sperm cell has manged to cross the egg’s zona pellucida. What protein does it release into the egg and what process does this protein initiate?

A

The sperm cell releases oscillin which initiates a series of calcium spikes within the egg. This ultimately activates the egg for mitosis with the sperm.

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28
Q

(L34) There are two mechanisms by which an egg prevents polyspermy. What are they?

A

Fast block: This process occurs within milliseconds of a sperm cell binding the egg. Depolarization of the egg’s plasma membrane prevents any other sperm from binding to it.
Slow block: This process occurs within 1-2 minutes of a sperm binding the egg. Cortical granules are exocytosed onto the egg’s membrane, containing proteases that prevent any additional sperm from binding.

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29
Q

(L34) Describe initial embryo development before the embryo implants onto the uterine horn.

A

After fertilization, the zygote is formed. Every 24 hours, here is cellular cleavage, producing new totipotent cells. The zygote transitions from a 2-cell, to a 4-cell, to an 8-cell embryo. A 16 cell embryo is called a morula. Eventually, the embryo is subdivided into an inner cell mass and the trophoblast.

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30
Q

(L34) What three cell layers does gastrulation form?

A

Endoderm
Mesoderm
Ectoderm

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31
Q

(L34) What is retrograde sperm loss?

A

Retrograde sperm loss is the first major loss of sperm cells within the female reproductive tract. After ejaculation, the withdrawal of of the penis also draws some semen out with it.

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32
Q

(L34) After ejaculation, sperm reaches the site of fertilization in one of two ways. What are they?

A

Rapid sperm transport occurs immediately after ejaculation. Myometrial contractions move sperm directly into the uterus and oviduct. However, these sperm cells do not participate in fertilization because they don’t undergo capacitation.
In slow sperm transport, sperm cells swim up through the oviduct to the site of fertilization. These cells undergo capacitation in the isthmus.

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33
Q

(L34) The female reproductive tract preferentially selects for morphologically and functionally normal sperm cells. How?

A

Only progressive, highly motile sperm will reach the egg to fertilize it. Only sperm cells that survive retrograde loss, uterine leukocytes, and undergo capacitation in the oviduct can fertilize an egg.

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34
Q

(L35) What is the gonadal determining region in goats and how can it cause intersexuality?

A

The gonadal determining region is an autosomal gene linked to the gene controlling the polled condition in goats. An individual homozygous for the polled gene will develop male pseudohermaphroditism or ovotestes.

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35
Q

(L35) What is XO monosomy? What species is it common in?

A

XO monosomy, or Turner’s syndrome, is common in mares. The presence of only one X chromosome causes the development of hypoplastic ovaries that lack germ cells or follicles with possible hypoplasia of the oviduct and uterus.

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36
Q

(L35) What are paraovarian cysts? What sturctures are they thought to arise from?

A

Paraovarian cysts are adjacent to the ovaries and are thought to arise from the remnants of Mullerian or Wolffian ducts. Usually, they are clinically insignificant and do not affect fertility.

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37
Q

(L35) What are the three ways that ovarian cysts can be clinically significant?

A
  1. If they are hormonally active and disrupt cyclicity
  2. They destroy ovarian parenchyma
  3. They physically impede ovarian function
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38
Q

(L35) What are subsurface epithelial structure cysts? Which species are they relevant in?

A

In dogs, subsurface epithelial structures are invaginations of the germinal cell epithelium. These cavitations can then become fluid-filled. These usually do not affect ovulation and follicular development.

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39
Q

(L35) What is cystic rete ovarii? What species is it relevant in?

A

In dogs and cats, a cystic rete ovarii arises from the ovarian medulla, near where the vessels enter and leave the ovary, and can compress the cortex.

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40
Q

(L35) What are epithelial inclusion cysts? What species are they important in?

A

Epithelial inclusion cysts are also called fossa cysts, which form in the equine ovulation fossa. They can physically impede ovulation.

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41
Q

(L35) What is cystic ovarian disease? What species is it relevant in?

A

In cows, anovulatory follicles are termed cystic ovarian disease. Without ovulation and the formation of a CL, these females present as either in persistent anestrus or estrus or possibly with nymphomania (most present in anestrus).

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42
Q

(L35) What are luteinized follicular cysts and how they are different from a cystic CL?

