Final Exam New Info Flashcards
What are some of the reasons you would administer fluids to a cow?
(Animal dehydration, rumen dehydration, carrier for medications, and to stimulate appetite)
What can impact your ability to assess dehydration using the sunken eyeball method?
(If a low BCS, retrobulbar fat pad may be small and eye can look sunken when not dehydrated)
What is indicated by an empty paralumbar fossa?
(Cow is off feed and/or dehydrated)
Any dairy cow that is off feed is likely at least what percent dehydrated?
(5%)
What is the fluid deficit in pints, gallons, and liters for a 1200 lb cow that is 7% dehydrated?
(84 pints (1200 x 0.07), 10.5 gallons (divide pints by 8 bc 8 pints in a gallon), or 38 liters (divide pints by 2.2))
What are the goals of fluid therapy in cattle?
(Rehydrate the animal, rehydrate the rumen, encourage appetite, and deliver any needed medications)
Pair the appropriate fluid therapy plan with the percent dehydration:
< 8%
A - Oral fluids alone
B - IV + oral fluids
C - Depends - if you choose this option, additional question of depends on what?
A - Oral fluids alone (< 8%)
Pair the appropriate fluid therapy plan with the percent dehydration:
> 8%
A - Oral fluids alone
B - IV + oral fluids
C - Depends - if you choose this option, additional question of depends on what?
B - IV + oral fluids
Pair the appropriate fluid therapy plan with the percent dehydration:
8%
A - Oral fluids alone
B - IV + oral fluids
C - Depends - if you choose this option, additional question of depends on what?
C - (Depends on if she has a condition that will cause her to have continuing losses/generally make her feel worse/less likely to be eating/drinking on her own after giving oral, then you’d choose oral + IV fluids)
How much does the cattle pump system pump in one stroke?
(A pint)
Why should you make sure you’re not pumping fluids too quickly with a cattle pump system?
(Prevents regurg and aspiration which is potential fatal)
How do you know if a cow you are pumping fluids into with a cattle pump system is going to regurgitate?
(She should normal be chewing while you have the pump system in place, if she stops, regurg is imminent)
How many gallons per 100 lbs of body weight can be administered orally in cows?
(0.5-0.75 gallon per 100 lbs of body weight, should be warm)
Why would you add 60-100 grams of calcium to a cows’ oral drench?
(Off feed and/or fresh dairy cows are typically hypocalcemic)
What is the purpose of adding 3-5 pounds of alfalfa meal to a cows’ oral drench?
(Gives the bacteria in the rumen a growth substrate, adding ¼-½ a lb of yeast also helps to accomplish the same goal)
If you’re going to add KCl to an oral drench to replace potassium losses, how much do you add?
(90 grams)
If you’re going to add propionate to an oral drench, how much do you add?
(12 oz)
If you’re going to add NaCl to an oral drench to replace losses, how much do you add?
(120-160 grams)
What is the dose of hypertonic saline in cattle, which is a great economical way to rehydrate moderate to severely dehydrated ruminants?
(2-3 ml/lb)
Why do you need to make sure a cow is either drinking or you administer oral fluids in a cow that you administer hypertonic fluids to?
(Bc in those cases, water will be drawn from the rumen by the hypertonic fluids so there needs to be fluids in the rumen to draw from)
In what conditions is hypertonic saline contraindicated and why?
(Salt intoxication and anemia; salt intoxication better make sense to you already or you should just quit while you’re ahead, for anemia hypertonic saline pulls water from the cells which will dilute that already minimal number of blood cells and then it’ll be time to kick the bucket)
What brand of bottled water is best for making homemade lactated ringers and why?
(Deer park (this part really was just for shits and giggles), or any company that uses reverse osmosis)
What electrolytes and how much do you add to 18 liters of reverse osmosis water to make homemade lactated ringers?
(140 grams NaCl, 90 grams of KCl, and 10 grams of CaCl)
What do you need to ask yourself when trying to decide if you are going to give a calf with scours oral versus hypertonic IV versus isotonic IV fluids?
(What is causing the diarrhea and is it malabsorptive or secretory diarrhea; oral obviously won’t work if it is malabsorptive and neither will hypertonic because they need to absorb fluid from the GIT for hypertonic to work)
If you have deemed a scouring calf a good candidate for oral fluid therapy (they are still drinking on their own just not enough, they don’t have abdominal distension, and they have secretory diarrhea), how much can you give and how often can you give it?
