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 |