A

Luteinized follicular cysts are anovulatory follicles with a rim of luteal tissue around them. A cystic CL suggests that ovulation has occurred and CL development was possible. In contrast, a luteinized follicular cyst is inovulatory and will not have a palpable crown.

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43
Q

(L35) Describe a granulosa-theca cell tumor and its clinical effects.

A

GCTs, usually seen in mares, are neoplastic granulosa or theca cells that are hormonally active; they can secrete inhibins, testosterone, and AMH. Affected females will have disrupted cycles and may exhibit male behavior.

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44
Q

(L35) What neoplasia is associated with the germinal epithelium of the ovary?

A

Cystadenoma

Carcinoma of the germinal epithelium

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45
Q

(L35) What are two germ cell tumors in the ovary?

A

Dysgerminoma

Teratoma

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46
Q

(L35) Which ovarian neoplasia is often seen in birds, especially chickens?

A

Adenocarcinoma of the germinal epithelium with carcinomatosis is common.

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47
Q

(L35) What is oophoritis?

A

Inflammation of the ovaries

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48
Q

(L35) Uterine hyperplasia can result from abnormally high steroid levels. However, how can hyperplasia occur when steroid hormone levels are normal?

A

Hyperplasia can occur if an animal is forced to continue cycling without ever achieving pregnancy. Endometrial proliferation overtakes apoptosis so there is net growth.

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49
Q

(L35) What are some neoplasia of the endometrium?

A

Adenomas

Carcinomas seen mostly in rabbits

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50
Q

(L35) What are some neoplasia of the uterine wall?

A

Leiomyoma/sarcoma
Fibroleiomyoma
(neoplasia of smooth muscle)

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51
Q

(L35) What are endometrial nodules?

A

They’re inflammatory-associated polyps seen in cats and dogs. These pedunculated masses of fibrous connective tissue and cystic glands should not be confused with endometrial carcinomas, which are rare except for in the rabbit.

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52
Q

(L35) How does progesterone exacerbate a uterine infection?

A

Progesterone stimulates the closure of the cervix, contributing to the development of a pyometra if any pathogens are trapped in the uterus. Additionally, since the cervix is closed, the infection can’t be cleared out.

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53
Q

(L36) What are some causes of female infertility with a normal cycle?

A
  1. The male is infertile
  2. There is a developmental or acquired anatomic abnormality
  3. There is a reproductive tract disease
  4. The management of breeding isn’t good
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54
Q

(L36) What are some anatomic abnormalities that would cause a female to be infertile (without affecting her cyclicity)?

A

Think things that would predispose to inflammation/infection:

  1. A hooded vulva, which predisposes to vaginitis
  2. Abnormal perineal conformation, where the vulva is misaligned to the uterus, possibly exposing it to fecal material
  3. A loose vulva, preventing the formation of a tight seal
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55
Q

(L36) What are some examples of a reproductive tract disease that could cause infertility (without affecting a female’s cyclicity)?

A
  1. Endometritis
  2. Metritis
  3. Fibrosis
  4. Endometrial cysts
  5. Neoplasia
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56
Q

(L36) What are some causes of female infertility that would disrupt cyclicity?

A

Think systemic issues/disease:

  1. Malnutrition
  2. Endocrine disorders
  3. Neoplasia
  4. The use of anabolic steroids

Think hormone disruption:

  1. Anovulatory follicles
  2. Persistent CL
  3. Developmental abnormalities
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57
Q

(L36) How would malnutrition impact fertility?

A

Only excess malnutrition would impair cyclicity. However severe metabolic stress and disease could also cause infertility.

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58
Q

(L36) Developmental abnormalities can cause infertility with or without disrupting cyclicity. Why is that the case?

A

There are some developmental abnormalities that are purely structural e.g. strictures, septae. However, intersex conditions in which hormone production is impacted e.g. sex reversal, freemartinism, segmental aplasia of the reproductive tract that will severely impair a female’s cycle.

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59
Q

(L36) An anovulatory follicle will cause infertility while disrupting a female’s cycle. How? How would you resolve an anovulatory follicle?

A

An anovulatory follicle is hormonally active. It will continue secreting estradiol and prolonging the follicular phase. These can be treated with GnRH or hCG to induce ovulation or with LH after the follicle has luteinized.

