Week 12 Flashcards
What are oxygen tensions in the foetus compared to a neonate?
Why conditions that affect blood supply have profound effect
What are the two major right-to-left shunts that by-pass the lungs in a foetus?
Where does the umbilical vein connect in the foetus? What does the aorta connect to in the foetus?
What happens at birth going from blood to air?
What happens when everything goes right with the lungs after birth?
What happens when everything goes wrong with the blood supply after birth?
What is the most important immunoglobulin in colostrum? How does a neonate absorb colostrum? Why is colostrum so important?
IgG.
* specialized enterocytes that absorb large molecules by pinocytosis (process becomes fairly inefficient relatively quickly; stopped after 24 hours)
** failure of passive transfer is associated with an increased risk of disease and mortality
When does a neonates own immunoglobulins become detectable?
* after 1-2 weeks of life, but do not reach significant levels for several months
* temporarily protected by the passive transfer
* half-life for equine maternal antibodies is approximately 20-30 days and most have gone by 6-months of age
Failure of passive transfer of antibodies can be a consequence of?
- Failure to ingest a sufficient quantity of colostrum: orphans, too weak to stand, unable to stand, unable or lack of desire to suckle (e.g. hypoxic-ischaemic encephalopathy)
- Ingested poor quality colostrum (low IgG content)- premature lactation (placentitis in mares), premature parturition (inadequate udder development), ingestion of grasses infected with specific endophytes (fescue associated agalactia in mares)
- Failure to absorb colostral components from gut lumen (seen in premature or dysmature neonates occasionally, delayed ingestion of colostrum)
How do you determine quality of colostrum?
* measure IgG e.g. > 800 mg/dL considered adequate for foals
* Assays or ELISA
Why is it important not to over feed or under feed the pregnant mare?
Over feeding increases foetal growth and can cause deposition of fat within the dam’s pelvic canal (increased risk of foeto-pelvic disproportion)
* poor nutrition in the final trimester of pregnancy leads to poor udder development and lactation
Why is low birth weight in a foetus a problem? Over feeding?
Neonates more likely to be susceptible to adverse environmental conditions- impaired heat conservation
* weak at birth–> impaired ability to consume colostrum and subsequently, adequate volumes of milk- immunity, starvation
* over-feeding increases foetal growth and causes deposition of fat within the pelvic canal–>increased risk of dystocia
What species is foetal-maternal disproportion a problem? Not a problem?
Cattle is more commonly a problem, not so much in horses
What are some common consequences when dystocia occurs?
* Hypoxic injury to neonate
* Neonates with hypoxic brain injury can be:
- slower to stand and nurse–> failure of passive transfer
- nurse poorly–> hypovolaemia/dehydration, hypoglycaemia, weak
* Neurologic signs are usually the most obvious consequence of hypoxia
- GI tract injury
- renal injury
What effect can decreasing ambient temp and inreasing precip have on neonates?
Greater relative surface area, evaporation of amniotic fluid, limited caloric reserve
* Newbown animals have stores of brown fat– stores rapidly depleted in cold weather if unable to consume enough milk
* compounded if dam’s milk production low
Discussion of pathogen load on neonates
* multifactorial in order to succumb to disease
* Inevitably exposed to organisms capable of causing disease
* Normal protective mechanisms can be overcome if environmental pathogen load very high
* Or a particuarly virulent pathogen is present
When can pathogen load become more of a problem? How can you reduce the risk?
* clean the mare’s perineum and udder before foal nurses
* removal of faecal material from foaling paddocks
High risk potential historical traits in a mare
High risk mare events during current pregnancy
High risk mare events during parturition
What is normal foal behavior (first 24 hours)?
Why do foals have dilute urine (except their first urine sample)?
Milk has a lot of water in it- (10% for a calf; 20-25% for a foal of bodyweight per day)
What are the reflexes you might look for in small animals?
When is the TB arbitrary birthday? SB?
When does mating season start?
What are the consequences of TB born later?
TB- 1st Aug
SB- 1st Sept
** Mating season starts 1st September– Melbourne foals may do better born August than July
** may be smaller than competitors at 2 yo (yearling)
* mare may be difficult to get pregnant early next season
What are the all the things that must happen to get a cow in calf?
* calve, clean up (endometritis), start cycling (post partum anoestrus), be detected on heat, be inseminated, conceive, stay pregnant
uterus at 12 hours after calving
how long after calving?
30 days after calving
When should a cow be mated in order to calve every year?
Cows are pregnant for approx 9 months so mating starts 3 months after calving
How long does post-partum anoestrus last in a cow?
20-80 days
What is the avg percentage of heat detection efficiency in cows?
60-90%
What is the range of avg conception rates in cows?
30-60%
How long is a horse’s post-partum anoestrus?
start cycling almost immediately
What is a submission rate in cows? Conception rate? What is the 6 week in calf rate? empty rate? Pregnancy rate?
% cows submitted in first 21 (or 30) days
* Conception rate- % cow pregnant per 100 inseminations
* % of the herd pregnant after 6 weeks of joining
* % herd empty (after a given number of weeks- 12 or 20)
* Pregnancy rate- % of the herd pregnant after a given time
How can a cattle herd be best managed in regards to pregnancy rates?
