Reading...
Play button
Play button
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;
146 Cards in this Set
- Front
- Back
|
CS of warfarin tox
|
hematomas and ecchymoisis of mm
epistaxis hematuria |
|
|
tx of warfarin tox
|
vit K1 admin q 6 hours until PT normal
|
|
|
why wont you give K3 for warfarin tox
|
because it will blow out the kidneys. it is especially toxic to horses.
|
|
|
how do animals get sweet clover tox
|
ingestion of moldy sweet clover in hay or silage
|
|
|
what type of sweet clover will cause tox
|
moldy
|
|
|
how long until signs occur with sweet clover tox
|
2-7 days
|
|
|
if you have chornic low levels of sweet clover how long until cs
|
3 months
|
|
|
CS of sweet clover
|
epistaxis, melena, subq hematomas, as dz progreses-> periarticular swelling, non painful swelling at point of trauma
|
|
|
treatment of sweet clover
|
remove contaminated feed
admin. vit K1 |
|
|
hemolytic anemia
|
increase erythrocyte destruction faster than replaced
|
|
|
cs of hemolytic anemia
|
pallor, fatigue, depression, anorexia, inc. pulse and resp rate, icterus
|
|
|
stress on animal with severe anemia may yield
|
bizarre behavior, mania, collapse, death
|
|
|
what might you see on your bw with hemolytic anemia
|
anisocytosis, polychromasia, reticulocytosis, nucleated RBC, decreased m/e ration, decreased serum haptoglobin, may see elevated LDH, inc. serum bilirubin
|
|
|
anaplasmosis
|
progressive anemia due to erythrocyte infected by: anaplasma marginal in cattle, and anaplasma ovis in sheep and gots
|
|
|
cs of anaplmasa
|
mild dz in cattle 6-9 moa
asymptomatic in calves < 6 mo SEVERITY INCREASES WITH AGE inc temp dec. in milk production anorexia and therapy dry muzzle decreased or absent ruminations aggressiveness stress may lead to sudden death |
|
|
incubation of anaplasma
|
15-30 days
|
|
|
recovered animal with anaplamsa are
|
infected for life
|
|
|
in sheep and goats what will you see with anaplasma ovis
|
not much unless there are other concurrent dz
|
|
|
d/dx of anaplama
|
babesiosis, bacillary hemoglinuria, lepto, toxins (heptotoxins), liver, copper toxicity in sheep
|
|
|
definitive dx of anaplama
|
see it in the rbc
|
|
|
what is the pcv about for anaplama
|
<30 at time of first CS
|
|
|
what does blood smear detect with anaplama
|
acute infection
|
|
|
when will regeneration of RBC be noted
|
several days post infection
|
|
|
perisitstenly infected animals or
|
will always have it and can give it to others
|
|
|
Elisa is high Sp and Sn and what do you have to know about canada for anaplama
|
have to be neg to import
|
|
|
what xmits anaplama
|
dermacentor ticks and rhipicepalus ticks
|
|
|
what else is another way to transmit anaplama
|
iatrogenic
|
|
|
tx for anaplama
|
tetracycline, +/- whole blood transfusion, treatment will not clear infection, allow young beef calves to become naturally infected so they don't have a problem unless they have something else that causes stress. key is prevention
|
|
|
where are endemic areas in the US for anaplasma
|
western/ southern
|
|
|
is there a vaccine for anaplasma
|
yes in australia its a live blood based vax, in the US no vaccine. there have been but they are taken off the market
|
|
|
what is the key for anaplasma
|
prevent transmission
|
|
|
babesiosis is transmitted how
|
tick borne boophilus, intraerythrocytic dz (also called piroplasmosis, texas fever, redwater, tick fever)
|
|
|
what are other names of babesia
|
pirplasmosis, texas fever, red water, tick fever
|
|
|
b. bigeminia
b.bovis |
big- large
bovis- small, most virulent |