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60
Q

(L36) A persistent CL will cause infertility while disrupting a female’s cycle. How? How would you resolve a persistent CL?

A

A persistent CL would extend the luteal phase and prevent short cycling through continued progesterone secretion. A persistent CL can be treated with PGF2-a to induce luteolysis.

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61
Q

(L36) What is diestral ovulation in mares?

A

Diestral ovulation, like a retained CL, will extend the luteal phase through extra progesterone secretion. However, the pathogenesis is different: a mare may ovulate normally during estrus, but during diestrus, one of the follicles associated with a follicular wave may also ovulate and form a second CL. Luteolysis will cause regression of the first CL, but the second one will be too immature to respond and will continue secreting progesterone.

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62
Q

(L36) What are some causes of early embryonic loss?

A
  1. Embryonic defect
  2. Maternal age
  3. Maternal infection
  4. Maternal Malnutrition
  5. Maternal Anabolic steroid use
  6. Maternal Luteal insufficiency
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63
Q

(L36) How would luteal insufficiency contribute to infertility? How can you treat it?

A

Luteal insufficiency describes when the CL does not produce enough progesterone to support the pregnancy, either secondary to endometritis, systemic disease, or maternal stress. It can be treated with administration of exogenous progesterone.

64
Q

(L36) What are some causes of late term abortion?

A

Think compromised placental blood flow:

  1. Uterine torsion
  2. Umbilical torsion

Think inadequate nutrition:
3. Twins in the mare

Think inflammation/disease:

  1. Placentitis
  2. Maternal infection
  3. Toxicity
65
Q

(L37) Briefly, what are the three stages of parturition?

A

Stage I - dilation and positioning
Stage II - fetal expulsion
Stage III - expulsion of fetal membranes

66
Q

(L37) Describe stage I of parturition. When does it end?

A

Stage I is characterized by cervical dilation, uterine contractions, and repositioning of the fetus to facilitate parturition. It ends with the fetus breaching the cervix and entering the proximal vagina, engaging the Fergusson reflex.

67
Q

(L37) Describe stage II of parturition. How long does it last across various species?

A

Stage II is characterized by fetal expulsion. In horses, this phase lasts only about 15-20 minutes, while stage II in cows can last anywhere from 1-4 hours. In litter bearing species, the length of stage II depends on the the size of the litter, lasting anywhere from 1-12 hours.

68
Q

(L37) Describe stage III of parturition. How does it vary across species?

A

Stage III is characterized by expulsion of the fetal membranes. How long the placenta is retained varies: mares should expel in about 2 hours, while, in ruminants, the placenta can be retained for up to 8 hours without issue. In dogs and cats, the placental membranes are delivered with the neonates.

69
Q

(L37) What are the four causes of dystocia?

A 
Think maternal issue:
1. Pathology of the maternal anatomy
2. Failure of the cervix to open 
Think fetal issue:
3. Fetal-maternal mismatch
4. Improper fetal positioning, presentation, or posture
70
Q

(L37) What is uterine inertia and how does it contribute to dystocia?

A

Uterine inertia is failure of the uterine muscles to contract during parturition. Primary uterine inertia is when there is a failure to initiate labor, often the result of hypocalcemia. Secondary inertia can be considered fatigue, where prolonged dystocia leaves the uterine smooth muscle depleted.

71
Q

(L37) What are the three different presentations possible for a fetus during parturition?

A

Anterior/cranial presentation
Posterior/caudal presentation
Transverse

72
Q

(L37) What are the four possible positions for a fetus during parturition?

A

Dorso-sacral
Dorso-pubic
Dorso-left
Dorso-right

73
Q

(L37) What is the normal posture for large animal fetuses during parturition?

A

Normally, large animals are born with their legs fully stretched in front of them in a diving position.

74
Q

(L37) What abnormalities to position, presentation, and posture are associated with a true breech?

A

In a true breech, the fetus is born with caudal presentation, dorso-sacral presentation, and with both legs flexed at the hips.

75
Q

(L37) You suspect a dam is experiencing dystocia. What diagnostics are possible to confirm this diagnosis and do they tell you?

