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ag med > Hematopoietic > Flashcards

Hematopoietic Flashcards

1
Q

What erythocyte morphology indicates regeneration?

A 
Increased MCV
reticulocytes
anisocytosis 
polychromasia
howell jolly bodies
nRBCs
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2
Q

What erythrocyte morphology indicated oxidative damage

A

Heinz body formation

Eccentrocytes

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3
Q

How long does it take for regeneration to show on blood work in a ruminant

A

5-7 days

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4
Q

What clotting factors are vitamin K dependent

A

II, VII, IX AND X

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5
Q

What are common causes of chronic blood loss in ruminants

A

bleeding GI lesions
some renal diseases
hemostatic dysfunction
parasites: lice and ticks and haemonchous

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6
Q

What are common causes of acute blood loss in ruminants

A 
epistaxis
surgery
ruptured liver/spleen/lung/vessel
clotting defects
gastric ulceration
hemoperitoneum 
hemothorax
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7
Q

Why can we safely give an unmatched blood transfusion in a ruminant?

A

because of high variability among blood groups and types amongst ruminant species

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8
Q

What are the 3 branches of the cascade model of coagulation?

A

Intrinsic
Extrinsic
Common

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9
Q

Hemophilia A has a deficiency in what factor? How common is this syndrome in ruminants?

A

VIII; rarely seen

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10
Q

what is another rare inheritable coagulation disorder?

A

Factor XI deficiency

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11
Q

What toxin does moldy sweet clover have that causes hemostatic disorders and what region do we see this condition in?

A

dicoumarol; seen in the northern plains states

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12
Q

How long after ingestion of dicoumarol do clinical signs appear? also do they need to ingest a large or small amount to become affected?

A

2-7 days; need to ingest large amounts for long periods eating this at consecutive meals.

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13
Q

What are some differentials for sweet clover toxicosis? How do you rule these out?

A

DIC, bracken fern toxicosis, mycotoxicosis

rule out by performing platelet counts - These will cause a thrombocytopenia while sweet clover does not.

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14
Q

What is the pathogenesis of sweet clover toxicity?

A

interferes with hepatic synthesis of factors II, VII, IX, AND X by inhibiting vitamin K

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15
Q

How do you treat sweet clover tox?

A

supplementation of vit K (1mg/kg IM q 6h)
or
whole blood transfusion

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16
Q

What are some infectious causes of hemolytic anemia?

A 
anaplasmosis
babesiosis
eperythrozoonosis
leptospirosis
bacillary hemoglobinuria
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17
Q

What is the most Prevalent tick born disease of cattle worldwide and how is it spread?

Also what time of year do outbreaks occur?

A

anaplasmosis - spread by ticks and biting flies
*carrier cattle are asymptomatic and serve as reservoirs!

outbreaks seen in late spring and summer.

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18
Q

How are persistently infected carriers created in anaplasmosis infection?

A

through primary exposure at calfhood - they are asymptomatic or have mild disease initially.

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19
Q

What clinical signs will be seen in acute anaplasmosis in an adult animal?

A

pyrexia for first 12-24 h followed by subnormal temp as the hypovolemia sets in

anorexia etc…

signs of anemia + pale or icteric MM and dark feces/urine

Later term abortion/abortion storms can occur in the face of an outbreak

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20
Q

How can you diagnose and treat anaplasmosis?

A

Blood smear (difinitive) (wrights stain or new methelene blue or geimsa)

Serology: cELISA (gold standard) – approved by USDA and OIE - highly specific and sensetive - but may not have seroconverted if in the acute pahase.

PCR - can confirm in acute phase.

Treatment: tetracyclines but does not eliminate the persistent infection. Cured animals will still be carriers.
Also consider transfusions if the PCV <12%; poor px if <8%

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21
Q

Is Babesiosis eradicated or reportable in the US?

A

YES and YES!!!

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22
Q

What genus of tick transmits babesia?

A

Rhipicephalus (boophilus)

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23
Q

What type of hemolytic anemia is caused by babesia and how does it occur?

A

INTRAcellular i.e. hemoglobinemia and hemoglobinuria will be seen?

escaping merozoites lyse the RBCs in circulation.

24
Q

What other system in the body can be affected by babesia and what does it cause?

A

CNS - causes cerebral babesiosis = hyperexcitability, convulsious, opisthotonous, coma and death

25
Q

Treatment for babesia?

A

imidocarb
diminazene
phenamidine
amicarbalide

26
Q

Causal agent for eperythrozoonosis/haemobartonellosis? What part of the RBC is this associated with?

A

hemotropic mycoplasmas - associated with the surface of RBC;

Perform blood smear quickly after drawing to prevent them from jumping off the RBCs

27
Q

How is eperythrozoonosis transmitted?

A 
Via blood (biting insects, needles, etc..) 
Also- intrauterine transmission is likely and will lead to life long infection of the offspring.
28
Q

Which species is eperythrozoonosis more common? sheep or cattle?

A

Sheep- they have marked depression anemia and significant death losses - will see marked rd cell destruction

In cattle they are mildly depressed have fever and modest anemia - the infection is usually latent. (decreased milk production may be the only presenting complaint in cattle).

29
Q

How do you treat eperythrozoonosis?

A

Oxytetracyclines

30
Q

Is leptospriosis zoonotic?

A

YES!!!

31
Q

What are some syndromes that are caused by leptospirosis?