(2 quarts 2-3 times a day)
What is the more common location for digital dermatitis lesions though it can be seen in the interdigital space?
(On the heels)
Animals in which stage of digital dermatitis are reservoirs?
(M4)
Accumulation of several animals in which stage of digital dermatitis usually occurs at the beginning of an outbreak?
(M2 lesions)
If a farm continues to cycle between having M2 and M4 digital dermatitis affecting their cows, what management practice should you examine?
(Foot bath management)
What is the main causative agent of digital dermatitis, though there are unknown synergistic bacteria that are necessary for disease to occur?
(Treponema spp.)
What antibiotic class is best for use against digital dermatitis?
(Tetracyclines, they work best on Treponema spp.)
Beef cattle in what stage of production are most likely to be impacted by digital dermatitis?
(Feedlot)
Why is digital dermatitis more difficult to treat in beef cattle cases?
(Do not have a set routine where they have an exact path the cows walk everyday to place a foot bath in)
Corkscrew claw is a heritable disease but what other factor can also play a role?
(Nutrition → subclinical ketoacidosis or heavy, fast gain specifically)
The lateral/medial (choose) claws on the hindlimbs and the lateral/medial (choose) claws on the forelimbs are typically corkscrew.
(Lateral claw on the hindlimbs and medial claw on the forelimbs)
What lesions can occur secondarily to corkscrew claw?
(White line disease and sole ulceration +/- digital sepsis)
Pair the following trace minerals with their function:
Zinc/biotin
A - Antioxidant and immunity, protects cell membranes
B - Joint structure and bone density
C - Hoof keratin formation
D - Synthesis/maintenance of ligaments, tendons, bone, and cartilage
C - Hoof keratin formation
Pair the following trace minerals with their function:
Manganese
A - Antioxidant and immunity, protects cell membranes
B - Joint structure and bone density
C - Hoof keratin formation
D - Synthesis/maintenance of ligaments, tendons, bone, and cartilage
B - Joint structure and bone density
Pair the following trace minerals with their function:
Copper
A - Antioxidant and immunity, protects cell membranes
B - Joint structure and bone density
C - Hoof keratin formation
D - Synthesis/maintenance of ligaments, tendons, bone, and cartilage
D - Synthesis/maintenance of ligaments, tendons, bone, and cartilage
Pair the following trace minerals with their function:
Selenium
A - Antioxidant and immunity, protects cell membranes
B - Joint structure and bone density
C - Hoof keratin formation
D - Synthesis/maintenance of ligaments, tendons, bone, and cartilage
A - Antioxidant and immunity, protects cell membranes
The toe length for a dairy cow should be how long?
(3 inches)
You should dish out more of the sole on the lateral or medial claw in the forelimbs?
(Medial)
You should dish out more of the sole on the lateral or medial claw in the hindlimbs?
(Lateral)
What is the purpose of quarantine?
(Prevent transmission of disease both from new to resident and resident to new, better observation of newbies, and to identify disease, behavioral, and nutritional diseases in newbies)
(T/F) Even if new populations of animals are of the same known health status as your resident animals, it is still best to have a short quarantine period.
(T)
Which of the following are appropriate topics to be discussed during a vet-to-vet call when bringing new animals into a herd? (Yeah this is a funny question, but there’s another question where I ask you to list the correct reasons so you best know them)
A - Your favorite colors +/- if you prefer the sparkly version of that color or not
B - Confirmation that source herd has not had any recent disease outbreaks
C - Your favorite coverall brands
D - To determine what disease have or have not been detected/tested for in the source herd
E - Your favorite season and why
F - To determine what vaccination programs are used (what are they given and when)
G - Your vet school crush and why
H - To determine what antimicrobials are being used in the source herd’s feed and/or water
(B, D, F, and H)
What are the main topics that should be discussed in a vet-to-vet call?
(Recent disease outbreaks in the source herd, what diseases have or have not been detected/tested for, what vaccination program is used, and what antimicrobials are being used in the feed/water)
How are diseases generally transmitted between pigs?
(Direct, makes quarantine real nice looking)
Diseases are generally transmitted through direct contact between pigs, what are additional routes of transmission?
(Rodent/bird vectors, fomites, environmental transmission via aerosol, water, food, or dirt)
What should be included in quarantine areas that can minimize fomite transmission, particularly pertaining to humans?