A
  1. A physical/vaginal exam - allows for assessment of the dam and p/p/p of the fetus
  2. Ultrasound - visualizes the fetus for assessment of viability and retained placentas
  3. X-ray - allows for enumeration and assessing viability
76
Q

(L38) Where is the uterine body normally located on a radiograph?

A

The uterine body is normally between the colon and the bladder.

77
Q

(L38) The uterine body isn’t always easily visualized on a radiograph or on ultrasound, even in a healthy female. Why?

A

The size of the uterus varies with cyclicity - it may enlarge during estrus or be very small during anestrus.

78
Q

(L38) You take a radiograph and suspect that the uterus is enlarged. What radiographic signs would confirm that?

A
  1. The colon cranially displaced in the caudal abdomen

2. Distended soft-tissue tubular structures in the middle and caudal abdomen

79
Q

(L38) You’re ultrasounding the bladder in transverse and you see a large thick-walled tubular structure immediately dorsal to it. The contents are a relatively echogenic fluid. What could this structure be? What type of fluid is it?

A

A diseased uterus, on U/S, can appear as fluid-filled tubular structure in the area of the bladder. The echogenic fluid inside it may be pus, blood, or high protein fluid - anything that would make it more echogenic than normal fluid.

80
Q

(L38) An enlarged uterus can sometimes be confused for bowel loops. What are two sonographic signs that would suggest what you’re seeing is bowel loops as opposed to a uterus?

A

Bowel loops are more likely to have gas in them than the uterus (though there are exceptions) and will show peristalsis.

81
Q

(L38) What are the advantages of using a x-rays to diagnose pregnancy vs. an ultrasound?

A

X-rays more easily allow you to count the number of fetuses, especially when fetal development has reached the point at which fully formed skeletons can be seen. They can also suggest fetal viability by indicating whether the fetuses are associated with gas or not and whether their skeletons are properly ordered. U/S similarly lets you check fetal viability by looking at the fetal heartbeat and at movement. Counting the number of fetuses is much harder on U/S.

82
Q

(L38) What imaging signs would indicate that a fetus is dead?

A
  1. Misalignment of the skull and cervical spine
  2. Gas surrounding the fetuses
  3. Lack of a heartbeat or movement
  4. Bones in the uterus that aren’t arranged in normal anatomy
83
Q

(L38) You’re ultrasounding the ovaries of an intact female in heat and you see fluid-filled structures ~1 cm in diameter in the ovarian parenchyma. What could they be?

A

Follicles

84
Q

(L38) What are some imaging characteristics of ovarian neoplasia?

A

Ovarian neoplasia is aggressive. They’re heterogenous and have mixed echogenicity. Secondary lesions include ascites, cysts, and carcinomatosis.

85
Q

(L38, 39) What is maceration? What type of pathogen is it associated with? What imaging sign might suggest maceration?

A

Maceration is liquefaction of fetal soft tissue, leaving behind only bones and emphysema may or may not be associated. It’s mostly caused by a bacterial infection, but can also be exacerbated by prolonged fetal retention. Bacteria are also gas-producing so seeing gas around the fetuses on a radiograph or ultrasound suggests that maceration is occurring.

86
Q

(L39) What is mummification? How is it different from maceration?

A

Mummification is desiccation of the fetus. Unlike maceration, mummification is more associated with viral infections and polytocous species.

87
Q

(L39) Differentiate abortion from stillbirth.

A

Abortion is death of the fetus before it’s capable of independent life. A stillborn is born fully developed, but dead.

88
Q

(L39) What is fetal macrosomia? What kind of issue would it contribute to?

A

Macrosomia is also known as fetal maternal size mismatch. In other words, the fetus is large for the female to easily birth, contributing to dystocia. There are a lot of potential causes include prolonged retention, genetics, diabetes, and dam obesity.

89
Q

(L39) What is schistosomus reflex? What are the different components of this abnormality?

A

Schistosomus reflex is a abortive fetal defect with several components:
spinal inversion, fissured abdominal wall, ankylosis, and lung and diaphragm hypoplasia

90
Q

(L39) What is an amorphous globosus?

A

An amorphous globosus is an acardiac twin that is supplied by the live twin. It resembles a ball of skin and fur surrounding fat.

91
Q

(L39) Why can’t a mare support twins?

A

With twins, the two placentas press up against one another, reducing the surface area available for nutrient supply.

