Anemia Flashcards
1
Q
How is Anemia classified?
A
- Morphologic classification via RBC size and Hgb concentration
- Bone Marrow responsiveness
- Presence of reticulocytes
- Pathophysiological mechanism
- underlying disorder
2
Q
What are the morphological classifications of anemia based on Size?
A
-
Microcytic anemia
- RBCs small
-
Normocytic anemia
- RBCs normal volume
-
Macrocytic anemia
- RBCs larger than ref interval
3
Q
What are the morphological classifications of anemia based on [Hgb]?
A
-
Hypochromic anemia
- Cells contain less-than-normal hemoglobin concentration
-
Normochromic anemia
- Cells contain normal hemoglobin concentration
-
Hyperchromic anemia - do NOT occur
- MCHC is falsely increased when the hemoglobin determination is falsely increased because of intravascular hemolysis, lipemia, or the presence of Heinz bodies
4
Q
How is Anemia classified based on Bone Marrow response?
A
- Based on number of circulating polychromatophils or reticulocytes
5
Q
What are Reticulocytes?
A
- Young, anucleate erythrocytes
- Released to the blood in increased numbers as a response to anemia caused by hemolysis or blood loss in most species
- horses are an exception
- Reticulocyte count is th % of total RBCs that are reticulocytes
- Used to determine marrow response to anemia
- Not all reticulocytes are seen as Polychromatophilic RBCs.
6
Q
What time frame is evidence of a regenerative response?
A
- Anemia that develops acutely (blood loss) will appear non-regenerative first
-
Within 2-4 days:
- Increased release of reticulocytes is seen after blood loss or RBC destruction (hemolysis)
- Peak reticulocyte count is reached in 5-7 days
7
Q
What time frame is evidence of nonregenerative anemia?
A
- If anemic >5 days with NO increase in reticulocytes
- Bone marrow is NOT responding
8
Q
How is Regenerative Response to Anemia assessed in Equids?
A
- Reticulocytes do not circulate in blood of non-anemic horses
- Reticulocytes are not generally released from marrow in regenerative anemia
- Can’t use polychromasia as an indicator of regeneration
- Regenerative response indicated by:
- Macrocytes
- Increased MCV
- Anisocytosis (+/- increased RDW)
- Erythroid hyperplasia in bone marrow
- Trends - increasing Hct and MCV over several days
9
Q
What is the diagnostic approach to anemia and laboratory data?
A
- History & Physical Exam
-
Regen or Non-regen?
- Morphologic classification
- Blood film assessment
- Reticulocyte
- Count
-
Regen:
- Blood loss or hemolysis
- External blood loss usually also results in loss of protein too
- patient may be dehydrated which can increase protein
-
Non-regen:
- Anemic >5 days with no evidence of regeneration
- Biochemistry indicated
- Are other cell lines affected
- Bone marrow aspirate may be indicted
- Cat - FIV/FeLV status
10
Q
What are the expected findings with Regenerative anemia?
A
- Macrocytic (high MCV)
- Hypochromic (low MCHC)
- Heterogeneous (RDW increased)
- Anisocytosis
- Polychromasia
11
Q
What are the expected findings in Nonregenerative anemia?
A
- Normocytic (normal MCV)
- Normochromic (normal MCHC)
- Homogeneous (RDW within normal limits)
- Minimal anisocytosis on smear
- No to minimal polychromasia
12
Q
What are the possible reasons for anemia?
A
- Regen:
- Blood loss
- Hemolysis
- Non-Regen:
- Blood loss or hemolysis <3-4 days duration
- Reduced erythropoiesis
- Defective erythrocytes
13
Q
What is Regenerative anemia?
A
- Implies there is an appropriate bone marrow response with increased erythropoiesis & RBC release
- Blood Film:
- Polychromasia
- Anisocytosis
- Macrocytosis
- Rubricytosis, Increased Howell-jolly bodies, target cells
- Possible basophilic stippling
- Erythrogram:
- Increased MCV
- Decreased MCHC
- Decreased MCH
- Increased Red cell distribution width (RDW)
14
Q
What are the types of Blood Loss Anemia?
A
- Acute blood loss:
- External hemorrhage - protein and iron are lost
- Internal hemorrhage - protein and iron recycled
15
Q
Hw does blood loss lead to Anemia?
A
- Persistent small volume blood loss
- Iron depletion
- Iron stores low, Normal Hct, normocytic normochromic homogeneous
- Early iron deficiency
- low serum iron, iron stores exhausted
- Normal Hct, normocytic normochromic heterogeneous
- Continued blood loss
- low serum iron
- Anemia, microcytic, normochromic heterogeneous
- Advanced iron deficiency
- Low serum iron
- Anemia microcytic, hypochromic heterogeneous
16
Q
Where does RBC destruction take place?
A
- Intravascular - w/in vascular system
- Extravasclar - intracellular (macrophages)
17
Q
What causes hyperbilirubinemia?
A
- Prehepatic:
- increased Bu production ⇢ hemolytic disorders
- Hepatic:
- ⇣ Bu uptake (fasting, ⇣ functional mass)
- ⇣ Bu conjugation (fasting horses, ⇣ functional mass
- Functional cholestasis
- Intrahepatic cholestasis (lipidosis, lymphoma, etc.