A

abortion
hemolytic anemia and septicemia (calves and lambs)
mastitis
combination of these

32
Q

Which serovars are associated with hemolytic syndrome most commonly

A

pomona and icterohemorrhagiae (these have hemolysins)

33
Q

What is the pathophysiology of anemia in lepto?

A

Immune mediated mechanisms - extravascular??

34
Q

Treatment for Lepto?

Prevention?

A

Oxytet (LA200) or Procaine Pen-G + supportive care

prevention via vaccination which covers most key serovars.

35
Q

common name for bacillary hemoglobinuria

A

redwater

36
Q

What is bacillary hemoglobinuria

A

acute fatal clostridial disease characterized by a liver infarct, toxemia, and intravascular hemolysis

37
Q

What clostridial species and toxin are associated with bacillary hemoglobinuria?
What is a major risk factor for this?

A

clostridium novyi type D

major toxin is betatoxin which causes hepatic necrosis, hemolysis, and damage to capillary endothelium

38
Q

pathophysiology of bacillary hemoglobinuria

A

spores ingested –> cross intestinal mucosa –> to liver and other organs via phagosomes of macrophages –> spores live in kupffer cells –> if liver becomes damaged and anaerobic (like with liver flukes) the spores germinate –> germination allows for release of toxins and increasing anaerobic area –> continuation causes hepatic necrosis and if toxins are absorbed intravascular hemolysis, icterus and hemoglobinuria occur followed by death

39
Q

Clin path evidence seen with clostridium novyi infection

A

anemia
elevated AST/GGT
Total bilirubin increased!
severe hemoglobinuria (port wine colored urine)

40
Q

Treatment for redwater

A

very grave prognosis - can give high dose penicillin or tetracyclines; and do supportive care - fluids, blood etc..

41
Q

Prevention of redwater:

A

control flukes and minimize exposure to natural water sources;
vaccinate - typically short lived (may need to booster every 6 months in endemic areas)
destroy infected carcasses to prevent sporulation into the soil!

42
Q

What are non infectious causes of RBC destruction in ruminants?

A

Heinz body anemias - caused by oxidation inducing plants (brassica sp (kale, rape, turnips) and onion/garlic)

Copper toxicity

Water intoxication

Post parturient hemogobinemia

43
Q

what is the toxin in Brassica plants and what species is most susceptible to intoxication?

A

S-methyl cysteine sulfoxide in plants and converted to dimethyl disulfide in the rumen.

Cattle are most susceptible to intoxication/heinz body formation and RBC damage

44
Q

What toxin is present in onions and what species are susceptible?

A

n-propyl disulfide and s-methyl cysteine sulfoxide

all ruminants susceptible

45
Q

typically what type of hemolysis occurs with heinz body formation?

A

typically extravascular as the spleen removes them as they’re filtered.

However, if there are micronutrient deficiencies that weaken the RBCs concurrently - you can have intravascular as well.

micronutrients include: P, Se, Cu

46
Q

what stain are heinz bodies best visualized with?

A

crystal violet or new methylene blue

47
Q

If you diagnose heinz body anemia due to these intoxications what organ system should you be worried about protecting during the recovery?

A

Kidneys – fluids fluids fluids!

48
Q

What species is most sensitive to copper toxicity?

A

SHEEP!

49
Q

What other mineral influences copper absorption?

A

Molybnenum - copper: molybdenum raitos >6:1 likely to result in Cu poisoning

50
Q

Pathophysiology of copper toxicity

A

ionized Cu is stored in hepatocytes and redistributed to bie bile , packaged into lysosomes in portein compleses or used for ceruloplasmin –> however, accumulation occurs because <1% oc copper is excreted daily so if intake it high it will build up.

Hepatocytes will continually store copper until they become saturated but it will all be released when they die.

Free inorganic copper is an oxidant that participates in the Fenton reaction allowing for the production of oxidative hydroxides and peroxides which damage cells.

This leads to heinz body formation and production of methemoglobinemia

51
Q

Clin path and dx of copper tox

A

Plasma Cu 2.4-20 ug/mL diagnostic for acute toxicosis

Heinz body formation, intravascular hemolysis, methemoglobinemia, decreased pcv

Increased bilirubin, AST, GGT, ALP, total bilirubin, CK, creatinine, BUN and ceruloplasmin

Dark brown to black urine with high protein, blood, and hemoglobin casts

52
Q

Treatment for copper tox

A

(poor px in sheep)
supportive care - whole blood transfusions (if pcv <8), insulfated with oxygen

chelators: d-penecilamine to increase copper excretion, anhydrous sodium sulfate
ammonium molybdate - reduces hepatic copper loads and enhances copper excretionq

53
Q

pathophysiology of water intoxication causing hemolysis

A

massive water intake can cause marked hypotonicity of body fluids leading to swelling and lysis of RBCs

54
Q

clinical signs and clin path of water intoxication

A

neurologic signs, respiratory distress, hemoglobinuria, death;

hemolytic anemia, hemoglobinuria, hyposthenuria, and marked hyponatremia

55
Q

pathophys of postpartureint hemoblobinuria

A

hypophosphatemia due to inadequate intake –> lower intracellular phosphate –> interferes with energy metabolism —> causes oxidative stress and comprimised cell viability –> hemolysis–> hemoglobinuria

56
Q

Treatment of postparturient hemoglobinuria

A

blood transmusion, supportive care, correct hypophosphatemia, correct dietary imballances.

likely to be a slow recovery - make sure to provide a source of PO4 - CMPK only has PO3

ag med (8 decks)

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