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clinical pathology > Ashley's 1am deck of tears > Flashcards

Ashley's 1am deck of tears Flashcards

1
Q

protein that picks up hemoglobin in the blood, transports to liver for recycling.

A

haptoglobin

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2
Q

If circulating hemoglobin in not captured by transport protein

A

hemoglobinuria

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3
Q

Bilirubin and hemolytic anemia

A

first is present in urine and feces
second backs up in plasma
third mucocutaneous(icterus)

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4
Q

How do we distinguish extravascular from intravascular hemolysis?

A

intravascular has hemoglobinemia/uria (worse prognosis)

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5
Q

poikilocytosis

A

abnormal shape

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6
Q

ancanthocyte v. shistocyte

A

acanthocyte - uneven star-like projections

shistocyte - chunk missing

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7
Q

acanthocytes and schistocytes can indicate

A

fragmentation hemolysis

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8
Q

spherocyte

A

immune mediated hemolytic anemia (extravascular)
perfectly round, 0 central pallor
MP @ spleen didn’t eat entire cell (hemoglobin leaks out ->hemoglobinemia/uria)

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9
Q

eccentrocytes

will often also see

A

oxidative damage, hemoglobin pushed to side

heinz bodies

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10
Q

immune mediated hemolytic anemia lab findings

A

regenerative anemia, macro/microagglutination, spherocytosis(dogs), neutrophilia, pigmentemia/uria, variable platelets, abnormal liver enzymes

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11
Q

agglutination

A

aggregates stuck due to binding of RBCs by antibodies (IMHA)

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12
Q

primary v secondary imha

A

primary is idiopathic or neonatal

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13
Q

ghosts indicate

A

intravascular hemolysis

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14
Q

spherocytes indicate

A

extravascular hemolysis

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15
Q

Lead Poisoning

A

metarubricytosis w/o polychromasia

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16
Q

intramarrow anemia

A

other cell lines may be involved (dec. WBCs - risk of infection, dec. platelet - risk of hemorrhage)

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17
Q

relative erythrocytosis v transient

A

relative is very common(hemoconcentration), transient common in horses(splenic contraction)

18
Q

absolute erythrocytosis

A

primary - not EPO issue

secondary - increased EPO production

19
Q

King Charles Spaniels

A

macrothrombocytopenia (large and less numerous)

20
Q

would need to lose ______ to result in significant throbocytopenia

A

nearly entire blood volume

21
Q

thrombocytopenia rarely due to

A

abnormal distribution

22
Q

buccal mucosal bleeding time

A

to test platelet function, normal time is under 3/4 minutes

23
Q

platelet function defect

A 
acquired(drugs, renal failure) 
or congenital (vonWillebrands disease)
24
Q

Vitamin K dependent coag factors

A

2(thrombin), 7, 9, 10

strong negative charge, syn in liver

25
Q

sodium citrate tubes

A

inhibit coagulation by binding calcium

26
Q

PT

prolonged PT?

A 
prothrombin time (test of extrinsic and common path)
deficiency of factor 7 or common path factors
27
Q

PTT

A

activated partial thromboplastin time

test of intrinsic and common

28
Q

extrinsic path occurs with

A

strong negative charged membrane

29
Q

feedback with extrinsic and instrinsic path to amplify

A

extrinsic - 10a -> more 7a

intrinsic - 7a -> 9a

30
Q

steps coag

A

initiation
amplification
prolongation

31
Q

when is thrombin burst?

A

prolongation

32
Q

only important in vitro

A

in vivo activated by negative charges instead…. but HMWK, PK

33
Q

responsible for degrading clot

A

plasmin
protein C with S
antithrombin 3
Tissue Factor pathway inhibitor(TFPI) (7 10)

34
Q

What to use for coagulation testing?

usually specifically?

A

Plasma!

citrate for anti-coag testing

35
Q

DIC formation

A

dec. platelets
anemia
shistocytes
acanthocytes

36
Q

inc. FDPs only?

A

inc. fibrinogenolysis

37
Q

inc. FDPs and D-dimers?

A

inc. fibrinolysis (DIC, internal hemorrhage)

38
Q

phases and consequences of DIC?

A

1- hyper coag - thrombus, ischemic necrosis

2- consumptive - bleeding

39
Q

ACT

A

activated clotting time
(uses patients own factors)
(95% deficiency before detected, vs. 70%)

40
Q

hypercoagable state when

A

protein losing nephropathy bc lose antithrombin 3 in urine

41
Q

von willebrands has a ______ platelet count

A

normal

clinical pathology (6 decks)

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