|
|
most common transmission of babesia in ticks
|
transovarially: preg female gives it to her babies
|
|
|
b. bigenmia can only be transmitted how
|
can only be transmitted once the tick larva molt to the nymph or adult stages
|
|
|
CS of babesia
|
begin 2-3 wks post tick
fever depression hemolytic anemia icterius CNS |
|
|
who is more resistant to babesia in the cattle world
|
bos inducius breeds
calves have natural immunity |
|
|
calves can have what with babesia
|
naturla immunity
<9 mo min. reactions calves become asymptomatic carriers adult carriers remain resistant to clinical dz for at least 4 years |
|
|
clinical path of babesia
|
blood smear for dx
positive serological test inoculation of splenectomized calves the number of parasitized RBCs decrease in chronic infections (makes dx difficult) |
|
|
pcv and urine of babesia cow
|
rapid decrease in pcv from normal to < 10 / in a week
K+ in urine |
|
|
when are antibodies detected from babesia cows
|
w/i 7 days and can exist 252 days after parasites are no longer detectable
|
|
|
which babesia is harder to treat
|
small species
|
|
|
prognosis of babesia
|
poor once you see CNS signs, or PVC less than 10
|
|
|
what drugs can be used for tx of babeisai
|
chemotherapeutic agents:
diminazine acetate phenamidine siisethionate imidocarb diproponate amicarbalide diisethionate |
|
|
px of babiesia
|
px of tick bites:
controlled burning, cultivation, prolonged pasture rest, repellants, px iatrogenic transmission, immunization (live organism inocluated into susceptible calves, live organism into older cattle followed by chemotherapy) |
|
|
hemobart bovis lives where in the body
|
on the RBC surface
|
|
|
eperythrozoon wenyoni
|
normally latent and doesnt cause much dz
|
|
|
theileriasis
|
infected lymphocytes and erthrocytes of ruminants
T. parvo causes: "east coast fever" |
|
|
trypanosmiasis
|
flagelated protozoal organism that cause a variety of dz in human and animals
tseste fly |
|
|
where can you see trypanosis
|
buffy coat
|
|
|
lepto
|
anemia if it caused some type of kidney problem
|
|
|
red water dz
|
clostriudm nobyi type D
naturally occurring in cattle experimentally reproduced in sheep poor drained areas of western US most common early summer and fall |
|
|
how is red water dz ingested
|
spores
the organisma thrives in anaerobic environment most common in liver fluke infestation |
|
|
px of red water dz
|
pv liver fluke
|
|
|
red water dz CS
|
anemia (regenerative)
icterus |
|
|
tx and px of red water
|
really tough to treat
high doses of penicllin tetracycline- tx of choice ivomec plus injection (anthelmintic with clorsulon to kill liver flukes) |
|
|
px of red water dz
|
fence off fluke infested water, vaccination (short lived ~ 5months), prophylatic treatment with ivomec plus
|
|
|
IMHA
|
associated with production of ab's against host RBC's
anbodies combine with complement and antigens not he RBC membrane- removal and destruction by the RES occurrence is rare as primarily idiopathic dz in lg. animals more common to occur secondary to some other primary dz process |
|
|
dx of IMHA
|
coombs test
|
|
|
indirect coombs test
|
detects anti-erythrocyte antibodies in the serum
|
|
|
what is IMHA assoc. with
|
secondary problem in lg. animals associated with neoplasm, viral, bacterial, rickettsial, protozal dz, exposure to some drugs, other immune mediated dz
|
|
|
tx for IMHA drug induced
|
discontinue or chane the drug therapy if they are on a drug that can cause this, can take up to 14 days for this to calm the fuck down.