92
Q

(L39) What are three mechanisms that could contribute fetal ischemia?

A

Uterine torsion
Umbilical cord torsion
Premature separation of the placenta

93
Q

(L39) What are the two routes of fetal infection?

A

Hematogenous

Transcervical

94
Q

(L39) Describe the hematogenous route of placenta infection.

A

A hematogenous agent crosses the placenta and ascends the vascular tree to infect the fetus. As a result, a hematogenous infection is often associated with inflammation of the cotyledons in ruminants or the chorioallantois in other species.

95
Q

(L39, 40) Describe the transcervical route of placenta infection. What other inflammatory processes can be secondary to a transcervical infection?

A

A transcervical agent will ascend up the cervix and infect the various cell layers of the placenta before reaching the fetus. Thus, a transcervical infection is associated with inflammation of the equine cervical star, the amnion, dermatitis, pneumonia, and peritonitis.

96
Q

(L40) What is placental hypoplasia in the horse? How does the placenta compensate?

A

Placental hypoplasia describes avillus areas on the placenta, often corresponding to areas of endometrial damage or inflammation. These avillus areas compromise normal placental function, so the placenta compensates with villous hyperplasia in other areas.

97
Q

(L39, 40) What would induce squamous metaplasia of the equine placenta?

A

Squamous metaplasia is caused by premature separation of the placenta from the endometrium. If the separation was diffuse, then it could compromise fetal oxygenation and contribute to ischemia.

98
Q

(L40) What is adenomatous allantoic hyperplasia in the horse? How is different from placental hyperplasia?

A

Adenomatous allantoic hyperplasia is secondary to chronic inflammation or infection. Unlike placental hyperplasia, which is villous hyperplasia, the former forms hyperplastic nodules on the allantois at the root of the umbilicus.

99
Q

(L40) What are hydrops allantois and hydrops amnii? How are they different?

A

Hydrops allantois is the accumulation of fluid in the allantois late in gestation, often associated with abnormal placental growth or placentitis. Hydrops amnii is fluid accumulation in the amnion. A hydroamnion is caused by anything that would impair normal fetal swallowing or renal function.

100
Q

(L40) How would an acute placentitis morphologically compare to a chronic placentitis?

A

An acute placentitis can be characterized by necrosis and suppuration. A chronic placentitis, on the other hand, will cause thickening, fibrosis and inspissated exudate formation.

101
Q

(L40) What is parvovirus and porcine reproductive respiratory syndrome (PRRS)?

A

PRRS is a viral infection of porcine placenta that causes stillbirth, mummification, and embryonic death.

102
Q

(L40) What is epizootic bovine abortion and what is it caused by?

A

Epizootic bovine abortion is an abortive disease caused by a tick-borne pathogen, Pajaroellobacter abortibovis.

103
Q

(L40) What is neospora caninum? What type of disease does it cause in cattle?

A

Neospora caninum in cattle is an abortive protozoan that can cause a variety of lesions ranging from early embryonic death, abortion, or neurological deficits in newborns.

104
Q

(L40) Describe mare reproductive loss syndrome. What is it primarily caused by?

A

Mare reproductive loss syndrome describes abortion caused by the ingestion of tent caterpillars. The setae, or hairs, on the caterpillar can travel from the GI tract to the placenta where they cause significant fetal damage and abortion.

105
Q

(L41) Traumatic injuries to the female reproductive tract e.g. uterine prolapse, uterine artery rupture, uterine torsion, uterine rupture are all predisposed by what?

A

Dystocia

106
Q

(L41) Describe normal post-partum involution.

A

After parturition, the uterus begins the gradual process of repair. First, the placental membranes are expelled and the maternal lochia is sloughed. Then the endometrium and myometrium begin remodeling. This process lasts about a month in cows, but up to 4 in dogs.

107
Q

(L41) Mastitis is inflammation of the mammary gland. In our commercial milkers, what the most common cause?

A

An ascending bacterial infection

108
Q

(L41) A normal healthy mammary gland has some innate defense mechanisms. What are they?

A

A teat sphincter which only opens during suckling
A rapidly changing squamous epithelial lining to the ducts
Milk flow, which flushes out microbes
Resident neutrophils and macrophages
Antibacterial secretions in the milk e.g. lysozymes, lactoferrin, lactoperoxidase

109
Q

(L41) Differentiate between mastitis and galactophoritis.

