Food Ani. Med- Neonatology 2

wilsbach's version from 2016-04-21 00:45


Question Answer
3 ways to prevent FPTI(1) colostrum (2) plasma (3) timing
if you pass the time of gut closure-- what else can you do? the cons of doing this?can give plasma with IgG in it-- but its missing some of the other nutrients, proteins, might not have locally relevant IgGs... and misses out on all those extra things in colostrum, and no IgA (which is good for mucosal barrier)
what dzs are calves at risk of developing? esp if FPTI?sepsis, umbilical infection, penumonia, joint dz, systemic infxn...
why do neonates get joint dz when theyre septic?perfusion of joint isn't great. Cartilage doesn't have a big blood supply-- most nutrients through diffusion. So if blood has lots of bact, and gets into place not well perfused, bact has more of a chance to settle in and cause issues. Also sepsis-->immune complexes--> can latch onto tissue or they can cluster and stim more cytokines and inflammatory mediators at site--> joint disease
ways to determine if has FPTI?RIA/RID, Zn sulphate turbidity test, ELISA, TP. Can also look at colostrum quality, and look for CSs of infection
if FPTI are they guaranteed an infxn?no- doesnt guarantee infxn, but HIGH risk (septic till proven otherwise)
****What is the definition of septicemia?bacterial infection of the blood associated with adverse systemic clinical signs
Most common G+, G- and anaerobic bacteria associated with septicemia?G-: Ecoli, klebsiella, salmonella, pseudomonas, mannheima haemolytica. G+: staph, strep, trueperella pyogenes, bacillus, listeria. Anaerobic: clostridia, bacteroides, prevotella
septicemia more commonly G+ or G-?G-
what generates the adverse clinical symptoms seen in septic pts?Mostly inflammatory cascade!! inflammatory mediators cause systemic reactions resulting in various clinical symptoms. Also the host's immune system's interaction with infectious agent. (so just remember: its not so much the bacteria themselves causing the symptoms as it is the inflammatory mediators)
CSs that might be associated with septicemia?hypotension (distributive shock), injected mucous membranes (vasculitis-->vasodilation. Also remember with distributive shock, at first lots of peripheral vasoconstriction but hypoxia to vessels eventually causes death and vasodilation and then blood pools in periphery. Also Hbg releases O2 and takes up the Co2 and high levels of that= purplish blood which isnt exiting the area) tachycardia, pyrexia, weakness and depression, resp distress (MULT AND VARYING EFFECTS ON EACH BODY SYSTEM)
what will CBC look like with septicemia if acute vs chronic?Acute: sequestration, not enough time to make more, so looks very low. Chronic (few days) then BM kicked out a bunch= high
what does blood gas usually look like with septicemia?acidosis (lactic acid) and not breathing well, so resp acidosis too.
what will glucose be like with sepsis?could be high OR low-- bact eating it= low or stress=high.
what is the serum chem thing you can look at for acute, ongoing inflammation? (ACUTE PHASE PROTEIN!!)serum amyloid A (fibrinogen, albumin is a neg one)
if on your chem of your septic neonate, you see elevated GGT, what do you think?THIS IS FROM THE MILK- DONT FORGET.
why might septic bb have thrombocytopenia?vasculitis--> inflammatory mediators--> sets off clotting--> DIC---> use up thrombocytes
calf comes out in front of you, pull blood, has elevated BUN-- what are you thinking?inc index of suspicion of sepsis in utero bc takes a while to inc
why is modulating inflammation really tricky, esp with sepsis?(1) Steroids: immunosuppressive. (2) NSAIDs: only mediate one part of inflammatory cascade, and can knock out good and bad prostaglandins
is drug absorption better or worse in neonates?better
what is drug distribution like in neonates?higher apparent Vd, less protein bound drug, inc permeability of membranes/barriers. (so overall more distribution)
what is drug excretion and elim like in neonates as compared to adults?in neonates, slower elim of drug, longer half life.
in general, if you are giving antimicrobials to neonates, what should the doses and inervals be?for neonates, higher doses with longer dosing intervals.
