• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/83

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

83 Cards in this Set

  • Front
  • Back

What is the number one cause of death in calves between birth and weaning?

Scours

What is the number one cause of death after weaning?

respiratory illness

What is uncomplicated scours?

Scours where the lesions/inflammation does not extend beyond the GIT

What is undifferentiated scours?

where the cause is unknown.

What are the most important mechanisms in calf diarrhea?

Hypersecretion and malabsorption/maldigestion

How does the villus change in secretion as you move from crypt to tip?

There is no NaCl secretion past about midway in the normal villus

How does damage to the villus lead to hyper secretion of NaCl?

By damaging the villus tip, there are now going to be more immature/crypt cells marching on up, causing more of the villus to be SECRETORY (like in heat labile toxin)

What do the basolateral pumps do?

Na/H and Cl/HCO3 exhanging

What is the mechanism behind maldigestion/malabsorption diarrhea?

Clubbing or blunting of the villus tip decreases absorption capacity (will see in combo with the secretory toxins as you are knocking out the tip in both instances)

Do you lose more bicarb through secretion or malabsorption processes?

Malabsorption.

What happens when more lactose is pushed into the lower GIT?

an osmotic diarrhea and increased intestinal bacterial fermentation

If you are losing H what else are you losing?

HCO3

Which e. coli attacks immature gut cells?

ETEC (enterotoxigenic e coli)

What are the major virulence factors of ETEC?

K99 pillus and heat stable enterotoxin

What does ETEC stimulate?

the secretion of NaCl and H2O (via increases in cGMP)

What is the basic mechanism behind ST (heat stable toxin)

Cl secretion from the crypt cells and no absorption of Na at the tip.

Which Na transport mechanism is NOT AFFECTED BY ETEC's ST toxin?

The glucose-Na transport!!!

What other factor can increase secretory crypt cells?

the Enteric Nervous system

What are the lesions seen in enterotoxigenic e coli?

hyperemia, superficial inflammation

How do we dx ETEC?

Fecal culture w/ anB- have confirm that the K99 pillus is there.

Where on the villus does rota attack

the tip

What type of diarrhea is seen in rota virus

Malabsorption/maldigestion

What does corona virus do to the villus?

It "cuts" - SI to LI - leading to tenesmus and bloody D+

Where does crypto colonize?

the tip of the villus enterocytes.

Where in the GIT does crypto like to live

the Ileum

How does crypto cause cellular dysfunction?

Inflammation

Does crypto have to sporulate in the environment to be infective?

NO -- can auto infection - sporulation within the gut can lead to relapses

How long can crypto survive in the environment

6 months

How can milk replaces lead to scours?

poor quality replacers -- increase in intestinal fermentation - and can exacerbate the D+ of an infectious agent.

Which pathogen is most common in calves < 4 days old?

E coli

Which pathogen is most common in those 4-14 days old?

Rotavirus

What are the clinical signs of scours?

watery D+, obtundation, weakness, anorxia, loss of skin tent and eye luster; can progress to coma.

What is commonly seen on clinical pathology?

Hyponatremia/chloremia, metabolic acidosis (secretional); hyperphosphotemia (renal damage), increased PCV (can be hard to appreciate in calves)

What are the direct causes for the acid/base imbalances seen in scours?

loss of HCO3 throughout the feces (mui important)

What are some secondary causes of the acid/base disturbances?

1. Lactic acid production (poor perfusion)


2. Retention of acids normally excreted by the kidneys.


3. absorption of VFA from colon fermentation (+lactate luminal production)

How does the respiratory system play into the acid/base disturbance?

Early -- will have respiratory compensation (hyperventilation)


Late - b/c of weakness - unable to ventilate well - hypoventilation leading to a respiratory acidosis

What will a mild/non clinical scours calf look like?

Profuse D+ -- Standing, suckling well. Minimal skin tent, no HCO3 deficit, < 5% dehydrated, pH of 7.35-7.5

What does a moderately affected scours calf look like?

Profuse diarrhea, dull but responsive, normal eye luster with increased skin tent. Low suckle reflex. Head held down, 7% dehydrated, blood ph at 7.10-7.25, HCO3 def of 5mEq/L

What does a severely affected scours calf look like?

Profuse D+, dull w/ minimum responses, very long skin tent, eyes are sunken and dull, stand only w/ assistance (5pt stance), but can remain sternal on own, minimal if any suckle, dehydrated 8-10%, pH of 6.9-7.1, HCO3 deficit of 10mEq/L

What does a VERY SEVERE calf look like?