(Foot baths, hand washing stations, changing area, +/- use of gloves)
What should be included in quarantine areas to minimize environmental transmission (aerosol, water, food, or dirt)?
(No common water or feed sources, easy to clean surfaces to minimize dirt, no contact b/w resident pigs and newbies)
Unless the newbie pigs/animals are entirely naive animals with no exposure to any diseases, when should quarantined animals be fed, watered, checked on, etc?
(Dead last)
What is a good general time period for quarantine?
(28-30 days, minimum is 2 weeks)
What occurs during an acclimation period that is an additional 15-30 days on top of quarantine time?
(Acclimatization period allows for the newbies to be exposed to or immunized for diseases affecting the resident pigs/animals)
What should be done during the acclimation period?
(Vaccinate for specific organisms that are proven to be an issue in your resident herd, exposure the newbies to a resident sentinel pig, and treat with antiparasitics (both internal and external) prior to entry into the resident herd)
What are the most common causes of death in piglets?
(Trauma, hypoglycemia, and hypothermia)
What are some of the skin related congenital disorders that piglets can be affected by?
(Epitheliogenesis imperfecta → monitor for QOL and manage as a wound, polydactyly → left alone or removed in show pigs, and cleft palates)
What are some of the CNS related congenital disorders that piglets can be affected by?
(Tremors → will grow out of it, splayed legs → if congenital can try to hobble them, if traumatic not much to do, hydrocephalus → will die)
What are some of the urogenital related congenital disorders that piglets can be affected by?
(Atresia ani → if partial will be fine, if not will die, intersex → fairly common, won’t affect growth but cannot be in the breeding herd)
Piglet losses increase when the piglets are what weight or less at birth?
(<2.5-2.75 lbs)
In which gestational status of mom pigs are stillbirths highest?
(Gilts and older sows)
If you are presented with 1-5 day old piglets with diarrhea, what all should be on your differential list?
(E. coli, Clostridium spp., coronaviruses (TGE/PEDv), and rotavirus)
If you are presented with >5 day old piglets with greyish diarrhea, what will be at the top of your differential list?
(Coccidia)
What diarrheal piglet diseases are associated with the highest mortality?
(TGE and PEDv)
Compare and contrast rotavirus and coronavirus in pathophysiology, clinical signs, and ages affected.
(Pathophysiology: rota takes the tips, corona takes the whole villi down to the crypts → villi take a week to regenerate, baby cannot absorb anything in the meantime and die; clinical signs: rota mostly diarrhea, corona diarrhea and vomiting so they get dehydrated fast and die; ages affected: rota is a baby pig dzs, TGE/PEDv can affect any age pig)
What are some of the strategies that can be used to obtain herd immunity against coronaviruses?
(Autogenous or commercially available vaccine and feedback (feed intestines of infected animals to the whole herd, found to not work for PEDv though))
When should creep feed start in piglets?
(Around 7 days of age)
If you note arthritis or polyarthritis in piglets, what are the possible causative agents and what can be used to treat?
(Strep spp, Staph spp, and T. pyogenes; tx with cephalosporins or penicillins)
In general, pigs are weaned at what age?
(3 weeks of age)
(T/F) Though nursery pigs still get diarrhea when they have E. coli infections, they will present more septicemic when compared to a piglet.
(T)
(T/F) Nursery is where exposure to Lawsonia intracellularis (causative agent of proliferative enteropathy) begins but clinical disease caused by Lawsonia is typically associated with growers/finisher pigs.
(T)
What parasitic infection is responsible for weaned pig diarrhea particularly when pastures are used instead of confinement?
(Trichuris suis, whipworms)
Why is coccidia associated with greyish-green diarrhea?
(Bc coccidia causes the intestinal lining to necrose which translates the greyish-green diarrhea)
What is the causative agent of edema disease which can cause CNS signs in nursery pigs?
(E. coli)
What are some of the CNS disorders that can cause ataxia, staggering, down and paddling, seizures, and convulsions in nursery pigs?
(Edema dz, Strep suis meningitis, salt poisoning, ascending paralysis from tail abscesses/infections, otitis interna +/- aural hematoma, pseudorabies, and Glasser’s dz (polyserositis mainly but can see some CNS signs))
What are some of the causative agents of polyserositis/arthritis in nursery pigs?
(Strep suis type 2, Haemophilus parasuis, Mycoplasma hyorhinis or hyosynoviae, Erysipelothrix, and other secondary invaders from neonatal infections)
What are some of the causative agents of respiratory disorders in nursery pigs?
