Food Animal Midterm 2

how many veins and arteries does the umbilicus consist of?

• 2 arteries

• 1 vein

and a urachus

What can an umbilical infection lead to?

• umbilical hernia

Are umbilical hernias inherited?

yes in holsteins

At what size do umbilical hernias tend not to resolve wuth conservative management and require surgery? Can the surgery be done in the field?

• >6cm

• yes with restraint and local anesthesia

Describe the conservative management options for umbilical hernias (3)?

• manually reduce with hand several times a day

• abdominal bandage

• clamping or banding but must ensure ut is well reduced before application.

Note: this is only for small hernias

What should you do if you want to do an umbilical hernia surgery but unsure if there is infection?

• ultrasound to examine before hand

How would you begin an umbilical hernia surgery? Describe the two approaches.

Do a local block (subQ cranially and to the sides with lidocaine). Make an elleptical incision through the skin. Blunt and sharp dissection down the edges of the hernial ring without entering the hernial sac

Open herniorrhaphy: enter abdomen lateral aspect of ring. Palpate content without entering. Better edges for healing.

Closed: don’t open abdomen so no infection risk. Less good edges for healing. Roughen body wall edges with scalpel.

_________ herniorrhaphy: enter the abdomen lateral aspect of ring. Palpate contents of sac, reducing without entering. Can open and undo adhesions, resect if abscess of umbilical remnant, better edges for healing, appositional suture. Often do open in calves as higher incidence of adhesions or infections. Appositional suture pattern with absorbable suture. Preplaced sutures to ensure you don’t include intestines. 

• open

___________ herniorrhaphy: don’t open the abdomen so no risk infection. Less good edges for healing. Roughen edges, appositional or overlapping suture pattern. Roughen body wall edges with scalpel. Use back of thumb forceps to take bites of wall without risk of intestines. 

• closed

How would you treat post op umbilical hernia repair?

• NSAIDs day of surgery

• confine for 2-4w to small area

• don’t need peri-op abx

If there is an umbilical infection on the urachus, what will occur? What about infected arteries? Where does the vein go? How do you diagnose?

• dribbling urine

• form abscesses

• liver

• palpation and ultrasound

What should you do if there was a patent urachus?

• can wait to see if it closes and regresses.

• can do a course of abx

• if this doesn’t work then surgery. If the vein infected all the way to liver then marsupialize the vein to give drainage.

What is one complication that can occur if there is infection following the umbilical remnant excision? How do you approach this surgery?

• hernia

• like a hernia and open into abdomen. larger incision. Deal with adhesions. Must ligate and excise proximal to the infection. Routine closure. Confine for 2-3w.

_________ hernias: often due to trauma, weakening with age. Uncommon in cows. If large can sometimes leave whereas small may require surgery due to risk of entrapment. 

Ventral

_______________: breakdown of surgical incisions. Most often due to incisional infections. All infections must be gone prior to repair, Appositional repair or placement of mesh. Most common reason for failure of repair is return of infection. 

Incisional hernias

What is the most common reason for failure of incisional hernias?

• return of infection

True or false: congenital inguinal hernias are usually not strangulating

true

How are acquired inguinal hernias be fixed?

• fix surgically with unilateral castration under GA at hospital to preserve other side.

• can herniate on other side later so warn owners

What are three reasons that newborns are more susceptible?

• fewer energy reserves

• high surface area to body mass (rapid heat loss and vulnerability to environmental stress)

• dependence on maternal passive immunity

What are 4 main components included in colostrum?

• IgG

• leukocytes

• antimicrobial components (lactoferrin, lysozyme, etc)

• growth factors and insulin effects to support intestinal mucosal development

What are the three failure points for colostrum management?

• colostrum quality (low IgG or excessive bacterial contamination)

• ingestion failure

• absorption failure (need in first 4-6h)

Which cows make better colostrum— beef or dairy? Older or younger cows?

• beef

• older

How long does it take to make colostrum?