Profuse D, skin tents forever, eyes are sunken/dull, non responsive, no suckle reflex, comatose, 10-12% dehydrated, pH of 6.8-7, bicarb deficit of 15-20mEq/L

How are calves that are over 1 week old different with scours presentation?

They get a lot worse prior to showing clinical signs - better coping mechanisms. Will have a higher bicarb deficit (+5mEq/L deficit) than younger animals.

What are the immediate treatment goals for scours?

1. Rehydrate


2. replace lost e-


3. restore acid/base balance

What are the long term goals for scours treatment?

Provide nutrition and provide for ongoing losses

How do you calculate the rehydration needed?

BW (kg) x (%) dehydration x (1L/kg)

What % of the bw is the gastric capacity?

5%

How do we figure out how to restore the acid/base disturbance?

Deficit (either know the amt based on presentation or calc based on blood gas) - then it is ECF (50%) x BW x Deficit x 1L/kg = mEq bicarb to give.

What is the main disadvantage of administration of oral fluids

you are limited to the gastric capacity!!!! only 5% of the calves body wt. (so you figure the amt needed to replace and split that up into enough feedings to get the amount that you want to admin)

Can you replace e- with oral fluids?

No! Need to give parenterally (they will not be absorbed if there is a maldigest/malabsorption occurring.

What is the main advantage of IVF?

You can RAPIDLY correct deficits

What is the disadvantage to IVF?

Can correct TOO fast. Plus you can cause hemolysis and it is $$$.

What types of fluids are you limited to in SQ use?

hypotonic or isotonic (hyper tonics will pull fluid from the vasculature)

Who can be treated with oral fluids

Those that are still suckling or have JUST lost the suckle.

When do you use SC fluids?

as an adjunct - those that you are also giving oral fluids too, or those you gave an IV bolus to as a support and prolong of effect.

How soon should you give IVF if the oral fluids did not lead to an improvement?

2-4 hours.

What will good milk replacers contain?

Salt, base, sugar (you add the water)

What should we be aware of in glorified milk replacers?

The ones that have whey, guar gum or xanthine as 1st ingredients == have abx in them that do not work on the concerning bacterium.

What should the first ingredient be in a milk replacer?

NaCl

What should the base be in a milk replacer?

bicarb, proprionate acetate or citrate

Why is glucose important in a milk replacer?

Increases the hypertonicity of the solution, and in sodium absorption

How does a hypertonic sol'n help?

Slows gastric emptying so it is better absorbed.

What if I am using an IVF method? How do I figure out what to give

Start with Normosol (has some base in it already about 25-30mEq/L). Then add in NaHO3 (which has 12mEq/g HCO3) or an 8.4% (1mEq/mL) sol'n to adjust for deficit

Why so careful with the base administration?

Too fast of a bi carb add'n can cause neuro deficits.

What do we need to be careful when adding in NaHO3?

Do not want IVF at more than 2x hypertonicity - and adding 100mEq of HCO3 this way is also adding in 100mEQ of Na. So spread out your base (give in 4L instead of in 2)

What if I did not want to add in IVF>

can give isotonic (1.4%) or hypertonic (8.4%) NaHCO3 (this will drop the K since it will shove all the K into cells by pulling out H)

How fast should we move calves to po fluids?

ASAP

What is the maintenance rate for a calf?

10%BW/day

How does D+ change our maintenance rate?

triples it (30% BW/day)

What is the difference between milk and fluids?

Milk has higher energy but less electrolytes with the exception of K

When do we want to start getting the calf back on milk?

by d2

What should we not mix with the milk?

Electrolytes - will curdle the milk.

When should NSAIDS be used?

in COMPLICATED scours cases only

When should abx be used in scours?

Only to cover the bases in complicated cases.

How do we minimize losses from scours?

management! Cleaning! boost immunity (vacc for K99, rota and corona -- mammas' otherwise oral AnB for calves)

What causes diarrhea in calves > 3 weeks old?

Coccidia

Where is the most severe damage caused in coccidiosis?

The ileum, cecum and colon

How long does it take coccidia to develop in the GIT

Weeks

Are coccidia infections self limiting?

yes

Can you relapse with coccidia?

YES -- but it is a REINFECTION (coccidia cannot auto infect)

What are the clinical signs of coccidia?

D, hematochezia, tenesmus, poor growth.

What lesions are seen in the GIT?

Effacement of the villi (from the "explosions" of merozoites)

how is coccidia dx?

Fecal floatation (a few days after signs start)

What is the treatment for coccidia

young - sulfas


amprolium (corid)

How do you prevent coccidia infection

Decoquinate (in feeds)


Monensin - ionophores


Good hygiene