(Atrophic rhinitis, PRRSv, circovirus, influenza, salmonellosis, and Mycoplasma hyopneumoniae)
What is the causative agent of greasy pig disease?
(Staphylococcus hyicus)
What is the typical presentation of pigs with Actinobacillus pleuropneumoniae and what will you find on necropsy?
(Presentation is sudden death in previously healthy pigs, necropsy you’ll find caudodorsal fibrinonecrotic lung lesions)
What is the causative agent of verminous pneumonia and how will affected pigs present?
(Ascaris suum, will have a wet cough that looks like they are trying to clear something from their lungs and be lethargic and generally sick looking)
What is the main concern when grower/finisher pigs have Mycoplasma hyopneumoniae or circovirus infections?
(Both limit growth)
(T/F) Salmonella is more of a concern in growers/finishers compared to piglets and nursery pigs.
(T)
Where will you see porcine circovirus dermatitis lesions at the beginning stages of the disease?
(At the hind end, then will migrate across the back of the pig)
Where are pityriasis rosea lesions typically found on pigs and how do you treat them?
(Usually found on the ventrum, no tx bc pigs will grow out of it)
Ringworm in grower/finisher pigs is typically treated with diluted bleach, what other skin disease is treated similarly in nursery pigs?
(Greasy pig disease)
How can you distinguish between mite and fly bites?
(Mite bite lesions will be widely distributed over the pig whereas fly bite lesions will not be)
Boars can have overuse issues so normally semen is collected how many times maximum in a week?
(2-3)
What gastrointestinal nematodes can be found in the abomasum of small ruminants?
(Haemonchus contortus, Teladorsagia spp., and Trichostrongylus axei (only trichostrongyle that is found in the stomach))
What gastrointestinal nematodes can be found in the small or large intestines of small ruminants?
(Trichostrongylus spp., Cooperia spp., Oesophagostomum spp., and Trichuris spp.)
What clinical signs are associated with parasitic gastroenteritis in sheep and goats that are economically unfavorable?
(Weight loss, slow growth, and lower production of milk, wool, or meat)
Are goats or sheep slower in developing immunity against parasites?
(Goats)
Are goats or sheep less likely to be exposed to parasites for behavioral reasons?
(Goats bc they are browsers instead of grazers like sheep)
What is the 70/30 rule?
(30% of a flock will have 70% of the worms and will therefore contribute to 70% of the contamination of pastures)
What is the goal of integral parasite management in small ruminants? )
(To keep worms at a level that does not have detrimental health effects
What are the three basic principles of integral parasite management in small ruminants?
(Reduce exposure of the host to infective stages (mainly achieved by grazing management strategies), development of a more favorable response of the host to GI parasite infection (achieved through breeding management), and deworming using the targeted selected treatment method)
Grazing animals in short/long (choose) pastures increases the ingestion of infective larvae.
(Short)
What is the difference between resilient and resistant animals?
(Resilient animals are healthy animals with high FEC whereas resistant animals are healthy animals with low FEC; resistant animals are more desirable)
What are some sheep breeds that have higher levels of resistance to parasites?
(Gulf Coast Native, St. Croix, Katahdin, and Barbados Blackbelly)
What are some goat breeds that have higher levels of resistance to parasites?
(Spanish, Myotonic, and Kiko)
What benzimidazole dewormers are approved for domestic sheep and goats?
(Albendazole and thiabendazole, fenbendazole is approved for goats but only wild sheep)
What macrocyclic lactones dewormers are approved for sheep and goats?
(Tricky me, none are approved for both sheep and goats, only ivermectin and moxidectin are approved for sheep, none are approved for goats)
What nicotinic agonists are approved for sheep and which are approved for goats (they do not overlap)?
(Levamisole is approved for sheep and morantel is approved for goats)
Some of the management practices that speed up development of resistance are frequent deworming, use of the same drug/group, anthelmintic underdosing, mass treatment, and purchase/movement of new animals because they all decrease what?
(Refugia)
What are the two sources of refugia?
(Free-living stages of helminths in the environment at the time of treatment and parasitic stages in untreated hosts)
How are animals that need to be dewormed when trying to maintain refugia mainly identified?
(FAMACHA scoring)
What is the most common causative agent of bacterial meningitis in goats, though there are other bacteria that can cause it?