don't use corticosteriods, this will change the immune system and fuck shit up IF YOU HAVE A DRUG REACTION CAUSING THIS |
|
|
tx for IMHA
|
glucocortiocoids
|
|
|
heinz body hemolytic anemia
|
Acute hemolytic anemia that develops after exposure to oxidizing agents-> aggregation of globulin (Heinz bodies)
penotiazine methyl blud actylphenlyhydraine plants such as onion, rape, kale willed dry red maple leaves |
|
|
heinz body anemia in sheep
|
more common in sheep that are fed diets low in molybdenum. results in chronic copper toxicity
|
|
|
tx of heinz body anemia
|
remove source
|
|
|
if you give iron will it help heinz body anemia
|
no
|
|
|
water intoxication
|
massive ater intake- marked hypotonicity of body fluids-intravascular hemolysis
|
|
|
heinz body anemia in sheep
|
more common in sheep that are fed diets low in molybdenum. results in chronic copper toxicity
|
|
|
CS of water intoxication
|
neuro signs
resp distress death |
|
|
tx of heinz body anemia
|
remove source
|
|
|
if you give iron will it help heinz body anemia
|
no
|
|
|
water intoxication
|
massive ater intake- marked hypotonicity of body fluids-intravascular hemolysis
|
|
|
CS of water intoxication
|
neuro signs
resp distress death |
|
|
tx of water tox
|
water restircion
supportive care for calves with marked hyponatremia and showing neuro signs: hypertonic saline, mannitol, coriticosteriods |
|
|
what is the goal of treatment for water toxicity
|
restoration of serum sodium concentration to 120-125 mmol/L is the goal of therapy (avoid over concentration)
|
|
|
how is warfarin toxicity diagnosed
|
history, clinical signs (large vessel hemorrhagic diathesis)
lab tests (prolonged PT is the earliest indicator. factor VII has the shortest half life of any other clotting factors, aPTT is prolonged as the dz progresses) |
|
|
so summary of warfarin tox dx
|
early- prolonged PT
later- prolonged aPTT |
|
|
how do you treat warfarin tox
|
vit K1 q 6 hours until PT is normal
plasma transfusion whole blood transfusion (for severe anemia) |
|
|
is warfarin or coumarin eliminated rapidly
|
warfarin is
|
|
|
what does sweet clover contain that becomes toxic
|
coumarins that are coverted to dicumarol when the mold forms
|
|
|
what is the toxic dose of dicumarol
|
10 mg/ kg
|
|
|
is grazing sweet clover a problem
|
no... not unless its moldy
|
|
|
what do you have to be careful of when you have an animal with dicumerol poisoning and it has a small wound
|
it can bleed out
|
|
|
what are the laboratory findings of dicumerol poisoning
|
early- prolonged PT
platelet count remains normal |
|
|
when should vitamin K 1 start to work with dicumerol poisoning
|
within 24 hours
|
|
|
how do you treat dicumerol poisoning
|
plasma or whole blood
|
|
|
what is bacillary hemoglobinuiria
|
redwater dz (C. novyi type D)
|
|
|
what kind of signs may a calf less than 9 months show
|
they show minimal reactions
|
|
|
what are the most widely used serum tests for babesia
|
compliment fixation (CF) (effective test until approximately 100 days post infection)
indirect fluorescent antibody (IFA) |
|
|
what are other serologic tests for babesia
|
gel precipitation
latex particle agglutination rapid card agglutination enzyme labeling immunoassay (EIA) recombinant DNA technique |
|
|
at what PCV will acute cases of babesia respond well to therapy
|
> 12 %
|
|
|
what is the toxin that causes bacillary hemoglobinuira
|
beta toxin that causes hemolyti syndrome as well as focal liver lesions
|
|
|
what is a direct coombs test
|
identifies the presence of anti-erythrocyte antibodies and the complement of the RBC membrane
|
|
|
how is autoimmune hemolytic anemia thought to be initiated
|
damaged RBC membranes, the immune system reacts inappropriately.
|
|
|
some RBC's are lysed intravascularly but most of the anemia of IMHA is caused by what?
|
the removal of the RBC's by RES
|
|
|
what can cattle eating rye grass on selenium deficient pastures cause
|
heinz body anemia
|
|
|
how can heinz body anemia be diagnosed
|
it causes an acute and profound anemia
heinz bodies are round protruding from RBC |
|
|
what will the plasma proteins be in an animal with heinz body anemia
|
normal
|
|
|
will a coombs test be neg or pos for heinz body anemia
|
negative
|
|
|
what will hematology show with heinz body anemia
|
inflammatory leukogram
|
|
|
what is the pathophysiology of heinz body anemia
|
the precipitation of hemoglobin that has undergone oxidative denaturation
|
|
|
what is the treatment of heinz body anemia
|
removal toxic source
blood transfusion in animals with severe anemia iron is of no use IV fluids are indicated with hemoglobinuria and azotemia |
|
|
what is the goal of treatment of heinz body anemia
|
goals of treatment is to improve tissue oxygenation and perfusion (control inflammation, control pain)
|
|
|
should you use corticosteriods for heinz body anemia
|
no
|
|
|
how can calves get water intoxication
|
raised on a milk diet with an unlimited amount of water
|
|
|
who gets postparturent hemoglobinuria
|
cows worldwide
occurs spontaneously more common in multiparous cows |
|
|
what are CS of postparurent hemoglinuria
|
CS in first month after freshening (depression, decreased feed intake, dec. milk production)
|
|
|
what will you see on lin path with a cow with postparurent hemogloniuria
|
intravascular hemolysis, hemoglobinuria, marked anemia, icterus, regenerative response strong after 4-5 days
|
|
|
what is postparuent hemoglobinuria related to
|
hypophosphatemia, due to inadequate intake late in gestation, low intracellular phosphate concentrations interfere with energy metabolism
|
|
|
what animals are most susceptible to copper toxicosis
|
sheep especially lambs
|
|
|
is acute copper toxicosis common
|
no, results from parenteral overdose with copper disodium edetate
|
|
|
how do animals get chronic copper toxicosis
|
excess copper relative to molybdenum levels
|
|
|
how do monogastrics absorb copper
|
in the stomach, jejunumn, duodenum, and ileum
|
|
|
how do ruminants absorb copper
|
in the lower small and large intestine
|
|
|
how is copper transported in the blood stream
|
actively, loosely bound to albumin, cerulopasmin, and transcuperin
|
|
|
where is bound copper transported to in the body
|
liver, kidney, bone marrow and brain for storage.
