ECAR prep Flashcards
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Canine prostatic hyperplasia
*Benign Prostatic Hyperplasia is the most common prostate disorder in dogs. Prevalence is 90% in entire male dogs >8years; common in dogs that are 5years (>50%)
Cause: Long term exposure to Dihydrotestosterone (DHT) = metabolite of testosterone (Testosterone + 5alpha-reductase =>DHT); DHT is the androgen active at cellular level of prostate.
Clinical signs
o Older dogs
o Uniform enlargement
o Most will be asymptomatic
o Sanguineous/Serosanguineous discharge = intermittent or continuous
o Haematuria, stanguria and pollakiuria
o Incontinence or anuria uncommon
o Constipation if very enlarged
o Infertility (May be a cause; haemospermia cases; freezing: poor quality due to ROS)
Diagnosis
o Enlarged smooth symmetrical gland on digital palpation
o Not painful on digital palpation
o Very little else in terms of systemic signs
o CBC & Biochem normal
o Canine prostatic specific esterase levels of >80ng/ml
o Radiography; prostatomegaly
o Ultrasonography; diffuse, relatively symmetric involvement with multiple, diffuse, cystic structures
o Cytology after wash; haemorrhage & mild non-septic, non-neoplastic inflammation
Differential diagnoses:
o Lower urinary tract infection/neoplasia/trauma
o Prostatic neoplasia (difficult to differentiate at advanced changes)
o Prostatic cysts
o Paraprostatic cysts
o Prostatitis (Acute/chronic)
o Urinary cysts (aspirate it to check blood urea:creatinine ratio)
Treatment
o Surgical castration if not intended for breeding; involution in 6 weeks (50% reduction)
+ Cycle of medical Treatment before castration (if there is doubt of prostatic neoplasia)
o Medical treatment
(i) Osaterone acetate potent anti-androgenic activity
0.25-0.5 mg/kg, PO for 7 days; 6-8 months duration of effect
4 months should pass after administration
Reduction in spermatogenesis after administration + Abnormality in sperm morphology (++coiled tails) is described
(ii)Delmadinone acetate (another potent anti-androgen)
1-2mg/kg once SC
4 months duration of effect
(iii) Deslorelin acetate (Suprelorin implant) may be used for medical castration but will have a negative effect on fertility (will arrest spermatogenesis)
Flare-up effect (not good in severe cases)
Combine initially with osaterone acetate to block receptors and avoid overstimulation.
Long-term control of BPH to avoid continuous use of other medical treatments.
Safer than castration in terms of risk of prostatic neoplasia.
(iv) Finasteride: blocks the action of 5 alpha-reductase, blocks T to DHT
0.1–0.5 mg/kg daily for up to 4 months; stop 2 weeks (2mths 1 months then restart)
This is a human product, don’t use it as a first choice
Use in cases of liver problems
Uterine prolapse in bitches
Uterine prolapse in bitches is uncommon, although it can happen as a consequence of parturition. The clinical sign is the presence of a solid tubular mass protruding from the vulva, it can also be confirmed by abdominal ultrasound (the uterus will be absent). Manual repositioning of the uterus is not possible due to the size of bitches, therefore the main treatment is a surgical approach by means of laparotomy. As the mucosa of the endometrium is often damaged, ovariohysterectomy is performed.
Abortion in sheep
Structure of the testes
The testes are paired dense organs responsible for reproductive function in males. The testes include:
(i) testicular capsule: composed by the visceral vaginal tunic (continuation of the visceral peritoneum) and by the tunica albuginea (made of connective tissue and smooth muscle fibers that contracts in response to norepinephrine and acetylcholine, causing the testicular capsule to have a pump effect that help spermatozoa progression within the tubules system); finger-like projection from the tunica albuginea enter in the testicular parenchyma and converge in the mediastinum.
(ii) mediastinum: dense connective tissue hosting the rete tubules (= rete testis), made of thin tubules though which the spermatozoa leave the testis.