(Mycoplasma)
Infection with Mycoplasma tends to occur in kids with failure of passive transfer, how do they get the infection? Two answers.
(Acquired through milk of asymptomatic dam within the first 2 months of life or post dehorning and tail docking)
Of the signs of bacterial meningitis, listed below, which are specifically caused by Mycoplasma infection?
A - Opisthotonus/stiff neck
B - Nystagmus
C - Swelling of joints
D - Diarrhea
E - Convulsions
F - Pneumonia
G - Crying abnormally
(C and F)
What does the spinal fluid of animals affected with bacterial meningitis look like?
(Cloudy with clots)
What four antibiotics can be used for cases of bacterial meningitis and which are specifically used for Mycoplasma infections?
(Ceftiofur (4-5 mg/kg IV QID), Nuflor (20 mg/kg IM), tetracycline (10 mg/kg IV), and Tylan (10 mg/kg IV), tetracycline and Tylan are abx of choice for Mycoplasma bacterial meningitis)
What is adequate colostrum intake for small ruminants?
(10-20% of their body weight within the first 12 hours)
Within what time period does aseptic meningitis occur post thermal dehorning?
(8-24 hours)
What is the most apparent clinical sign of caprine arthritis encephalitis in kids?
(Progressive rear limb ataxia, will be afebrile and BAR, condition will progress to tetraplegia, facial paralysis, and opisthotonus)
Listeriosis tends to live in material with a pH above what value such as spoiled silage, residual hay at round bale feeders, spoiled feed in feed bunks, and wet pastures or boggy soil?
(pH above 4.8)
Of the clinical signs for Listeria, listed below, which may not be present at the time of examination?
A - Depression and anorexia
B - Dysphagia, protruding tongue, drooling
C - Head tilt +/- walking in circles
D - Fever
E - Lack of menace and palpebral reflexes
F - Nystagmus, ear droop
G - Upper respiratory obstruction
(D)
What antibiotics can be used to treat Listeria and how long do you need to administer them?
(Procaine penicillin (22-44,000 IU/kg BID), oxytetracycline (5-10 mk/kg IV BID), or florfenicol (20 mg/kg IM SID); treat for a minimum of 10 days)
What is the causative agent of cerebrospinal nematodiasis?
(Parelaphostrongylus tenuis)
(T/F) The neurological clinical manifestations of P. tenuis infections (ataxia, paresis, knuckling) are accompanied by a change in mentation (dull, depressed).
(F, animals will be bright and alert, will eat and try to get up)
What dewormers should be used to treat P. tenuis infections?
(Some sort of macrocyclic lactone (Dr. P mentions ivermectin, doramectin, and moxidectin (500 ug/kg then 200 ug/kg for 5 days) and fenbendazole (15 mg/kg for 3-5 days))
What deficiency or what toxicity causes polioencephalomalacia?
(Thiamine deficiency or sulfide toxicity)
Which of the following is NOT a clinical sign associated with scrapie infections?
A - Apprehensiveness, loss of herding instinct
B - Clumsy gait
C - Aggression
D - Head and body tremors
E - Dysphagia, drooling
F - Ataxia, wide based stance
G - Droopy ears
(E)
What occurs to QQ, QR, and RR animals when a scrapie positive animal is identified from their birth cohort?
(QQ (susceptible) and QR (resistant but not entirely) are euthanized, RR (resistant) are kept and should be bred)
How are animals infected with Corynebacterium pseudotuberculosis?
(Organism enters through a wound → tail docking, castration, ear tagging, shearing, bites from external parasites, and barnyard hazards such as nails, board, etc.)
Corynebacterium pseudotuberculosis causes abscesses that are typically external in goats/sheep (choose) and internal in goats/sheep (choose).
(External in goats, internal in sheep)
In addition to treating goats or sheep with caseous lymphadenitis with penicillin (10,000 IU/lb BID for 4-6 weeks), what can be infused directly into the abscesses?
(Iodine, formaldehyde in pet goats)
What are the two causative agents of contagious foot rot in sheep and goats?
(Dichelobacter nodosus and Fusobacterium necrophorum)
What antibiotics can be used for treatment of contagious foot rot in sheep and goats?
(Pen-G (20,000 IU/lb one dose), oxytet (9 mg/lb), and gamithromycin (6 mg/kg))
What are the footbath/foot soak types that are commonly used for prevention/treatment of contagious foot rot in sheep and goats?
