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Rumi Hematological Dz

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sihirlifil's version from 2018-04-28 23:47

Intro, blood loss

Question Answer
Types of anemiaBlood loss: acute & chronic; thrombocytopenia; clotting defects
Hemolysis: infx & noninfx
Inadequate erythropoiesis
Acute blood loss: how does it happen? e.g.?Internal or external!
Epistaxis
Large vessel bleed
Ruptured organ
Gastric ulcers
Clotting defects
Epistaxis e.g.CVC thrombosis
Large vessel bleed e.g.Mammary v/a, uterine or vaginal vessel
Acute blood loss: CSSeeing blood loss
Pale/white mucus mb
Increased CRT
Tachycardia, tachypnea
Weak pulse
Hypovolemic shock, death
Chronic blood loss: how does it happen?Losses over time (days-weeks)
Parasitism: lice, flukes, Haemonchus
GI ulcers
Chronic hemorrhage (bladder)
Chronic blood loss: CSIll thrift, poor BCS, rough hair coat
Pale mucus mb
Weak, lethargic
Edema if concurrent protein loss
This sheep comes in weak, lethargic, & poor BCS. what’s wrong?
Chronic blood loss (edema from protein loss), from e.g. Haemonchus
Causes of thrombocytopenia?BVDV type 2
Bracken fern (ptaquiloside)
Causes of clotting defects?Liver disease
Moldy sweet clover (dicoumarol --> inhib Vit K epoxide reductase)
Rat poison (GOATS & PIGS!)
DIC
Inherited factor deficiencies
Hemolytic anemia: what does extravascular look like?NO HBURIA, NORMAL URINE!
Hemolytic anemia: what does intravascular look like?Hemoglobinuria & red urine
(Inadeqate erythropoiesis: caused by?)(Nutritional deficiency: Fe, Cu, Co, folate, B12
AKD
2ry to BM dysplasia/dysfxn)
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Infectious Hemolytic anemia

Question Answer
Which dzs cause hemolytic anemia?Anaplasmosis
Babesiosis
Eperythrozoonosis (now Mycoplasma, Haemoplasma)
Leptospirosis
Bacillary hemoglobinuria
Anaplasmosis: agent? found where?Rickettsial organisms (A. marginale, centrale, ovis). Obligate intracellular, highly mutagenic
Anaplasmosis: how is the organism maintained?Insect vector (19 tick spp., mainly Dermacentor in USA), mechanical vector (biting flies & needles), & carrier animals
Anaplasmosis: how common is infection? mortality?Common! mortality 30-50% if clinical
***Anaplasmosis: CS?Subclinical in young cows, sheep, camelids
Adults: Peracute (death, fever, anemia, icterus) or Acute (over a few days) (cyclic fever, extravascular hemolysis, regenerative anemia)
**Anaplasmosis prototypical case2-3 y.o. bovine exposed that season for the 1st time
Anaplasmosis: Clin PathExtravascular hemolysis = no hburia
Anemia, reticulocytes
Organ effects of hypoxia
Anaplasmosis: DxArea, Hx, CS
Parasitemia
cELISA, PCR best
See this on a blood smear, think?
Anaplasmosis
Anaplasmosis: what is necropsy like?Anemia, watery blood, icterus
Hepato- & splenomegaly
Anaplasmosis: TxDaily/long-acting oxytetracycline (can clear infxn, but ubiquitous in environment so re-infxn is possible)
Supportive: reduce stress, high quality feed
Blood transfusion
Anaplasmosis: PreventionMove into endemic areas when young
Control biting insects & blood transfers (ear tags, parasitacides), new needles, clean palpation sleeves, calving hygiene
(Vax in some conuntries; VFD = no tetracyclines in feed anymore)
Babesiosis: aka? agents?
Texas (cattle) fever, red water fever, cattle tick fever
B. bigemina & bovis
Babesiosis: CSINTRAVASCULAR hemolysis! --> hbemia, -uria
Depression, weakness, tachycardia, tachypnea, icterus, abortion (fever), neuro
Who’s this
Mycoplasma haemolamae
Which species get mycoplasma? which agents?
Mycoplamsa: risk factors? how does infxn happen?Immunosuppression (usually postpartum, shipping, weaning)
Transmitted by carrier animals, biting insects(?), intra-uterine/transplacental w/ M. haemolamae
Infection is lifelong!
Mycoplasma: CS in camelidsNO IV HEMOLYSIS! urine is normal! infection is common
Mycoplasma: CS in sheepIV hemolysis with sudden death (urine is red)
Hburia, icterus (Ddx copper toxicity)
Mycoplasma: DxBlood smear (see on surface of RBC, fall of easily & can look like debirs in stain)
Often HYPOGLYCEMIA (weird for camelids who are usually hyperglycemic)
Serology
PCR (M. hemolamae)
Mycoplasma: Tx? prevention?Oxytetracycline, blood transfusion, supportive
Vax (short-lived immunity so use every year)
***Bacillary Hburia: aka? causes what?Redwater (other is babesiosis)
Acute, fatal clostridial disease (Liver infarcts, toxemia, IV hemolysis) from C. haemolyticum, a g(+)
Bacillary Hburia: mechanism?Spores ingested/inhaled, persist in soil >1y, latent spores hang out in liver until damaged
Bacillary Hburia: what triggers CS?Liver damage! Flukes (REGIONAL!), liver abscesses, liver biopsy/trauma
Explain what’s happening
(Bacillary bhuria) Bacterial replication in infarcted, anaerobic liver lesions. Clostridial spores --> vegetative form, proliferate, produce exotoxin --> tissue necrosis & IV hemolysis --> DEAD
Bacillary Hburia: CS? what’s mortality like?100% fatal
Acute anorexia, drop in milk production, fever 105-106*F!!, abdominal pain, vasculitis, abortions, hemoglobinuria & die before icterus can happen
Bacillary Hburia: bloodworkUsu dead before able to run! Hburia & -emia, anemia, degenerative LS
Bacillary Hburia: NecropsyRapid rigor & autolysis
Ischemic liver infarcts
Edema, he
Bacillary Hburia: DxRegional risk factors (flukes), r/o other causes hburia
Hepatic US (infarcts)
Hepatic aspirate & cytology (risk! inflame w/ G(+) rods)
Blood smear: G(+) rods
Fecal NOT HELPFUL! Fasciola hepatica ova still in liver!
Bacillary Hburia: Tx/controlHard to tx… die :/
Control: Ivermectin + clorsulon or albendazole for flukes (only tx adults so timing is critical; snail control; *** 8-way clostridial vax 2x/year in endemic areas; incinerate carcasses to destroy spores
Leptospirosis: dz syndromes?Abortion
Hemolytic anemia & septicemia
Mastitis
(any combo of these)
Lepto: etiologyNumerous serovars! Pomona, icterohemorrhagica; swajizik, grippotyphosa, bratizslava, hardjo
Lepto hemolytic crisis: happens more often in who? at what time?Neonates > adults! Incubation 3-7d, death 2-3d after
Long recovery period if survive initial event
Lepto hemolytic crisis: CSHigh fever, anorexia,depression
Mucosa petechiation
IV hemolysis, hburia, anemia, icterus
Tachycardia & dyspnea
memorize

