Week 4 - March 3 Day 2 Flashcards
What is the facial nerve responsible for? Damage to this nerve results in?
Provides motor innervation to the muscles of facial expression. Damage to this nerve may result in:
- Inability to blink
- Muzzle deviation
- Ear droop
- Lack of nostril flare
- Loss of menace and palpebral response
What is the oculomotor nerve responsible for?
Provides motor innervation to the dorsal, medial, and ventral rectus muscles. Additionally, this nerve innervates the palpebral levator, which is responsible for raising the upper eyelid.
What is the trochlear nerve responsible for?
The trochlear nerve innervates the dorsal oblique muscle of the eyeball. Injury to this nerve = dorsomedial strabismus.
What is the trigeminal nerve responsible for?
Provides sensation to most of the face and also motor innervation to the muscles of mastication.
What is the abducens nerve responsible for?
Motor innervation to the lateral rectus and part of the retractor bulbi muscles.
Topic: African Horse Sickness
- How is this disease transmitted?
- Where is this disease endemic to?
- What are the clinical signs?
- How is it diagnosed?
- How is it treated?
- How can this disease be prevented?
African horse sickness (AHS) is a viral disease of equids that is transmitted by insects, primarily Culicoides.
African horse sickness is endemic in sub-Saharan Africa and outbreaks have periodically extended to the Middle East and southern Spain. The primary and biological vector is Culicoides but the virus may also be transmitted by mosquitoes. The virus has been isolated from certain ticks but arthropod transmission is not believed to play a significant role.
Clinical signs of AHS typically develop 5-7 days after infection and begin with fever and conjunctivitis.
Some animals may recover but many go on to develop the pulmonary and/or cardiac forms of AHS.
The pulmonary form consists of acute respiratory distress, coughing, sweating, and foaming from the nostrils; this form is usually fatal. The cardiac form consists of edema of the head and neck as well as abdominal pain and depression. A characteristic sign is swelling in the indentation above the eyes (also referred to as swelling of the supraorbital fossa). About 50% of animals with the cardiac form die from heart failure while the rest gradually recover after about one week.
Diagnosis can often be made based on history of exposure to endemic areas, clinical signs and lesions but must be confirmed by viral isolation and/or serology. There is no effective treatment and prevention/control can be accomplished by vector control and vaccination. There are multiple serotypes of virus and animals immunized against certain serotypes are still susceptible to others. In an outbreak situation, affected horses should be removed/euthanized and remaining horses should be vaccinated with a polyvalent vaccine until the specific serotype can be determined and then animals should be revaccinated with the corresponding vaccine.
For importing equids from Africa, a 2 month quarantine is required and then horses must test free of virus. Presence of antibodies does not disqualify a horse from importation. Because of the vector-borne nature of the disease, it is recommended that planes flying from endemic areas be sprayed with insecticides on arrival to disease-free countries.
Stable all horses in insect-proof housing, particularly at night because the disease is transmitted primarily by Culicoides flies
Topic: Equine Recurrent Uveitis
- This is also referred to as?
- List the etiologies.
- Recurrent bouts of uveitis can lead to?
- Recurrent uveitis is the most common cause of ?
- How should this condition be treated?
Equine recurrent uveitis (also referred to as periodic ophthalmia, recurrent iridocyclitis, and moon blindness) is common in horses. There are many proposed causes for this condition, but it is thought to usually be from infection (Onchocerca, Leptospira, or Borrelia) or immune-mediated processes. Because recurrent bouts of uveitis can lead to serious problems including cataracts, lens luxation, and glaucoma, it should be treated aggressively with topical and systemic anti-inflammatory drugs and topical atropine to prevent synechiae and ciliary spasm.
Systemic antibiotics are usually not indicated unless the horse is febrile or an infectious cause is identified.
How can you tell the difference between a central vs peripheral vestibular lesion?
Peripheral vestibular dysfunction causes signs of head tilt, nystagmus, circling and asymmetric ataxia with preservation of strength. The head tilt is toward the affected side as is circling towards the lesion.
Comparatively, central vestibular disease has similar clinical signs but general conscious proprioceptive deficits, weakness and cranial nerve deficits may also be present along with depression.
Describe the pathophysiology of Intraosseous desmitis in horses.
Intraosseous desmitis occurs when there is inflammation of the intraosseous ligament, located between the 3rd metacarpal or metatarsal bone with the small metacarpal or metatarsal bones.
Periostitis occurs when there is new bone formation along the splint bones or small metacarpals or metatarsal due to repetitive concussion, excessive training, poor conformation, or improper shoeing.
Do xrays to rule out a fracture of the splint bones.
What is the dental formula for a horse?
2(I3/3 C1/P P3-4/3 M3/3)
Horses may have 3 or 4 maxillary premolars
What AV blocks are considered a normal finding in horses?
First and second degree AV blocks are normal and are usually due to high vagal tone.
What is the definitive host of Dictyocaulus arnfeldi?
Donkeys!!!!
You are called to a horse ranch that has an ongoing problem controlling infection and transmission of Streptococcal infections (Streptococcus equi subsp. equi) among its horses. You attempt to identify carriers by collecting wash samples from the guttural pouch since this is the most common place that horses harbor the organism. On endoscopy, you detect several hard, smooth, stone-like structures within the guttural pouch. Which of the following is the most important intervention?
These objects are chondroids which are hardened pus filled concretions with bacteria. They most commonly occur when horses develop guttural pouch empyema which is an accumulation of purulent exudate in the guttural pouch due to mucosal infection or drainage from the retropharyngeal lymph nodes from Streptococcus equi subsp. equi (Strangles). The persistence of pus provides a refuge for the bacteria and allows for continued bacterial shedding. When exudate persists, it can become increasingly dense, forming solidified concretions that are difficult to extract and serve as a source for continued prolonged shedding of the organism.