A

Mastitis is inflammation of the mammary gland itself, while galactophoritis is inflammation of just the ducts, teat, and teat canal.

110
Q

(L41) Morphologically differentiate acute mastitis from chronic mastitis. How are these two forms different from gangrenous mastitis?

A

Acute mastitis will look angry - redness, edema, vasculitis, and lots of neutrophil infiltration. A chronic mastitis will have signs of tissue repair - fibrosis, the formation a granuloma, lymphocytic infiltration, and inflammatory polyps. Both of these differ widely from gangrenous mastitis, where there could be necrosis of the gland and the overlying skin.

111
Q

(L41) Fibroadenomaotous hyperplasia involves the mammary glands in young cycling cats. How is this different from a neoplastic process?

A

Fibroadenomatous hyperplasia is hormonally-driven hyperplasia of the mammary glands. Unlike neoplasia, this hyperplasia arises suddenly d/t hormones, affects all mammary glands uniformly, and can be corrected with spaying.

112
Q

(L41) How could you morphologically differentiate between a benign mammary tumor and a malignant one?

A

Benign mammary neoplasia are well demarcated, do not locally invade other structures, and freely movable. Malignant masses usually have poor margins and will invade and anchor onto local tissues.

113
Q

(L41) Dogs get what type of mammary tumors?

A

Benign ones - adenomas, papillomas, and benign mixed mammary tumors

114
Q

(L41) Cats get what type of mammary tumors?

A

Malignant ones - fibroadenomas and adenocarcinomas

115
Q

(L42) How would you calculate the rate of abortion in a herd?

A

The number of assumed or observed abortions/the number of diagnosed pregnancies

116
Q

(L42) Distinguish between endemic and epidemic abortion rates. What is a normal rate?

A

An endemic rate describes a rate of abortion that falls within the expected frequency, ~5-10%. An epidemic abortion rate would exceed normal.

117
Q

(L42) With an abortion, the owner may want to know if death occurred before, during, or after parturition. There are 6 tissues that you could look at. What are they and what might they tell you about time of death?

A
  1. Umbilicus - a rupture of the umbilicus, with the subsequent formation of clots, would suggest that the animal was alive at the time of birth
  2. Skin - the presence of subcutaneous hemorrhage suggests that the neonate had a functional cardiovascular system and, thus, was alive at birth
  3. Lungs
  4. Abomasum - if there’s milk in the abomasum, then the neonate would suckle so death had to have occurred after parturition
  5. Kidneys/heart
  6. Hooves - if the eponychium, or the gelatinous covering on the hooves, is in no longer intact, then the neonate must’ve survived long enough to walk
118
Q

(L42) How would a neonate that survived a viral infection before the development of immunocompetency compare to one that survived an infection post-immunocompetency?

A

A neonate that survived a viral infection before the development of its immune system will be persistently infected - when tested, it will be positive for the virus, but negative for antibodies against it. In comparison, a neonate that survived an infection post-immunocompetency will be negative for the virus and positive for virus antibodies.

119
Q

(L43) What are two reasons that might contribute to failure of passive transfer?

A

The first reason is if the mother fails to produce adequate antibodies in the colostrum. The second is if there is insufficient uptake by the neonate.

120
Q

(L43) Pregnancy ketosis is a common pre-partum issue for a lot of dams. Describe it.

A

Pregnancy places dams under high metabolic stress, especially if they’re gestating multiple fetuses. Dams risk developing ketosis or other metabolic diseases without the proper nutritional supplementation.

121
Q

(L43) Vaginal prolapse is a common pre-partum issue for dams. Describe the underlying problems and predisposing factors.

A

A vaginal prolapse can result from increased intra-abdominal pressure and attenuation of peri-pelvic ligaments. A dam could be made more susceptible to a prolapse with a larger than normal litter or prior trauma to the pelvic region. Less common factors include exceptionally short tail docking and heritability.

122
Q

(L43) What are the four differentials for a down cow in puerperium?