(iii) parenchyma: the testicular parenchyma is divided into
a) interstitial compartment: including blood and lymph vessels, nerves, and Leydig cells.
b) Tubular compartment: including peritubular cells, Sertoli cells, seminiferous epithelium, and developing germ cells (spermatogonia, primary and secondary spermatocytes, spermatides, and spermatozoa). Seminiferous tubules form highly convoluted loops, and each loop presents a convoluted portion (i.e., tubulus contortus, where majority of the spermatogenesis happens) and a straight portion (i.e., tubulus rectus). The tubular compartment can be divided into a basal compartment and a deep and a peripheral adluminal compartments. The peritubular cells that surround the seminiferous tubules contribute to the blood-testis barrier, together with the tight junction between Sertoli cells. This prevents WBC and immunoglobulins to reach the developing germ cells and recognizing secondary spermatocytes, spermatides, and spermatozoa (aploid germ cells with different genetics due to crossing-over during meiosis) as non-self.
What are the peculiarities of camelid reproduction?
Non-seasonal polyestrus.
Induced ovulators (neural stimulation is required for LH peak and ovulation to occur, in camelids mechanical stimulation is less important than biochemical stimulation by an ovulation inducing factor (GnRH-like)).
Long mating (hours).
Late puberty (around 2-3 years in Camels, 1-2 years in Llamas and Alpacas)
Types of estrous cycle
Polyestrous cycles (seasonal or non-seasonal), monoestrous cycles.
Non-seasonal polyestrous = cow, sow (in the wild sow are seasonal polyestrus, with reproductive season in autumn), camelids, rabbits, mice, guinea pigs, rats.
Seasonal polyestrous = ewe, doe (short day breeders), mare, queen, jill (long-day breeders).
Monoestrous = bitch.
Describe the differentiation phase of spermatogenesis
The differentiation phase of spermatogenesis is responsible for undifferentiated spherical spermatids becoming highly specialized spermatozoa. At the end of this process the nucleus is highly condensed, the acrosome is formed, and the spermatozoon is partially motile. The differentiation phase (also referred to as “spermiogenesis”) consists of four main phases: (i) the Golgi phase, in which the highly developed Golgi apparatus consisting of many small vesicles that fuse, gives rise to an acrosomic vesicle containing a dense acrosomic granule. In the meantime, the cetrioles migrate to the base of the nucleus.The proximal centriole will give rise to the implantation apparatus that will anchor the flagellum to the nucleus, whereas the distal centriole will give rise to the axoneme. (ii) During the cap phase, the acrosome forms a cap over the anterior part of the nucleus. The Golgi apparatus moves away towards the caudal end of the spermatid and will eventually disappear. (iii) In the acrosomal phase spermatids become deeply embedded into Sertoli cells, in the meantime, the acrosome continues to spread over the nucleus until it covers two thirds of it, and a system of microtubules (i.e., manchette) develops near the posterior nucleus attaching just posterior to the acrosome, this will form the post-nuclear cap during the (iv) maturation phase. In this phase the mitochondria cluster around the base of the flagellum assuming a spiral conformation to form the middle piece and the fibers of the flagellum are produced. Finally, the spermatozoon is released into the lumen of the seminiferous tubule by the Sertoli cell in which it was embedded (i.e., spermiation). During differentiation, the DNA of the spermatozoon becomes inert due to high kerathinization. Specifically, histones of the nucleus are replaced by protamines, which are small arginine-rich nuclear proteins with many sulphydryl groups forming disulfide bonds that create nuclear condensation. This way the DNA is not transcripted and translated and it is protected from possible damage occuring prior to fertilization. During fertilization, when the spermatozoon enters the oocyte, the glutathione of the oocyte reduces the disuphide bonds and histone proteins of the oocyte replace the proteamines, leading to nuclear decondensation and formation of the male pronucleus.
What are the characteristics of ovulation in bitches?