To reduce shedding and transmission, these chondroids should be removed and the guttural pouch should be flushed and infused with 5 million units of penicillin G in 3% gelatin. Chondroids can be removed surgically or via endoscopic basket removal.
In addition, these horses should be treated with penicillin G intramuscularly for 7 days, isolated for 30 days, and then retested with 3 consecutive series of nasopharyngeal swabs and culture. Animals that remain positive should go through a repeat treatment and culture cycle
As of 2017, S. equi is a reportable disease in all states within the US.
Vitamin K3 should NEVER be given to horses because it is?
Nephrotoxic
How would you tx warfarin toxicosis in a horse?
Vitamin K1 subq every 6 hrs
1-2 L of Plasma to replenish clotting factors
Which of these drugs has the greatest potential for causing acute renal failure in the horse?
Neomycin
Dexamethasone
Diphenhydramine
Oxytetracycline
Xylazine
The correct answer is neomycin. Aminoglycosides are one of the most common causes of renal tubular nephrosis and acute renal failure. Of the aminoglycosides, neomycin is probably the most nephrotoxic, followed by gentamicin, amikacin, and streptomycin. The other big class of nephrotoxic drugs is non-steroidal anti-inflammatory drugs.
A horse gets into cow feed that contains the ionophore, monensin. What is your biggest concern?
Cardiotoxicity
Monensin is a coccidiostat used to increase productivity in cattle. Horses are much more susceptible to toxic effects of monensin than cattle and mistakes in feeding or
accidental access to cattle feed can lead to toxicity. Monensin toxicity results in myocardial necrosis and development of dilated cardiomyopathy in horses. Clinical signs include progressive respiratory distress, heart murmur, weakness, and hypovolemic shock. Acutely, mild colic and diarrhea can occur as well but is less of a concern than the cardiovascular effects.
Topic: Equine Repro
- What is the average equine gestation length?
- What type of estrous cycle do horses have?
- When do horses naturally start cycling?
- When is artificial lighting used?
- 330-365; Average is 345
- Seasonally polyestrous
- April or May
- Artificial lighting is used starting in Mid-Dec=ember to promote estrus in mid- February
When performing a fundic exam on a horse with uveitis, you notice multiple dark dots on the tapetum as shown here. What do these dots most likely indicate?
The equine tapetum is penetrated by small choroidal vessels that appear as dark dots. These are sometimes affectionately referred to as the stars of Winslow.
Melanomas occur in up to 80% of gray horses. They occur most commonly on the perineum and tail base but can arise anywhere on the body. Most melanomas of gray horses are benign with varying degrees of invasiveness. They have the potential to develop into malignant tumors. Treatment includes surgery or cryosurgery. Horses that develop one melanoma are predisposed to developing others in the future.
If a horse is in seasonal anestrus, which of these is the most effective means of hastening the start of the breeding season?
Provide atifealighe fort6 hoursper day 6o days pierto the start of breeding
Provide artificial light for 12 hours per day 60 days prier to the start of breeding
Provide artificial light for 12 hours per day 30 days prior to the start of breeding
Provide artificial light for 16 hours per day 30 days prior to the start of breeding
The correct answer is to provide 16 hours of artificial light 60 days prior to the start of breeding. To get a horse to transition out of seasonal anestrus, you can gradually increase the amount of light to 15-16 hours per day to initiate ovarian activity. It usually takes at least 60 days until physiologic breeding will occur. There are hormonal methods to promote cycling, but they are less consistent than altering light.
Topic: PPID In Horses
- What is the pathogenesis of PPID?
- This condition is a result of hypertrophy, hyperplasia,
and micro- or macroadenoma of the pituitary pars intermedia that secretes increased amounts of
propiomelanocortin peptides. Adjacent pituitary tissues are compressed and secrete less of some other peptides. Data suggest that horses with this disease have hypothalamic dysfunction and decreased amounts of dopamine.
What is the treatment for a persistent corpus luteum that will allow a return to estrus in a mare?
Gonadotropin-releasing hormone (GnRH) injection
Progesterone injection
Human chorionic gonadotropin (hCG) injection
PGF-2-alpha (prostaglandin) injection
PGF will cause lysis of the corpus luteum in mares if the corpus luteum is more than about 5 days old. If you are unsure how old the corpus luteum is, you can repeat the injection in about 7 days. This will allow a return to normal cycling.
Remember, injection of PGF may cause mild-moderate abdominal pain (colic, cramping) after administration.
Progesterone injection would not change things because the horse already has high levels of progesterone due to the persistent corpus luteum.
hCG stimulates ovulation, but if the horse has high progesterone from the corpus luteum, it will not exhibit a behavioral estrus. GRH would have similar effects.
For neonatal isoerythrolysis to occur, what antigens does the sire and dam need to possess when they mate? Describe the pathophysiology
stallion positive for Qa and mare negative for Qa. For neonatal isoerythrolysis to occur, the mare must develop antibodies to the foal’s red blood cell antigens. Aa and Qa are the two antigens most frequently implicated in this condition. For this condition to occur, the foal must inherit the Aa or Qa antigen from the stallion, and the mare must be negative for the antigen (if she was positive, meaning she has the Qa antigen on her RBCs, she would not make antibodies against it).
Then, when the mare becomes exposed to the foal’s red blood cell antigens, she makes antibodies.
When she passes these antibodies to the foal through colostrum, an acute hemolytic event will occur in the foal. In most cases, the first time a mare has a foal with the antigen, she will not produce sufficient antibodies to cause severe damage to the foal. Therefore, this condition is usually seen in multiparous dams or in mares that have previously had a blood transfusion that exposed them to the red blood cell antigens.