3w

How many grams of IgG should calves get? In what time frame? What should the brix read?

• 150g

• 4-6h for high absorption

• >22% (bets is >25%)

How do high bacterial loads in colostrum affect absorption?

• high bacterial loads can bind to IgG and interfere with translocation across the GIT

What is the 4×4×4 colostrum rule?

4L in 4h with 4 characteristics (good, clean, quality, and colostrum)

What are 3 ways to assess FTP in calves?

• serum IgG concentration

• serum total protein by refractometer (practical)

• GGT rises after colostrum ingestion

How do you treat FTP?

• plasma at 20ml/kg IV ir whole blood.

• Treat infection and support perfusion, glucose, temp and nutrition

___________: infection associated with a dysregulated systemic inflammatory response. __________ occurs when the sepsis is worsened with persistent circulatory dysfunction and inadequate tissue perfusion. _________ is systemic inflammatory response syndrome. __________ is severe sepsis with multiple organ dysfunction syndrome. 

Septicemia

Shock

SIRS

MODS

What are 4 gram negative bacteria that cause septicemia?

• E. coli

• Klebsiella

• Salmonella

• Campylobacter

What are two common entry routes for septicemia? What are two ways this commonly happens to calves?

• GIT and umbilicus

• contaminated colostrum and environment

True or false:

Hypothermia and fever are both possible during septicemia

true

6 lab findings for septicemic calves?

• neutropenia or philia with toxic changes and bands

• increased fibrinogen

• hypoglycemia

• metabolic acidosis

• hypoxia

• hypoproteinemia

What are the 4 steps of treating septocemic animals?

1. stabilize airway, breathing, circulation, glucose and temp

2. obtain cultures

3. begin empiric therapy (Sodium ampicillin, TMS or ceftiofur)

4. ID and control focal infections

5. provide fluids, O2, nutrition, anti-inflammatories

6. reassess

_________________: when sepsis becomes neurological. Occurshypoglycemia, electrolyte abnormalities, hypoxic ischemiaere bacteremia and hematogenous CNS. Usually E. Coli. See endotoxin and inflammatory injury which cause infarction, necrosis, and neuro dysfunction. 

• ddx: hypoglycemia, electrolyte abnormalities, hypoxic ischemia, trauma after birth congenital CNS, toxic or metabolic encephalopathy, CNS infection

Neonatal Bacterial Meningitis

Most common bacteria that causes neonatal bacterial meningitis?

E. coli

Where is most of the calcium and phosphorus found in the body? Where is the remaining 1% found?

• the bone

• most found in cells and very small amounts found in the extracellular space.

2 times where there is huge demand for calcium and phosphorus?

• lactation

• fetus (especially when there are multiple)

Which two ions are membrane stabilizers?

calcium and magnesium

What happens when there is low calcium and magnesium?

• there is incomplete closure of sodium channels and the membrane potential becomes less negative to easier to conduct an AP—> tetany and hyperexcitability

• Calcium also is needed to release Ach at neuromuscular junctions. If there is low Ca then there is low Ach release and decreased muscle contractions

so there can be hyper or hypo muscle contractions

What is the role of PTH? What ion is excreted?

• increases osteoclastic activity, increase bone resorption, increase Vit D3 activation.

• phosphorus

________________: seen in first 72h. Risk factors include high milk producers, increasing age (>5y, rare in heifers due to lower milk production and more response to hormones from bones), jerseys, milk fever in previous lactation, improper feeding in dry period (grasses have a lot of Ca but straw doesnt however need to maintain BCS. Can also feed anions and trick the body into mobilizing calcium). 

Bovine Parturient Paresis

Why doesn’t PTH just fix the calcium drop seen when there is a new sudden demand for calcium?

• it takes 24h for optimal GI Ca absorption and 48h for optimal bone resorption so it takes time to come into effect.

Describe the three stages of bovine parturient paresis (milk fever)?

