Exam 1 Flashcards

(40 cards)

1
Q

Low TP, Low PCV

A

Substantial ongoing or recent blood loss

Over-hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Low TP, Normal PCV

A

GI protein loss
Proteinuria
Liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Low TP, High PCV

A

Protein loss combined with relative or absolute erythrocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Normal TP, Low PCV

A

Increased erythrocytes destruction
Decreased erythrocyte production
Chronic hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Normal TP, High PCV

A

Splenic contraction
Absolute erythrocytosis
Dehydration masked hypoproteinemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

High TP, Low PCV

A

Anemia of inflammatory disease

Multiple myeloma or other lymphoproliferative disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

High TP, Normal PCV

A

Increased globulin synthesis

Dehydration masked anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

High TP, High PCV

A

Dehydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What clinical findings differentiate intravascular and extravascular hemorrhage?

A

Intravascular: hemoglobinemia, hemoglobinura

Both have bilirubinemia, bilirubinuria, icterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What RBC morphology accompanies extravascular hemolytic anemia?

A

Spherocyte = immune/other causes, erythrocytes coated with antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What RBC morphology accompanies intravascular hemolytic anemia?

A

Ghosts = immune-mediated attack, Hgb leaks out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What does the presence of Heinz Bodies indicate?

A

Oxidative damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

RBC changes seen with oxidative damage

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Hemostasis
Interaction of blood vessels, platelets and coagulation factors to stop hemorrhage without obstructing blood flow - balance between fibrin clot formation and degradation
26
4 proteins that inhibit coagulation or regulate fibrinolysis
Plans in Antithrombin 3 Protein C with protein S Tissue factor pathway inhibitor (TFPI)
27
Is plasma or serum used for coagulation testing, why?
Plasma = fluid that remains if blood is prevented from clotting (citrate preferred) Serum - lacks fibrinogen, factor 5 and 8 (consumed during clot formation)
28
PT
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
PTT
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
ACT
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
Significance of FDP/FSPs
Increased concentration inhibits coagulation, promotes bleeding
32
Increased fibrinogenolysis
Only increases FDPs
33
How are D-dimers formed and how can they be detected?
Plasmin degradation of CROSS-LINKED fibrin = more specific than FDPs D-dimer test or TEG DIC***
34
Fibrinogen estimate
Better at detecting decreases than increases Increase = inflammation (especially LA) Decrease = DIC
35
What is DIC? What are the two phases? Potential causes?
``` 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
Classic lab findings with DIC
Anemia Thrombocytopenia (mild to mod) Fragmentation morphology = acanthocytes, schistocytes May also have prolonged clotting tests, or faster if phase 1 Increased FDPs
37
What are two other major coagulation abnormalities (acquired) other than DIC?
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
What is the major congenital coagulopathy?
vW disease - vWF important for platelet adhesion and aggregation = primary hemostasis Factor 8 = major carrier of vWF
39
Lab findings for vW disease
Bleeding, cutaneous bruising, hemorrhage Prolonged BMBT* Normal platelet count Normal PT, PTT (PTT prolonged in horses)
40
Primary vs secondary hemostasis, tests
``` Primary = platelets (BMBT - only if platelet number normal/elevated - platelet function) Secondary = coagulation, fibrin plug (PT, PTT, ACT) ```