If you suspect omphalophlebitis, what anatomical structures and organs do you want to assess?check arteries and the vein. (2aa and 1v) and check urachus and make sure bladder isnt involved. and do US for that. rule out infection of each of those structures. (prolly look for liver too)
4 possible sequelae for omphalophlebitis?death, sepsis/septic arthritis, peritonitis, hepatitis (abscesses in liver) cystitis (ascending nephritis.<--RARE but possible)
anatomical structures in in umbilicus?1 umbilical vein (to liver), 2 umbilical arteries(go to round lig of bladder), urachus
if you see a calf covered in meconium, what dz are you thinking they are at risk of developing?aspiration pneumonia (distress=gulping/breathing uterine fluid and meconium)
what type of pneumonia if aspirated meconium? milk?meconium= STERILE pneumonia (bc meconium is sterile). However meconium is highly inflammatory and can set off inflammatory reaction, which can lead to edema. Can also just obstruct and perhaps cause atelectasis. Usually die from SECONDARY infection in lungs after this. (esp bc tons of inflammation dec effectivity of fighting bact) Milk=infection pneumonia (milk is not sterile)
big thing on serum chem on a baby that came out with a not-good placenta?FIBRINOGEN
what CSs do calves exhibit with colic (abdominal discomfort)bruxism (teeth grinding) (bc in pain), dull/depressed, laying down (flat or sternal), rolling, pulling legs up, vocalizing, tail flagging, flank watching, stomping feet
2 common places for atresia of the intestines?ascending loop of spiral colon, atresia ani.
who is atresia of the intestines a genetic risk in?autosomal recessive in holsteins
how to dx meconium impaction?US
how common is intussusception in neonates?common, esp in >36hrs.
6 major ddx for colic in the neonate?atresia of intestines (ascending loop of spiral colon, ani), meconium impaction, intussusception, enteritis(diarrhea), abomasal ulcers/peritonitis, rupture of bladder+peritonitis
what does meconium look like on US?starry, speckly lumps in colon
3 major ddx's for weakness, difficult walking, with elevated CK?WMD, Copper deficiency ("swayback")
ddx's for weakness, difficult walking, depressed, dysphagic, want to nurse but can'tWMD, Cu deficiency, SC damage (vert malformation, vert osteomyelitis, fx, abscess in CS), peripheral nn damage from birth, mm damage from birth, border dz/hairy shaker lamb, encephalitis
common causes for encephalitis?CAE (think goats and pyrexia, cerebral abnormalities and depression), listeria, mannheima haemolytica (pyrexia, cerebral involvement)
when is WMD usually seen, but when can it be seen?can be congenital, but usually 2-4 mo (when rapid growth and deficient foods)
WMD aka?nutritional myodegeneration
WMD has what two forms, describe them(1) CARDIAC form: manifests as acute onset cardiac failure and death w/in 24hr (common for congenital form) (2) skele mm form: slower onset, mm weakness, stiffness, trembling, recumbency with notably hard and painful mm on palpation. mm affected in groups. diaphragm and intercostals can also be affected. Mm of tongue-->dysphagia. violent abdominal pain possible.
what enzyme can be affected by WMD (low, not high)glutathione peroxidase
what are skele mm like in WMD?pale, dry appearance, white streaks, calcification (gritty when cut), mm edema
how is cardiac mm affected by WMD? which 2 parts of the heart are most commonly affected in calves? lambs?similar to skele mm, in calves LEFT VENTRICLE AND SEPTUM most frequently involved. in lambs, both ventricles usually involved. Myocardial degen usually extends through the full thickness of the vent wall.