• stage 1: SM stops working to there is less eating, lethargy, decreased ruminal contractility (so may have mild bloat), ears dropped etc

• stage 2: skeletal muscle stops working right so the abimals goes down and can’t get back up but in sternal.

• stage 3: cardiac muscle starts getting affects so they are in lateral and can’t get up to eruct. Get tachycardic.

What are three things we can see when there is subclinical hypocalcemia?

• mastitis (bc increased recumbency)

• uterine inertia (dystocia, uterine prolapse, retained fetal membranes)

• DAs

Describe what you would expect to see on clinical pathology of a cow with bovine parturient paresis? (5)

• ionized calcium <1.6 (normal is 2.11-2.75mmol/L)

• mild hypophosphatemia

• hypermagenesemia (or normal)

• hyperglycemia (cortisol)

• elevated CK (increased recumbency)

How would you treat a clinical bovine parturient paresis case?

• IV 1 bottle of 23% Ca borogluconate and 1 subQ slowly and stop if there is bradycardia or arrhythmias

• can so oral Ca drenches or SQ Ca for stage 1

What is the prognosis for bovine parturient paresis? Indicators? best way to prevent?

• excellent if not recumbent long (25% relapse in 48h)

• if not standing in 24h or if CK is >10 000 then prognosis is guarded

• manage diet too increase PTH prior to lactation by feeding a low calcium transition diet or by adding anionic salts

In sheep when do we see hypocalcemia and what signs do we see?

• pregnant ewes—> see flaccid paraltsis

• transport tetany in lambs and ewes with concurrent low Mg (bc off feed)—> see tremors and tetany

Do you see paralysis or hyperexcitability in goats with hypocalcemia? When do you see it? How would you treat a case?

• hyperexciteability

• in first month of lactation

• Ca boro 1g per 45kg slowly IV and can use Mg containing products if there is tetany.

For hypomagnesemia in cattle (grass tetany, staggers, lactation tetany), what do levels depend on? What are three things that decrease Mg bioavailability? When is it seen? Breed?

• depend on diet and NOT hormonal control

• potassium, higher protein diets and CH diets (potatoes in feed are low Mg and high K and can cause issues)

• poor diet or lush pasture

• European beef breeds

What are some clinical signs of hypomagnesemia?Heart? Clin path?

• hyperexciteability, erecting ears, muscle fasciculations, eyes snap hard when blink

• LOUD heart sounds, tachycardia

• VERY low Mg (<0.4mmol/L) and may have low Ca and P

How would you treat hypomagnesemia in cattle? Prognosis?

• Ca and Mg borogluconate or half IV and half subQ. SLowly. NO K IN SOLUTION.

• supplement with Mg enema

• control seizures with diazepam then RUN

• good unless there is convulsing. ALWAYS watch for other animals too. Add some grain to prevent further cases.

Is acute hypophasphatemia common? How would you treat it?

• rare

• IV calcium phosph or fleet enemas

When does hypokalemia syndrome of dairy cattle occur? (2) High or low HR? CS?

• anorexic cows with metabolic alkalosis waste K in their urine

• following multiple treatments of isoflupredone (predef)

• high

• recumbent with S curved neck, usually >48h PP.

What is ketosis? When does it occur? Main ketone that causes issues?

• negative energy balance

• <6w PP

• B-hydroxybutyrate

What are the two types of ketosis classification?

• Primary (type 1): early lactation. NEB with absence of disease.

• Secondary (type 2): NEB due to disease causing decreased feed intake

______________ : no overt signs but there are production issues. Seen increased ketones. At risk for lower milk production, early culling, progressing to clinical ketosis. 

Subclinical ketosis

What are the main CS for subclinical ketosis?

• poor production, sweet breath, and occasionally nervous ketosis (twitching, licking walls, etc)

What level is considered subclinical for ketones? Clinical? Treatment? (5)

>1.2mmol/L

>3mmol/L

oral propylene glycol 300mL. Can do 1-200mL dextrose iV but its not really recommended now. Can give GC to suppress milk production for 3d (only if primary and not pregnant). Also can so insulin if there is hepatic lipidosis or B vitamins

What is one vitamin that may be deficient if a herd has chronic issues with ketosis?

cobalt

2 ways to prevent ketosis?