Ovulation is spontaneous, multiple follicles ovulate at the same time, ovulation occurs 48-60 h after the LH peak, the oocyte is ovulated immature (primary stage) and will then mature in the oviduct. The preovulatory LH peak lasts longer than in other species (36-55 h) and is accompained by a FSH peak (lasting 110 +/- 8 h). The delay between the LH peak and fertilization allow superfecundation (i.e., possible fertilization by different males).
What are protein kinases?
Protein kinases are a family of enzymes located in the cytoplasm of cells. These are important components of hormone action on target cells. Specifically, either protein or steroid hormones can bind to their membrane receptor, inducing a transformation of a G protein that will cause activation of a second messenger (adenylate cyclase) that converts ATP in cAMP. This links to the regulatory subunit of a proteine kinase, and this bond will activate the catalytic subunit in order to mediate the transformation of existing substrates into new compounds (protein hormones) or change the permeability of calcium channels (steroid hormones).
When does progesterone peak in bitches?
Progesterone peaks about 25 days after ovulation in bitches, then it gradually declines, reaching 1.5 ng/mL about 70 days after ovulation in non pregnant bitches, and < 2ng/mL around 62-63 days after ovulation in pregnant bitches (parturition normally starts within 24h from the drop of progesterone below 2 ng/mL).
Endometritis in cows
Endometritis in cows
PVD => solo PVD + <5% PMN
Clinical endometritis => PVD + > 5%PMN (Cytobrush)
Subclinical endometritis => no PVD + > 5% PMN
Vaginoscopio = fuoriuscita di pus dalla cervice
Glove hand technique = score 0-1 (non patologico)-2-3 (endometrite)
Metricheck = Stesso score
Ecografia = ispessimento endometrio, presenza di pus, eco-score 0-1-2-3
Impatto su fertilità 30-50% vacche da latte (meno da carne => 20%). Depends on breed, parity, farming system and management (nutrition), dystocia, placental retention, immunodepression
Batteri: microbiota differenze + Trueperella pyogenes, Fusobacterium, Prevotella, Porfiromonas, E.coli
Treatment: antimicrobial intrauterine (good result with probiotics LAB and ozone)
FSH (biochemical classification, source, target tissue, primary actions)
Describe the hormonal changes that occur during parturition in pigs.
Describe the blood-testis barrier
The blood-testis barrier has the function of preventing white blood cells and immunoglobulins to reach the developing germ cells within the adluminal compartment of the tubular compartment of the testicular parenchyma. The blood-testis barrier includes
(i) peritubular cells, surrounding the seminiferous tubule and preventing the passage of large molecules and cells from the interstitial compartment to the tubular compartment.
(ii) tight junctions between Sertoli cells, located in the basal compartment and preventing the passage of large molecules and cells from the basal to the adluminal compartment.
Functions of the increased mucus secretion under the effect of estrogens
Lubricate the cervix and vagina in preparation for copularion, flushes out foreing material, in cows low-viscosity mucus provides a preferential pathway for spermatozoa to traverse the cervix and enter the uterus
Explain sexual differentiation of the reproductive tract
Sexual differentiation of the reproductive tract starts by 20% of gestation and is completed around 33% of gestation. It depends on the presence or absence of the SRY gene. Specifically, the SRY (sex determining region) gene is found only on Y chromosome in the male (XY), whereas this is absent in females (XX). This gene controls the syntesis of the SRY protein. In the first phase of development. When the protein is synthesized by the sex cords, the sexual differentiation of the male starts. Therefore, the testes develop, including Sertoli cells producing anti-Müllerian hormone (AMH) that inhibit the development of the paramesonephric duct, thus that of the female reproductive tract and dihydrotestosterone. Moreover, the Desert Hedgehog Gene (DHH) causes the differentiation of fetal Leydig cells, leading to production of testosterone and dihydrotestosterone. The first stimulates the development of the male duct system, whereas the latter promotes the development of the penis, scrotum, and male accessory sex glands. In females, the SRY gene is not present, although sex differentiation is anyway an active process, because in the absence of the SRY protein, female genes are activated and ovaries will develop from the bulk of the genital ridge. The sex cord fragments into clusters of primitive follicular cells that will enclose one primitive germ cell per cluster. Primordial follicles forms on the surface of the ovary and this region will become the ovarian cortex (except in mares).