how can you tx WMD?with cardiac form usually too late to treat. can suppliment dam with vit E/selenium during preg for prevention. injectable BoSe at time of birth in deficient areas (E and Se)
what can a high anion gap mean again?high anion gap= acidotic. (remember: (Na+K) - (Cl+HCO3) ) DUELS= diabetic ketoacidosis, uremia, ethylene glycol, lactose, salicylic acid. (possible DDxs came up with in class: ruptured bladder/stomach, toxin ingestion? flora out of balance-- parasites? (do FAMACHA- but what about anion gap) clostridial infxn? meningeal worm? leukoencephalomalacia form of CAE (but what about blat and anion gap). Floppy kid syndrome. Ruminal acidosis (hard to explain in a kid- but rumen drinking maybe), NM junction dz. Atresia ani or coli (bc no diarrhea- but hard to explain how that didnt happen before 1.5wk) rumen drinkers can be acidotic and bloated )
what is the metabolic disturbance characterized like with floppy kid syndrome?METABOLIC ACIDOSIS with a HIGH ANION GAP without diarrhea!!!
usually see floppy kid syndrome in what kinda kids?aggressive eaters
What is the pathophys of floppy kid syndrome?eats too much milk--> prolif of lactate-producing intestinal flora (drops pH, metabolic acidosis and ileus)--> HIGH ANION GAP WITH NO DEHYDRATION--> overproduction of organic acid rather than loss of bicarb. Thought to coincide with a high plane of nutrition and overgrowth of clostridium perfringens type A.
how can you tx floppy kid syndrome?(remember: too much milk--> prolif lactate producing organisms) giving bicarb can help even tho losing bicarb isnt the problem, might need gastric lavage. Prevention: feed restriction and large pens to encourage exercise. Prog good but can be recurrance if they are a greedy bully

General diarrhea stuff, NCD (neonatal calf diarrhea)

Question Answer
most prevalent dz in calves?DIARRHEA
when is the most likely age calves will die due to enteritis?during 2nd week of life
how are herd size and diarrhea related?bigger herd, higher risk
what is one of the most important prevention measures for neonatal enteritis?colostrum management
what can inc risk of NCD?feeding waste milk
what should you know about dx the cause of the diarrhea?dont always figure out etiological agent-- usually just end up giving supportive care. (isolation of one agent does not mean causative agent. Age groups can tell you a bit but there can be mixed infections, etc)
*MOST COMMON mode of transmission of diarrhea?FECAL ORAL
4 most common causes of neonatal diarrhea in calves?E. coli K99/F5, Rota, corona, cryptosporidium. (other common causes include: salmonella, ETEC, clostridium difficile, clostridium perfringens, torovirus)
annnndd the rest she is not testing, refer to ReussReusssssss shit
young calf (<3wk diarrhea)?rota (usually 6d) and corona (7-10d)
zoonoticsRota, crypto
E coli virulence factors?K99 (attach) F5 (ID), STa (virulence- binds and causes secretion of Cl-/HCO3/H into intestinal lumen= SECRETORY diarrhea)
rota of villi. Malabsorptive diarrhea--> leads to osmotic diarrhea. Also secretory bc have toxins (NSP4 toxin)
3 probs corona causes?(1) diarrhea in neonates (<3wk), resp dz in older calves, winter dysentery in adults
corona destroysboth tips and crypts apparently.
cryptosporidium- which is the neonate one?NEONATE: parvum. (think parvo), bovis and ryanae also affect youngstock, andersoni gets everyone
gold standard for dx cryptosporidium?acid fast stain
coccidiosis caused by?eimeria sp
what problem might coccidiostats cause?PEM (thiamine deficiency)
floppy kid syndrome might be associated with what kinda bact?clostridium perfringens type A
alpha toxin of clostridium?ulcers
clostridium type B toxin?lamb dysentery
clostridium type C toxin (beta toxin) (oh thanks guys)necrotic enteritis/hge diarrhea.
Type D (epsilon toxin)over eating/ pulpy kidney dz-- enterotoxemia