• decrease energy density of diet in late lactation and dry cow.

• good transition diet and can add monensin to increase proprionate formation in rumen.

When is fatty liver seen in cows? Two risk factors?

• over conditioned cows that calved and then have increased energy demand so fat is mobilized to liver

• over conditioned in late lactation/dry period, prolonged days open

What are 4 things that can be noted on bloodwork for cows with fatty liver?

• high SDH

• high bile acids

• high ketones

• hypoglycemia

What test might you do with liver biopsy if you suspect hepatic lipidosis? How does it work?

• float test in CuSO4

• float in water then >34% (poor prognosis), float in copper sulfate then 25-34% infiltration. If it floats in 8% solution then 15-24% fat infiltration (may be normal in high producing animals)

Note: there is a 26% fatality and grave prognosis if >34% infilitration

How would you treat hepatic lipidosis? Should you add in steroids?

• IV dextrose and propylene glycol. Consider insulin. Treat concurrent disease.

• NO GC bc already immunosuppressed

When is pregnancy toxemia seen? CS? Why? Treatment? Prognosis?

• late gestation in sheep and goats

• neuro signs, anorexia, star gazing, etc

• high energy demands and decreased rumen space

• remove fetuses**

• fair

At what level can there be invisible milk fever? Why is this an issue (2)?

• 2.1mmol/L Ca

• lost 2.6Lmilk/cow/d

• increase DIM by 15d

You are suspecting milk fever in a down cow but when you listen to the rumen, she is ruminating perfectly. Do you still suspect hypocalcemia?

no—> if ruminating well then not a calcium issue

Subclinical milk fever cows are 2.6x more likely to have ___ and ____, 2.4x more ______ and 2.3x more risk of a ____.

• dystocia

• RP

• ketosis

• DA

What are two ions that we should limit in a dry cow diet? How do we get a negative DCAD equation (2 common options)?

• limit high Ca and K diets (so corn is a good option and avoid manured land for crops)

• anionic salts (sulfur and tastes gross)

• calcium binders (A Zelit)

What is an easy way to test to see is DECAD is working? How early before calving do you want this?

• acidic pH (5.6-5.8)

• 2w before calving atleast

What is the transition period? What is the close up period? What do we need to maximize during this period?

• -21d to 21DIM

• 3w before calving

• Dry matter intake

You see an early PP cow with an extremely high milk fat (>5%) in her first milk test. What do you suspect caused this?

• subclinical ketosis where there is extra fat mobilization

True or false: Every dairy cow goes through a negative energy balance during lactation.

true but don’t want them to lose more than half a BCS point

What ketone is best to measure? What is the cut off for subclinical ketosis?

• BHB

• 1.2mmol/L—> give propylene glycol if above this

Two ways to prevent ketosis in cows?

• kextone boluses: monensin selects for bacteria that make more proprionate

• AVOID OVERWEIGHT COWS

Can also feed niacin for 2w.

How do we monitor for fatty liver?

Non-esterified fatty acids (NEFAs)**

if the liver has a hard time keeping up, it will tell the body to release NEFAs

Two of the main signs of rumen acidosis?

• cyclic intake of feed

• milk fat depression

can also have laminitis, SARA, liver abscesses, etc

5 ways to prevent rumen acidosis?

• maintain proper fibre mat

• avoid slug feeding

• proper chopping and forage length

• use buffers (sodium bicarb but be careful with dry cows)

• make sure feed is in front of them

What should be look at if examining whether a cow had a rough transition period?

• transition management index where we want them above 0. If negative then rough.

3 ways to monitor for rumen acidosis?

• milk fat inversions

• manure scores (two knuckles deep)

• rumenocentesis (5.5pH or higher, if 30% of ten cows if higher then you have a herd issue)