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Clinical Pathology 2017 > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Low TP, Low PCV

A

Substantial ongoing or recent blood loss

Over-hydration

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2
Q

Low TP, Normal PCV

A

GI protein loss
Proteinuria
Liver disease

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3
Q

Low TP, High PCV

A

Protein loss combined with relative or absolute erythrocytosis

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4
Q

Normal TP, Low PCV

A

Increased erythrocytes destruction
Decreased erythrocyte production
Chronic hemorrhage

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5
Q

Normal TP, High PCV

A

Splenic contraction
Absolute erythrocytosis
Dehydration masked hypoproteinemia

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6
Q

High TP, Low PCV

A

Anemia of inflammatory disease

Multiple myeloma or other lymphoproliferative disease

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7
Q

High TP, Normal PCV

A

Increased globulin synthesis

Dehydration masked anemia

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8
Q

High TP, High PCV

A

Dehydration

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9
Q

What clinical findings differentiate intravascular and extravascular hemorrhage?

A

Intravascular: hemoglobinemia, hemoglobinura

Both have bilirubinemia, bilirubinuria, icterus

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10
Q

What RBC morphology accompanies extravascular hemolytic anemia?

A

Spherocyte = immune/other causes, erythrocytes coated with antibody

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11
Q

What RBC morphology accompanies intravascular hemolytic anemia?

A

Ghosts = immune-mediated attack, Hgb leaks out

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12
Q

What does the presence of Heinz Bodies indicate?

A

Oxidative damage

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13
Q

IMHA lab findings

A 
Regenerative anemia
Agglutination
Spherocytosis (no central parlor)
Neutrophilia
Pigmenturia/emia - bilirubinuria, bilirubinemia, icterus (NOT HEMOGLOBINEMIA/URIA BC IMHA IS EXTRAVASCULAR)
Variable platelets
Abnormal liver enzymes
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14
Q

RBC changes seen with oxidative damage

A

Heinz bodies
Eccentrocytes, pyknosis
Methemoglobin - can’t carry O2

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15
Q

Lab findings for hemolytic anemia caused by oxidative damage

A 
Regenerative anemia = polychromasia
Heinz bodies (NMB stain)
Eccentrocytes, pyknocytes
Methemoglobinemia on spot test filter 
Hgb crystals
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16
Q

Diagnostic tests for IMHA

A 
Saline test (agglutination)
Coomb's test - when agglutination is absent, detects immune system proteins on RBC, but doesn't distinguish cause
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17
Q

Regenerative Anemias

A

Hemorrhage - external, internal, chronic, acute

Hemolysis - extravascular, intravascular, acquired, congenital, IMHA, oxidative damage

18
Q

Common non-regenerative anemia lab findings

A

Normocytic, normochromic anemia (mild to moderate)
Non-regenerative - no polychromasia
Other cells lines affected with intramarrow disease - leukopenia, thrombocytopenia

19
Q

Conditions that depress intramarrow activity, seen with non-regenerative anemia

A

Chronic renal failure - inadequate EPO production, also serum biochem changes consistent with renal disease
Chronic inflammation/infection
Chronic liver disease - inadequate iron delivery/decreased RBC lifespan, also see decreased MCV/MCHC, acanthocytes

20
Q

Lab findings with iron-deficiency anemia

A

Microcytic, hypochromic/normochromic anemia
Fragmentation: schistocytes, keratocytes, acanthocytes
THROMBOCYTOSIS
Panhypoproteinemia
Early polychromasia, then diminished

21
Q

Two classic signs of lead toxicity

A

Metarubricytosis

Basophilic stippling

22
Q

Lab findings with relative erythrocytosis, common causes

A

Increased PCV, TP

Dehydration, edema

23
Q

Lab findings with transient erythrocytosis, cause

A

Increased PCV, normal TP

Splenic contraction

24
Q

Lab findings with absolute erythrocytosis; primary vs secondary

A

Increased PCV, normal TP
Primary - decreased PaO2, neoplasticism RBC growth, sludgy blood unable to carry O2
Secondary - normal PaO2, increased EPO production

25
Q

Hemostasis

A

Interaction of blood vessels, platelets and coagulation factors to stop hemorrhage without obstructing blood flow - balance between fibrin clot formation and degradation

26
Q

4 proteins that inhibit coagulation or regulate fibrinolysis

A

Plans in
Antithrombin 3
Protein C with protein S
Tissue factor pathway inhibitor (TFPI)

27
Q

Is plasma or serum used for coagulation testing, why?

A

Plasma = fluid that remains if blood is prevented from clotting (citrate preferred)
Serum - lacks fibrinogen, factor 5 and 8 (consumed during clot formation)

28
Q

PT

A

Prothrombin time - measure of extrinsic and common pathway
Measures time for fibrin clot to form
- 70% deficiency before prolonged
- inhibition/deficiency of factor 7 or common pathway
- 7 = shortest half-life, first one to be affected in Vitamin K antagonism/deficiency

29
Q

PTT

A

Partial thromboplastin time - measure of intrinsic and common pathway
Measures time for fibrin clot to form
- 70% deficiency before prolonged
- inhibition/deficiency of intrinsic or common pathway
- Factor 12 deficiency doesn’t cause bleeding in some species
Can be artificially prolonged by warm/delayed sample, low plasma:citrate

30
Q

ACT

A

Activated clotting/coagulation time - measure of intrinsic and common pathway
Measures time for fibrin clot to form (uses patients own Ca2+)
- 95% deficiency before prolonged
- severe thrombocytopenia can cause slight prolongation

31
Q

Significance of FDP/FSPs

A

Increased concentration inhibits coagulation, promotes bleeding

32
Q

Increased fibrinogenolysis

A

Only increases FDPs

33
Q

How are D-dimers formed and how can they be detected?

A

Plasmin degradation of CROSS-LINKED fibrin = more specific than FDPs
D-dimer test or TEG
DIC***

34
Q

Fibrinogen estimate

A

Better at detecting decreases than increases
Increase = inflammation (especially LA)
Decrease = DIC

35
Q

What is DIC? What are the two phases? Potential causes?

A 
Uncontrolled, continued activation of coagulation and fibrinolysis
Hypercoagulable phase (thrombosis) followed by consumptive phase (platelet/coagulation bleeding)
Hypercoagulable states: inflammatory diseases, heat stroke, HW
36
Q

Classic lab findings with DIC

A

Anemia
Thrombocytopenia (mild to mod)
Fragmentation morphology = acanthocytes, schistocytes

May also have prolonged clotting tests, or faster if phase 1
Increased FDPs

37
Q

What are two other major coagulation abnormalities (acquired) other than DIC?

A

Liver disease - liver is where coagulation factors are made

Vitamin K deficiency/antagonism - affects 2, 7 , 9, 10 = PT decreases first then PTT, ACT (rodenticide toxicity)

38
Q

What is the major congenital coagulopathy?

A

vW disease - vWF important for platelet adhesion and aggregation = primary hemostasis
Factor 8 = major carrier of vWF

39
Q

Lab findings for vW disease

A

Bleeding, cutaneous bruising, hemorrhage
Prolonged BMBT*
Normal platelet count
Normal PT, PTT (PTT prolonged in horses)

40
Q

Primary vs secondary hemostasis, tests

A 
Primary = platelets (BMBT - only if platelet number normal/elevated - platelet function)
Secondary = coagulation, fibrin plug (PT, PTT, ACT)

Clinical Pathology 2017 (4 decks)

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