What are the functions of Sertoli cells in the process of spermatogenesis?
(i) Hormone production: Estrogens, Inhibin, Activin, Transferrin, Androgen Binding Protein (ABP), SGP1 (involved in fertility acquisition by spermatozoa) and SGP2 (detergent effect allowing sperm cells to move in the seminiferous tubules)
(ii) Tight junctions between Sertoli cells contribute to the blood-testis barrier
(iii) Determine the reproductive potential of the male as each Sertoli cell host a maximum number of developing sperm cells (more Sertoli cells = higher reproductive potential)
(iv) During the acrosomal phase of the spermiogenesis the spermatids become deeply embedded into a Sertoli cell with only the flagellum protruding towards the lumen of the seminiferous tubule. After the maturation phase, Seroli cells release the spermatozoa into the lumen of the seminiferous lumen (= spermiation). The cytoplasm of the spermatid remains as a residual body within the cytoplasm of the Sertoli cell.
IVM
What is necessary for luteolysis
Luteolysis is the irreversible degeneration of the corpus luteum that ends the luteal phase. In mammals, except for primates and canids, an intact uterine endometrium producing PGF2a is necessary for luteolysis. In primates PGF2a is produced by the corpus luteum, whereas in canids there is no luteolysis, but a gradual regression of the corpus luteum. Secretion of PGF2a by endometrial cells in other species is promoted by oxytocin (oxytocin is produced by the hypothalamus and stored and release by the posterior pituitary, in Ruminants oxytocin granules can also be found in the cytoplasm of large luteal cells). Therefore, to achieve luteolysis oxytocin receptors on endometrial cells, critical levels of oxytocin, and synthesis of PGF2a are needed.
Since progesterone blocks the formation of oxytocin receptors, luteolysis cannot happen in the first part of the luteal phase. When progesterone levels start decreasing, the block is removed, oxytocin receptors are synthesized and expressed by endometrial cells, oxytocin can bind the receptors activating the synthsis of PGF2a. PGF2a is secreted in pulses (e.g., 5 pulses in 24 h are needed in ewes for luteolysis to happen) and it binds to plasma membrane receptors on plasma membrane cells, acting via proteine kinases, the binding cause the opening of Ca2+ channels and a consequent Ca2+ influx that starts apoptosis of luteal cells. Moreover, the binding of PGF2a with the plasma membrane receptor on luteal cells causes the activation of proteine-kinase-c that inhibit the synthesis of progesterone. WBC are present in the CL at the moment of lutheolysis and they also play an active role by releasing cytokines that activate macrophages (phagocytosis of damaged/dead luteal cells), inhibit progesterone synthesis, and may trigger agents of apoptosis in luteal cells.
Vulvoplasty bitches
Vulvoplasty or episioplasty is a reconstructive procedure mainly performed to excise the excess of skin folds around the vulva, which can cause vulvar dermatitis (to be treated before surgery), recurrent vaginitis, and recurrent urinary tract infections. The bitch is placed in a perineal (sternal) position with limbs supported. A purse-string suture is performed prior to vulvoplasty to reduce the risk of contamination from feces. Beginning near the ventral vulvar commissure, a crescent-shaped incision is performed around the vulva. Afterwards, a second crescent incision is made medial and parallel to the first one. After excision of the outlined segment of skin and subcutaneous tissue, interrupted sutures are placed at 3 o’clock, 9 o’clock, and 12 o’clock positions to assess the effectiveness of the resection. The margins are brought together and suturing of the subcutaneous tissue using interrupted sutures with buried knots is performed. The skin margins are sutured either with intradermal patterns. Once the vulvoplasty is completed, the purse-string suture is removed. Post-operative management include the placement of an Elizabethan collar.