(10% zinc sulfate, 10% copper sulfate, and 5% formalin)
Of the footbath options for treatment of contagious foot rot in sheep and goats, which is the most desirable to use and why?
(10% zinc sulfate, least toxic of the three soaking agents; copper is toxic if drunk and it stains wool, formalin can scald the feet)
What are the causative agents of ovine interdigital dermatitis?
(Fusobacterium necrophorum and Trueperella pyogenes)
Foot scald aka interdigital dermatitis is usually seen during what weather conditions?
(Wet weather conditions, or if there is a lot of morning dew)
What clinical sign being present in a case of foot scald would indicate the necessity of injection antibiotics (penicillin or tetracycline) versus just spraying between the toes with 4g of tetracycline powder diluted with 1 quart of isopropyl alcohol?
(Swelling of the coronary band → indicates cellulitis)
What is the most common sign of CAE in mature goats?
(Chronic hyperplastic polysynovitis-arthritis → carpal joints almost always affected, may involve stifle, hock, coxofemoral, and atlanto-occipital joints)
How can animals obtain CAE infections?
(Via colostrum and milk from an infected doe, iatrogenically from shared surgical equipment (blood), via inhalation, and in utero)
How do you heat treat colostrum to aid in prevention of spread of CAE, Mycoplasma, and lots of other diseases that are transmitted via colostrum?
(Heat to 135-140 F for 60 minutes)
Pregnancy toxemia is caused by abnormal metabolism of carbohydrates and fats in the last trimester in sheep and goats, a lot of things contribute to that cause, what are those things?
(Rapid fetal growth, increased metabolic demand (kinda associated with the rapid fetal growth, stress, decreased rumen capacity, and individual animal susceptibility (genetics))
What are the types of pregnancy toxemia?
(Primary pregnancy toxemia which occurs in animals with a normal BCS who have larger litters, fat ewe/doe pregnancy toxemia, starvation pregnancy toxemia, and secondary pregnancy toxemia which results from a concurrent dz)
Propionate is the most important glucose precursor and is derived from ruminal fermentation of what type of feed?
(High carbohydrate content feed so grain)
What is tissue fat broken down into when lipase activation occurs in animals with a negative energy balance?
(Glycerol (which goes to the liver to be converted into glucose) and NEFAs (which can be used for energy production or converted into ketone bodies)
What are some of the clinical signs of hypoglycemia encephalopathy, which is a more advanced presentation of pregnancy toxemia?
(Head pressing, circling, muscle tremors, blindness, star-gazing, and ataxia; these signs could also be related to a secondary thiamine deficiency)
What ketone value or greater found on blood work is considered clinical pregnancy toxemia in sheep/goats?
(> 2.4 mmol/L)
Listed below are blood work changes you might see in advanced cases of pregnancy toxemia, pair them to their cause:
Hyperglycemia
A - Hepatic/renal failure
B - Dehydration/renal failure
C - Fetal death
D - Anorexia
Hyperglycemia - fetal death
Listed below are blood work changes you might see in advanced cases of pregnancy toxemia, pair them to their cause:
Hypokalemia/hypocalcemia
A - Hepatic/renal failure
B - Dehydration/renal failure
C - Fetal death
D - Anorexia
Hypokalemia/hypocalcemia - anorexia
Listed below are blood work changes you might see in advanced cases of pregnancy toxemia, pair them to their cause:
Azotemia
A - Hepatic/renal failure
B - Dehydration/renal failure
C - Fetal death
D - Anorexia
Azotemia - dehydration/renal failure
Listed below are blood work changes you might see in advanced cases of pregnancy toxemia, pair them to their cause:
Hypoproteinemia
A - Hepatic/renal failure
B - Dehydration/renal failure
C - Fetal death
D - Anorexia
Hypoproteinemia - hepatic/renal failure
What is the mainstay treatment for mild cases of ketosis in sheep/goats?
(Oral glucogenic precursors → propylene glycol (60-200 ml PO q6-12h up to 6 days) or glycerol (60 ml PO q12 for 3-6 days), some alternatives are calcium propionate, sodium propionate, liquid molasses, sodium lactate, ammonium lactate but these are not metabolized as quickly as propylene glycol)
What is the treatment for moderate to severe cases of ketosis in sheep/goats?