Noninfectious anemia

Question Answer
Causes of noninfectious anemiaPlants (brassicas, allium, bracken fern)
Cu toxicity
Water intoxication
Post-parturient hburia
How does copper toxicity happen? in who?Excessive accumulation in body
Sheep, preruminant calves > goats > camelids > adult cattle
Cu tox: Acute CS if ingested?Abdominal pain, severe D+, V+, shock, dehydration, dead in 24h
Cu tox: Acute CS if injected?Anorexia, depression, dehydration
Ascites, pleural transudate, dyspnea
Head pressing, ataxia, wandering
(Hburia is RARE!)
Chronic Cu tox: what happens?Accumulates in liver (plants dmg liver & enhance storage). Slow elim in sheep! Often never ID source (stressed, all of a sudden liver releases)
Chronic Cu tox: risksPlants, soils, H2O, feeds, minerals w/ high Cu, Mo deficiency (binds Cu)
Chronic Cu tox: CSAcute onset depression, anorexia, thirst
Anemia, hburia, icterus (24-36h)
Seizures, death in 1-2d (renal failure, anemia)
Chronic Cu tox: what does Clin path look like?Elevated blood, liver, & kidney Cu
Marked elevation SDH, AST, GGT
Hburia, icterus, anemia
Dx?
Chronic Cu tox! Swollen yellow liver, large spleen, “gun metal” sheen to kidneys
Cu tox: TxAmmonium molybdate, sodium sulfate, ammonium tetrathiomolybdate
D-penicillamine to chelate Cu
Water intoxication: what does it look like?Neuro disease! Blindness, staggering, dullness, head pressing --> seizures, coma, death. IV hemolysis (rapid drop in plasma osmolality after water intake --> osmotic rupture of RBCs)
Postparturient hburia: happens in who? how?Dairy cows esp mature, high producers, pastured animals = nutrition issue (low Cu & Se)
Hypophosphatemia --> RBC lysis = IV hemolysis
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