** can get all cows in calf in 9 weeks
Replacement rate of 25-30%— more sustainable if self replacing herds
What is the “six pack”? What is it for?
Improve reproduction rates in a herd
- Calving pattern
- Condition score
- Heat detection
- AI technique
- Growing heifers
- Bulls
How long should calving go for? Why?
6-8 weeks (beef farm particularly)
* 3 months after calving start to join. The last cow has 6 weeks before joining- it is enough time. IN a good year 91% of cows can be pregnant. Calving them sooner makes them way more likely to be fertile and is far more profitable.
What is the major determinant of fertility?
Time since calving
What is the optimal range for a body condition score of a cow pre calving to improve the 21 day submission rate & conception rate?
What does using different colours of tail paint help with?
Determining how long a cow has been pregnant, or if she is in post partum anoestrus
Why is it better to have larger heifers?
* Give an extra 23 litres per Kg Liveweight at calving– calving at 500 instead of 420= $460
How do twins affect cattle repro herd numbers?
How does RFM affect herd repro rates?
How does lameness affect a herds repro rates?
Cystic rete ovarii
Epithelial inclusion cysts
Cystic subsurface epithelial structures- ovarian carcinomas can develop there
Dysgerminoma
* can also say inappropriate mammary development
* can also say inappropriate mammary development
Technically derived from mesoderm since that is what lines the ovaries
What is Cloud Burst?
Pseudopregnancy in goals– progesterone causes prolonged cervical closure– fluid builds up
Pathogenesis?
Combination of both: a complex interaction between disease processes
Reproductive toxins
Effects:
Impaired fertility due to impaired sperm migration, impairment of ovulation
- temporary effects if transient exposure
- Permanent effects if exposed for > 6 months
* Mammary hyperplasia and galactorrhoea
- due to secondary increased prolactin secretion
- affects males as well
* Oedema and hyperplasia of the uterus (cystic), vagina and vulva
* Vaginal Prolapse: swollen reproduction tract+ relaxation of perineal musculature and softening of connective tissue by oestrogen
Reduction in the palpable size of the scrotum, Testicular/ epididymal hypoplasia or degeneration/ atrophy associated with cryptorchidism… or may be agenesis, previous castration, aplasia of scrotal contents
Most common developmental anomaly of the male repro tract. Predisposes to testicular or spermatic cord torison–> oedema–> venous infarction.
* more often unilateral
* may lie anywhere from immediately caudal to the kidney to the scrotum itself, often intra-abdominal near the inguinal ring, in the inguinal canal, or subcutaneously immediately external to the external inguinal ring
** A higher than optimal temperature results in hypoplasia of the retained testis and epididymis– this is compounded by superimposed atrophy post-puberty
** Also prone to neoplasia (in dogs, sertoli cell tumours in intra-abdominal testes and seminomas in inguinal testes; in horses, teratomas)
Palpable enlargement of the scrotum: Scrotal hernia, inflammation of testicle or epididymis, testicular neoplasia, peritoneal neoplasia, accumulation of oedema fluid or inflammatory exudate in the tunica vaginalis, spermatic cord torsion or inflammation, enlargement of scrotal lymph nodes (superficial inguinal lymph nodes), herniation of abdominal contents into the tunica vaginalis
Spermatic granuloma
May develop post-pubertally in any species but especially bulls and rams. Often unilateral, associated with a lot of scarring, nearly always in the HEAD OF THE EPIDIDYMIS. Cause: outflow efferent ductules that are blind ended- pressure builds up- one ruptures–> granulomatous response.
Epididymitis and orchitis
Orchitis less common because testis lie further upstream than epididymis in ascending bacteiral infections and is a privleged immunological environment with anti-inflammatory characteristics.
** C. pseudotuberculosis in rams; B. abortus, M. bovis in bulls; B. suis in boars; FIP.
** Necrotizing orchitis is the most severe form of orchitis and is typical of bruceloosis in bulls and boars
Seminomas. Germ cell tumours of spermatogonial cell origin and are the most common testicular neoplasms in aged stallions, second most common in dogs. More often developed in retained than in descended testes.
** metastatic potential
Sertoli cell tumour (a lot of connective tissue, hard as opposed to seminoma)
* 1/3 make inhibin and oestrogen which can lead feminisation syndrome- testicular degeneration and atrophy, penile atrophy with a pendulous prepuce, hyperplasia and squamous metaplasia of the prostate, bilaterally symmetrical alopecia, and/or gynecomastia. The amount of hormone produced is generally proportional to the size of the tumour.
Varicoele- veins of the pampiniform plexus undergo varicose dilation and sometimes thrombosis. Most often in older rams (trauma), often as a bilateral condition. INfertility may result from associated testicular congestion, hypoxia, and degeneration/ necrosis (can be an incidental finding)
Most common in dogs. Prostatic hyperplasia can occur from constipation, stenosis of the prostatic urethra may also occur. Prostatic carcinoma (asymmetrical enlargement), prostatitis (ascending bacterial infection E. coli or Proteus vulgaris from urethra), prostatic and paraprostatic cysts- may develop in hyperplastic, squamous metaplasic or inflamed prostates.
** can press on autonomic nerve endings– can end up with a perineal hernia as a consequence because it has caused them to strain