(Oral/IV fluids and IV dextrose optimally in a hospital setting so dextrose can be given as a CRI, follow up with daily propylene glycol and fluids, and can give hypertonic bicarbonate if acidotic but need to give oral fluids if you do this; can also give insulin but these cases definitely need to be hospitalized for BG monitoring and dextrose CRI)
What gestational ages are safe minimums for induction in sheep and goats?
(Sheep 140 days, goats 143 days)
What two drugs are given for induction in sheep and goats?
(Prostaglandins (1-15mg dinoprost) and steroids (10-20 mg dex))
What is the difference in when hypocalcemia may be experienced in non-dairy versus dairy small ruminants?
(Non-dairy → greatest calcium demand is 3-4 weeks before parturition; dairy → usually post-partum)
What early clinical signs result from lack of membrane stabilization in cases of hypocalcemia?
(Stiff gait, tremors +/- hyperesthesia, and ataxia)
What later clinical signs result from the inability to release acetylcholine at the neuromuscular junctions in cases of hypocalcemia?
(Hyposensitivity, weakness, recumbency)
What clinical signs related to hypocalcemia result from inability of muscle to contract?
(Constipation and decreased rumen motility → bloat, absence of PLR, increased heart and respiratory rate)
What is the treatment for uncomplicated hypocalcemia? Be specific.
(30-60 ml IV calcium borogluconate heated to 35-40 C and slowly administered while monitoring heart rate; alternatively can give CMPK and dextrose IV)
Why should you avoid IV administration of calcium in hypocalcemia ewes/does that have concurrent pregnancy toxemia?
(Calcium solutions are fatal in animals with impaired liver function)
What dietary compound should be avoided because they precipitate formation of nonabsorbent compounds with calcium, therefore making it inaccessible to the animal?
(Oxalate)
What are the two main risk factors for hypomagnesemia in sheep/goats?
(Increased potassium and/or reduced sodium with an increased milk yield → reduced Mg absorption from the GI tract)
What clinical signs are caused by the spontaneous activation of neurons in the CNS in cases of hypomagnesemia?
(Excitability, paddling convulsions, tonic-clonic muscle spasms, and increased respiratory rate)
When does hypomagnesemia typically occur postpartum in small ruminants?
(2-4 weeks)
What are the suggestive and diagnostic levels of magnesium in the blood in cases of hypomagnesemia?
(Suggestive is <1.5 mg/dL, diagnostic is <1.0 mg/dL)
What is the treatment for hypomagnesemia?
(IV adm of 4-5% magnesium chloride and 50 mls of 20-25% CMPK solution with additional SQ or oral adm 12-24 hours later to prevent relapse)
If there is an outbreak of hypomagnesemia on a farm, what can you suggest to the owner?
(To give 7 g/animal magnesium oxide PO to clinically healthy animals and in the future prevention can be achieved by appropriate mineral supplementation and properly balanced fertilizers)
What are the typical weight ranges for kids versus lambs?
(Kids 5-8 lbs and lambs 8-10 lbs)
How much colostrum should a kid or lamb receive within the first two hours of life?
(20ml/lbs or 0.75 oz/lbs, should then intermittently give 100-125 ml/lbs or 3.5 oz/lbs over the next 24 hours)
How much should kids and lambs be fed per day in % of body weight?
(20% of their body weight per day)
How many times a day should kids and lambs be fed during the first 3-4 days of life?
(A minimum of 4 times a day, first thing in the morning and last thing at night with at least two feedings between those times)
How many times a day should kids and lambs be fed during the first two weeks of life after the initial 3-4 days?
(3 feedings per day)
After kids and lambs reach two weeks of age, how many times a day should they be fed?
(Two times a day)
How long should kids and lambs be fed 90-100 F milk and what temp should it be once that time period is over?
(Should be fed 90-100 F milk for the first week of life, room temp afterwards)
Hypothermia is considered what degree and colder in kids and lambs?
(98 F or colder)
What are the clinical signs of floppy kid syndrome and in what time period do they occur after birth?
(Clinical signs are muscle weakness, anorexia, depression, all of which will occur within the first two weeks of life)
What would you expect to see on blood work of a kid with floppy kid syndrome?
(Metabolic acidosis with a high anion gap)
What is the treatment for floppy kid syndrome?
(Oral baking soda (0.5-1 teaspoon mixed with water) or IV bicarb (125-200 ml of 1.3% bicarbonate solution or 20-25 ml of 8.4% bicarb added to saline))