A

Metritis
Mastitis
Musculoskeletal e.g. soft tissue trauma or pelvic fracture
Metabolic e.g. hypocalcemia

123
Q

(L43) Expulsion of the lochia is a normal process during puerperium. What would that discharge look like in a dog or cat? In a cow?

A

In dogs and cats, the lochia, when discharged, will be dark greenish due to the presence of biliverdin. In cows, it’s brownish red to yellowish white.

124
Q

(L43) Uterine contamination results in a whole spectrum of outcomes, from uterine inflammation to a pyometra. How would these processes impact involution?

A

Inflammation of infection of the uterus may delay the completion of involution, and subsequently, the return to cyclicity and fertility.

125
Q

(L43) Galactorrhea is the inappropriate lactation. In what groups of animals might we expect to see galactorrhea?

A

Dogs with overt pseudopregnancy
Goats that exhibit precocious lactation
Males with gynecomastia

126
Q

(L44) How does mammary development compare to the rate of body growth before puberty?

A

Mammary development is isometric to body growth rate until puberty.

127
Q

(L44) What three hormones regulate mammary development around puberty?

A

Estradiol, cortisol, and growth hormone

128
Q

(L44) Which hormones regulate mammary development during pregnancy and around birth?

A

Progesterone and prolactin

129
Q

(L44) Involution of the mammary glands between lactations is incomplete. What does this result in?

A

Since mammary gland regression never returns a mammary gland to pre-pregnancy size, there is an accumulation of mammary tissue of subsequent lactation cycles. This makes following lactations more efficient, which is especially important in litter bearing species.

130
Q

(L44) What role does progesterone play in mammogenesis and lactogenesis?

A

Progesterone is important to mammary development, especially during pregnancy, but inhibits lactogenesis by inhibiting the expression of a-lactalbumin.

131
Q

(L44) What enzyme complex is essential for lactogenesis? What are the two component enzymes?

A

Lactogenesis is mediated by lactose synthase, a complex of a-lactalbumin and b-galactosyltransferase.

132
Q

(L44) How does lactose synthase create milk?

A

This protein complex converts glucose and galactose into lactose. Lactose creates an osmotic gradient which draws fluid into the mammary gland, making milk.

133
Q

(L44) How do prolactin and cortisol increase milk production?

A

Prolactin (and cortisol when paired with prolactin) increases the expression of a-lactalbumin.

134
Q

(L44) In dairy cattle, what hormone plays a major role in setting the lactation curve? What would happen to lactation if this hormone was inhibited around the time of parturition? Several days after parturition?

A

Prolactin sets the lactation curve. If the normal increase in prolactin around the time of parturition is suppressed, then lactation, as a whole, suffers. However, inhibition of prolactin a couple of days after parturition will have little to no effect on the amount of milk produced. In other words, prolactin sets the level of milk production, but does not sustain it.

135
Q

(L44) In dairy cattle, what hormone sustains lactation?

A

bST, or bovine somatomammotropin, is involved in the maintenance and extension of the lactation curve.

136
Q

(L44) Which species are sensitive to changes in prolactin throughout lactation? What happens to lactation when a dopamine agonist is given during the middle of the cycle?

A

Dogs and humans are reliant on prolactin throughout lactation. If a dopamine agonist is administered, then milk synthesis is inhibited.

137
Q

(L44) In the canine female, how do progesterone and prolactin interplay to initiate lactogenesis?

A

Progesterone, through most of gestation, suppresses prolactin via dopamine. However, the progesterone withdrawal near parturition allows prolactin to increase, initiating lactogenesis.

138
Q

(L44) Which hormone is involved in milk letdown? How?

A

Oxytocin released by the posterior pituitary binds to and causes the contraction of myoepithelial cells in the mammary glands. These cells line milk-filled alveoli and when they contract, they induce milk letdown.

139
Q

(L44) What is lactational anestrus? What hormones play a role?

A

Lactating females normally do not cycle because suckling or stimulation of the teats inhibits the hypothalamic release of GnRH. More specifically, the stimulation of the teats causes the release of oxytocin from the posterior pituitary which then inhibits GnRH release.

140
Q

(L44) Beef cattle exhibit lactational anestrus while dairy cows don’t. Why?