Patterns of GnRH, LH, FSH, and testosterone in males
GnRH pulses last a few minutes and have a frequency of 4-8 times per day (every 3-6 hours); LH and FSH have the same pulse frequency, although LH pulses last 30-75 minutes, whereas FSH pulses last longer. Finally, testosterone is produced about 30 minutes after each LH pulse and it is released for about 20-60 minutes.
Describe the approach to a case of testicular hypoplasia in a stallion.
Hypoplastic testis in a horse refers to a condition where the testis is underdeveloped, resulting in smaller size and reduced function compared to a normal testis.
- Signalment and history
(i)Age: Testicular hypoplasia may be congenital or acquired, so knowing the age of onset is important.
(i)Breeding history: Has the stallion been used for breeding, and if so, has there been a history of poor fertility or failed pregnancies?
(i)Developmental abnormalities: Any history of abnormal development during growth.
(i)Previous illness or trauma: Any past infections, trauma, or surgeries related to the reproductive system.
2.Clinical examination
(i)Overall health and body condition of the horse, as systemic illnesses or poor nutrition can affect reproductive development.
(ii)Reproductive tract examination:
a.External palpation to evaluate both testes, paying attention to size, consistency, symmetry, and presence of pain or heat. Compare the hypoplastic testis with the contralateral testis (one is hypoplastic or the other one is enlarged?).
b.Testicular size: Hypoplastic testes are typically smaller and softer than normal testes. Measure the dimensions of both testes using a caliper.
c. Epididymis palpation: check for position and abnormalities in the epididymis, which may also be underdeveloped in the case of hypoplasia.
d. Examine the scrotal skin for signs of trauma, infection, or developmental abnormalities.
e.Penis and prepuce: Evaluate for any additional abnormalities in the external genitalia.
3.Differentials:
Testicular degeneration: This could be secondary to infection, trauma, or systemic illness.
Cryptorchidism: One or both testes fail to descend into the scrotum, leading to reduced testicular size and function. Use hormonal testing (AMH or hCG stimulation) to differentiate cryptorchidism from true hypoplasia.
Testicular atrophy: Often occurs secondary to infections (e.g., orchitis), trauma, or systemic conditions like fever.
Neoplasia: Although rare, testicular tumors can alter the size and function of the testis.
4.Ultrasound
Look for parenchymal abnormalities such as reduced testicular echogenicity, abnormal architecture, or cystic areas.
Measure the testicular volume to provide a more accurate assessment of testicular size and function.
Evaluate the blood flow using Doppler ultrasound to rule out vascular issues (such as testicular torsion) that could mimic hypoplasia.
- Hormonal testing
(i)Basal testosterone levels (hypoplastic testes may produce less testosterone).
(ii) hCG stimulation test:
Perform an hCG stimulation test to assess the ability of the testis to produce testosterone. After administering hCG, testosterone levels should increase in a normal horse. Failure to respond suggests testicular dysfunction.
(iii) AMH levels can help differentiate between cryptorchidism and true hypoplasia. Cryptorchid testes often produce higher levels of AMH, whereas a truly hypoplastic testis may produce very low levels. - Semen Evaluation
(i)Semen collection: if the horse is used for breeding or is of breeding age, collect semen via artificial vagina or electroejaculation.
(i)Sperm analysis:
assessment of semen volume, sperm concentration, motility, and morphology.
A hypoplastic testis may result in oligo and/or terato and/or asteno-zoospermia.
If sperm production is severely impaired, the horse may be considered subfertile or infertile.
7.Testicular biopsy
DD testicular degeneration?
8.Management
Unilateral testicular hypoplasia: the prognosis for fertility is generally fair if the contralateral testis is normal. The stallion may still be capable of producing enough sperm for natural breeding or artificial insemination.
Bilateral testicular hypoplasia: The prognosis for fertility is poor in cases where both testes are significantly hypoplastic. The horse is unlikely to be fertile, and castration may be considered for management.
Sertoli cell tumors
What are the stages of parturition in dogs, and how is normal delivery monitored?