- Post-hepatic:
- Obstructive cholestasis (cholangitis, bile duct neoplasia, cholelith, etc.)
18
Q
What happens in prehepatic hyperbilirubinemia?
A
- Increased production
- Caused by hemolytic disease
- Also see Anemia, bilirubinuria, +/- hemoglobinemia/hemoglobinuria
- Bilirubin processed by liver as in health but at an accelerated rate
- increased mounts of unconjugated bilirubin overwhelms the capacity of hepatocyte membrane carriers or the hepatocyte itself
19
Q
What are the mechanisms of extravascular hemolysis?
A
- RBCs are removed from circulation by macrophages
- Splenic clearance predominant
- Presence of spherocytes is common
20
Q
What is the mechanism of destruction in intravascular hemolysis?
A
- RBCs rupture in circulation nd release hemoglobin
- makes plasma pink/red - hemoglobinemia
- may enter the urine causing it to be red - hmoglobinuria
- ‘Ghost cells’ ma be seen on a blood smear
21
Q
What is the Pathogenesis of Immune Hemolysis?
A
- RBCs coated with *ESAIg (Erythrocyte surface-associated immunoglobulin) undergo extravascular hemolysis in macrophages
- RBCs coated with ESAIg are converted to spherocytes by macrophages removing the RBC membrane
- Spherocytes undergo either extravascular or intravascular hemolysis because of their rigidity and fragility respectively
- Some ESAIg may bind complement which activates the complement cascade leading to intravascular hemolysis via the membrane attack complex
22
Q
What laboratory findings are associated with Immune Mediated Hemolytic Anemia?
A
- Always:
- ⇣ Hct, RBC & Hgb
- ~Always:
- Positive for RBC-surface associated immunoglobulin (ESAIg)
- Evidence of regeneration
- Inflammatory leukogram
- Case dependent:
- Hemoglobinemia, hemoglobinuria
- Hyperbilirubinemia and bilirubinuria
- Spherocytosis on the blood film
- Agglutination
- Coombs’ Test + (antibody or complement on RBC)
23
Q
Wat is Coombs’ Test?
A
- Direct Antiglobulin Test
- Not as sensitive as RBC-surface-associated immunoglobulin test
- Detects antibody or complement bound to the RBC surface
- RBCs are washed with saline to remove unbound proteins, and ten incubate w/species specific anti- IgG, antiIgM, and anti-complement
- Coombs’ reagent binds Ab or complement that is already bound o the RBCs
-
positive result is indicated by RBC agglutination or Hemolysis if complement is added
- False negatives are common
24
Q
What are the exceptions for IMHA?
A
- Rarely anemia may be nonregenerative on presentation
- Short duration (<2-3 days)
- Marrow precursors are also a target for destruction
- Other concurrent disease interferes with erythropoiesis;
- Spherocytes are usually seen but NOT always
- if rapidly removed from circulation they may not accumulate in blood
- In suspected cases without siderocytes recommend RBC surface associated immunoglobulin assay recommended
26
Q
What is Mycoplasma haemocanis?
A
- Opportunistic Organism
- usually causing in severely immunosuppressed dogs, or dogs w/out a spleen
- Active infection may manifest days to weeks after a splenectomy
27
Q
What is Mycoplasma haemofelis?
A
- Results in IMHA
- Agglutination may be present
- Transmission not well understood
- Present throughout the world
- Latent carriers
- Stress may initiate recurrence of clinical disease
28
Q
what is mycoplasma wenyonii?
A
- Occurs worldwide
- Similar to Mycoplasma haemocanis in dogs
- Usually only causes severe anemia in immunosuppressed or splenectomized cattle.
29
Q
What is Mycoplasma Haemosuis?
A
- Pathogenic in very young pigs and splenectomized pigs
- Causes sever hemolytic anemia and some times death
- In older animals - poor weight gain
30
Q
What is Anaplasma marginale?
A
- Intracellular, bt appear to project from cell
- Organisms most numerous in acute (early) disease
- When Hct is falling
- 4-5 days later, typically difficult to find organisms
- Resulting anemia is immune-mediated
- Extravascular hemolysis typically predominates
- Moderate to sever anemia, polychromasia, reticulocytosis on NMB, basophilic stippling, mild to marked hyperbilirubinemia +/- bilirubinuria
31
Q
What is Babesia/Theileria?
A
- Several species of babesia cause hemolytic anemia and thrombocytopenia
- Transmitted via:
- Protozoal Tick-born disease
- Transplacental transmission & iatrogenic
43
Q
What is Pure red cell aplasia?
A
- Markedly decreased to absent concentration of red cell precursors
- Normal granulopoiesis
- Normal Thombopoiesis
- Severe non-regenerative anemia with normal WBC and platelet concentrations
- Dogs - usually immune-mediated destruction of RBC precursors
- =/- spherocytes and agglutination
- Cats - FeLV, subgroup C
- Dogs - usually immune-mediated destruction of RBC precursors