A

Under normal management practices, beef cattle are suckled by their young, which causes the release of oxytocin and inhibition of GnRH. Thus, beef cattle usually don’t cycle until 4-6 weeks after calving. Dairy cattle are milked by machines, which does not provide the same type of stimulation. Dairy cattle can ovulate within 2 weeks of calving.

141
Q

(L44) Differentiate between agalactia and failure of letdown.

A

Agalactia is a lack of mammary development or the inability to synthesize milk. With failure of letdown, milk can be synthesized, but there’s no release of it.

142
Q

(L44) Ergot alkaloid fescues are dopaminergic. What would ingestion of them entail for lactation?

A

If ingested around the time of paturition, ergot alkaloid fescues can inhibit prolactin secretion, ultimately causing agalactia.

143
Q

(L44) Differentiate between the manifestations of hypocalemia in dairy cattle and in dogs.

A

Hypocalcemia in dairy cattle, or milk fever, causes paresis because its thought that it disrupts the release of acetylcholine at neuromuscular junctions. In dogs, hypocalcemia is called eclampsia and it disrupts cell membrane potentials, predisposing them to tetany.

144
Q

(L45) How do avian sex chromosomes differ from mammalian ones?

A

Female birds are heterogametic (ZW) while males are homogametic (ZZ).

145
Q

(L45) Gynandromorph chickens exhibit cell/tissue sex autonomy. What does that mean?

A

A gynandromorph is an individual chicken that exhibits characteristics of either sex on each half of its body, whether it be gonad type or secondary sexual features. Cell/tissue sex autonomy describes how, for a given side of their body, these chickens’ phenotypes did not necessarily have to match the gonad e.g. one half of their body may exhibit characteristics of a female, but said side didn’t have to have an ovary.

146
Q

(L45) Say you remove the left ovary in a ZW chick soon after hatching. What would happen to her right gonad?

A

Removal of the left ovary will cause the regressed right gonad to develop into a testis, effectively bringing about sex reversal.

147
Q

(L45) Chicken follicles are hierarchical. What does that mean?

A

Chicken follicles are arranged in a hierarchy, where only the largest yellow follicle will ovulate per ovulation. Every time a follicle is ovulated, more immature ones are recruited for development.

148
Q

(L45) What hormones do the small white follicles in a chicken ovary secrete? What about the pre-ovulatory follicle? How is this different from mammals?

A

The small white follicles secrete androgens which are eventually converted into estrogens. The pre-ovulatory follicle secretes progesterone. In mammals, the pre-ovulatory follicle secretes estradiol.

149
Q

(L45) What hormone induces the LH surge in chickens? What structure secretes this hormone? How is this different from mammals?

A

Progesterone secreted by the pre-ovulatory follicle induces the LH surge. In mammals, the pre-ovulatory follicle secretes estradiol which causes the LH surge.

150
Q

(L45) List the parts of the avian oviduct and their functions. About how long does an egg spend in each region?

A

Infundibulum
Magnum - deposition of albumin; ~3 hours
Isthmus - deposition of the shell membranes; ~1.5 hours
Shell gland - deposition of the shell; ~18-22 hours

151
Q

(L45) Birds’ reproductive behaviors, like mammals, are photosensitive. Describe the role of the pineal gland in these two groups.

A

In mammals, the pineal gland, through the stimulation of photoreceptors in the eyes, controls the secretion of melatonin.

In birds, the pineal gland appears to have no role in reproduction. Instead, light directly penetrates the cranium to directly stimulate receptors in the brain to affect GnRH secretion.

152
Q

(L45) How is the liver involved in avian reproduction?

A

Most of the fats that would go into yolk are first processed by the liver.

153
Q

(L45) How are long bones involved in avian reproduction?

A

To accommodate for the calcium demand involved in shell formation, calcium stores in long bones are mobilized.

154
Q

(L45) Describe the pattern of LH secretion that goes into laying a clutch of eggs.

A

The LH surge associated with ovulation occurs only at night. Since the process of ovulation to oviposition takes a little more than 24 hours, after each egg, the LH is pushed further and further back. Eventually, when the LH surge coincides with morning, it stops and resets itself, meaning that there is no egg laid the next day. A clutch is an uninterrupted sequence of eggs laid without skipping any days.

155
Q

(L45) What hormone drives brooding behavior in chickens?

A

Prolactin

VET410 Endocrine/Reproduction (5 decks)

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