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
sodium citrate tubes
inhibit coagulation by binding calcium
26
PT | prolonged PT?
``` prothrombin time (test of extrinsic and common path) deficiency of factor 7 or common path factors ```
27
PTT
activated partial thromboplastin time | test of intrinsic and common
28
extrinsic path occurs with
strong negative charged membrane
29
feedback with extrinsic and instrinsic path to amplify
extrinsic - 10a -> more 7a | intrinsic - 7a -> 9a
30
steps coag
initiation amplification prolongation
31
when is thrombin burst?
prolongation
32
only important in vitro
in vivo activated by negative charges instead.... but HMWK, PK
33
responsible for degrading clot
plasmin protein C with S antithrombin 3 Tissue Factor pathway inhibitor(TFPI) (7 10)
34
What to use for coagulation testing? | usually specifically?
Plasma! | citrate for anti-coag testing
35
DIC formation
dec. platelets anemia shistocytes acanthocytes
36
inc. FDPs only?
inc. fibrinogenolysis
37
inc. FDPs and D-dimers?
inc. fibrinolysis (DIC, internal hemorrhage)
38
phases and consequences of DIC?
1- hyper coag - thrombus, ischemic necrosis | 2- consumptive - bleeding
39
ACT
activated clotting time (uses patients own factors) (95% deficiency before detected, vs. 70%)
40
hypercoagable state when
protein losing nephropathy bc lose antithrombin 3 in urine
41
von willebrands has a ______ platelet count
normal