Ashley's 1am deck of tears Flashcards
protein that picks up hemoglobin in the blood, transports to liver for recycling.
haptoglobin
If circulating hemoglobin in not captured by transport protein
hemoglobinuria
Bilirubin and hemolytic anemia
first is present in urine and feces
second backs up in plasma
third mucocutaneous(icterus)
How do we distinguish extravascular from intravascular hemolysis?
intravascular has hemoglobinemia/uria (worse prognosis)
poikilocytosis
abnormal shape
ancanthocyte v. shistocyte
acanthocyte - uneven star-like projections
shistocyte - chunk missing
acanthocytes and schistocytes can indicate
fragmentation hemolysis
spherocyte
immune mediated hemolytic anemia (extravascular)
perfectly round, 0 central pallor
MP @ spleen didn’t eat entire cell (hemoglobin leaks out ->hemoglobinemia/uria)
eccentrocytes
will often also see
oxidative damage, hemoglobin pushed to side
heinz bodies
immune mediated hemolytic anemia lab findings
regenerative anemia, macro/microagglutination, spherocytosis(dogs), neutrophilia, pigmentemia/uria, variable platelets, abnormal liver enzymes
agglutination
aggregates stuck due to binding of RBCs by antibodies (IMHA)
primary v secondary imha
primary is idiopathic or neonatal
ghosts indicate
intravascular hemolysis
spherocytes indicate
extravascular hemolysis
Lead Poisoning
metarubricytosis w/o polychromasia
intramarrow anemia
other cell lines may be involved (dec. WBCs - risk of infection, dec. platelet - risk of hemorrhage)
relative erythrocytosis v transient
relative is very common(hemoconcentration), transient common in horses(splenic contraction)
absolute erythrocytosis
primary - not EPO issue
secondary - increased EPO production
King Charles Spaniels
macrothrombocytopenia (large and less numerous)
would need to lose ______ to result in significant throbocytopenia
nearly entire blood volume
thrombocytopenia rarely due to
abnormal distribution
buccal mucosal bleeding time
to test platelet function, normal time is under 3/4 minutes
platelet function defect
acquired(drugs, renal failure) or congenital (vonWillebrands disease)
Vitamin K dependent coag factors
2(thrombin), 7, 9, 10
strong negative charge, syn in liver
sodium citrate tubes
inhibit coagulation by binding calcium
PT
prolonged PT?
prothrombin time (test of extrinsic and common path) deficiency of factor 7 or common path factors
PTT
activated partial thromboplastin time
test of intrinsic and common
extrinsic path occurs with
strong negative charged membrane
feedback with extrinsic and instrinsic path to amplify
extrinsic - 10a -> more 7a
intrinsic - 7a -> 9a
steps coag
initiation
amplification
prolongation
when is thrombin burst?
prolongation
only important in vitro
in vivo activated by negative charges instead…. but HMWK, PK
responsible for degrading clot
plasmin
protein C with S
antithrombin 3
Tissue Factor pathway inhibitor(TFPI) (7 10)
What to use for coagulation testing?
usually specifically?
Plasma!
citrate for anti-coag testing
DIC formation
dec. platelets
anemia
shistocytes
acanthocytes
inc. FDPs only?
inc. fibrinogenolysis
inc. FDPs and D-dimers?
inc. fibrinolysis (DIC, internal hemorrhage)
phases and consequences of DIC?
1- hyper coag - thrombus, ischemic necrosis
2- consumptive - bleeding
ACT
activated clotting time
(uses patients own factors)
(95% deficiency before detected, vs. 70%)
hypercoagable state when
protein losing nephropathy bc lose antithrombin 3 in urine
von willebrands has a ______ platelet count
normal