liver is the main storage area |
|
|
where does copper metabolism take place
|
in the liver
|
|
|
what is the pathogenesis of copper toxicity
|
excessive copper damages hepatocyte cell membranes-> hepatocyte death
copper is then released into the blood stream-> damage to RBC cell membranes-> intravascular hemolysis-> anorexia -> centrolobular necrosis-> more copper leakage |
|
|
where does copper accumulate
|
in the kidneys
|
|
|
what are clinical signs of copper toxicity
|
rarely seen in sheep until the animal is stressed.
hemoglobinuria, icterus, anorexia, and death |
|
|
what color urine will an animal have with copper toxicity
|
dark red urine
|
|
|
what are signs of copper toxicity in swine
|
anorexia, depression, poor weight gain, icterus, hemoglobinura, bloody feces
|
|
|
what is the treatment for copper toxicity
|
ammonium molybeate
sodium thisulfate d-penicillamine |
|
|
prevention of copper toxicity
|
do not give cattle, swine or horse feeds to sheep or cameleids
|
|
|
what can increase copper levels in young animals
|
monensen
|
|
|
what can be given to prevent hepatic compensation though inhibition of cell replication in copper toxicity
|
pyrrolizidine alkalois
|
|
|
what should the copper:molybdenum ratio be in feed
|
6:1-10:1
|
|
|
what can be given to assist in lowering copper availabilty
|
35% sulfur levels
|
|
|
is iron defiency a common cause of anemia
|
it is rarely the sole cause of anemia unless animals are raised on cement, in barns, or in hutches, with no access to soil
|
|
|
why would neonates have iron deficiency
|
congenital iron deficiency
|
|
|
what is the most common cause of iron deficiency
|
chronic blood loss, parasitism, or hemostatic disorders
|
|
|
what causes iron sequestration
|
inflammation/ infection cause iron sequestion by the RES and lactoferrin
|
|
|
what accounts for 2/3 body iron stores in the body
|
circulating erythrocytes the remaining 1/3 are distributed between the liver, spleen, and bone marrow
|
|
|
as blood loss contiues serum iron becomes more depleted what happens to the affinity of iron binding
|
increases
|
|
|
how is bone marrow evaluated
|
via bone marrow aspirate stained prussian blue stain
|
|
|
treatment of iron toxicity
|
correction of problem causing chronic blood loss
oral iron suppletment iron dextran is used in baby pigs |
|
|
what can iron dextran cause that you need to be careful when using htis
|
anaphylaxis
|
|
|
what kind of diets can cause copper defiency
|
milk only diets or in animals pastured in copper deficient areas
|
|
|
when does copper deficiency often occur secondary to
|
other trace mineral imbalances
excess molybdenamun influenced by sulfur and zinc content of the diet |
|
|
what is copper essential for
|
for cofactors of various enzyme reactions
|
|
|
what are clinical signs for copper
|
decreased growth rate
rough and depigmented hair -> black cattle have reddish hair diarrhea osteoporosis with SPONTANEOUS FRACTURES anemia decreased growth rate |
|
|
what is the pathophysiology of copper toxicity
|
important for transport of iron from the gut to the marrow
causes moderate and slowly progressive anemia resembling iron deficieny anemia (microcytic. hypochromic) |
|
|
what is the treatment of copper toxicity
|
dietary supplementation
cooper glyciante injection |
|
|
what does deficiency of B12 and folate cause
|
anemia. essential role for DNA synthesis.
|
