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Clinical Pathology > Erythrocytes > Flashcards

Erythrocytes Flashcards

1
Q

What is an erythron?

A

All erythroid cells in an animals

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2
Q

What is erythropoiesis a part of?

A

Hematopoiesis

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3
Q

What is erythropoietin produced by?

A

Fetal liver and adult kidney

Renal peritubular interstitial cells in response to hypoxia

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4
Q

What is hypoxia?

A

Anemia
Poor oxygenation of the blood
Decreased renal perfusion

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5
Q

What signals erythrocytes to stop dividing?

A

Increasing Hgb concentrations

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6
Q

What is produced for protein synthesis including Hgb?

A

RNA

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7
Q

What leads to nucleus extrusion in mammals?

A

Maturation of erythrocytes

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8
Q

What is a reticulocyte?

A

An erythrocyte without the nucleus but with high concentration of RNA

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9
Q

What happens to old erythrocytes?

A

Loose metabolic ability to keep deformability

Expose hidden antigens in the membrane that naturally occurring antibodies bind to mediating erythrocyte destruction

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10
Q

What is hemoglobin?

A

Tetramer of four globin molecules and bound to a internal Heme molecule

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11
Q

Why can heme alone not transport O2?

A

It has a Ferrous ion associated and that cannot transport O2

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12
Q

What percent of CO2 from tissues binds to Hgb? What happens with the rest of CO2?

A

20%

It reacts with H2O to form H+ hand HCO3-

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13
Q

What happens in order to excrete CO2 from the lungs?

A

The reaction is reversed

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14
Q

What is porphyria?

A

Increased concentration of porphyrins in erythrocytes, plasma, or urine
Can be acquired or congenital

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15
Q

What percent of iron is in erythrocytes?

A

50-70%

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16
Q

What percent of iron is in storage?

A

25-40%

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17
Q

What is absorption of iron regulated by?

A

Hepcidin

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18
Q

What is hepcidin produced by?

A

Hepatocytes

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19
Q

What decreases hepcidin production? What then happens to iron absorption?

A

Hypoxia

Fe absorption decreases

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20
Q

What increases hepcidin production?

A

Inflammation

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21
Q

What stains RNA and mitochondria?

A

New methylene blue causing a reticulated or punctuated structure look in erythrocytes cytoplasm

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22
Q

What are the types of reticulocytes?

A

Most species are all RNA rich erythrocytes will be called reticulocytes
Cats have punctuate with 2-6 granules and aggregate with large aggregates

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23
Q

What is reticulocytosis?

A

Semiquantitative evidence of erythropoiesis

Cats: aggregate started at 2 days, peaks at 4 days; punctate is mild in day 1, peaked at 7-14 days

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24
Q

What is the level of reticulocytes like in cattle and dogs when looking for erythropoiesis?

A

Starts 3-4 days and peak 7-14 days

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25
Q

What is the level of reticulocytes like in cats when looking for erythropoiesis?

A

Aggregate started at 2 days, peaks at 4 days

Punctate is mild in day 1, peaked at 7-14 days

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26
Q

What is the level of reticulocytes like in horses when looking for erythropoiesis?

A

They rarely will have circulating reticulocytes

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27
Q

What is polychromasia?

A

Increased numbers of basophilic erythrocytes in the blood smear

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28
Q

What does increased reticulocytes mean?

A

That bone marrow is responding to EPO

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29
Q

What is an erythogram?

A 
Morphologic evaluation
Hematocrit or PCV
Hgb concentration Erythrocytes count
Wintrobe's erythrocytes indices
Nucleated erythrocytes
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30
Q

What is a part of the Wintrobe’s erythrocytes indices?

A

MCHC
MCV
MCH

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31
Q

What is MCHC?

A

Average of 100 mL of erythrocytes [Hgb]

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32
Q

What is MCV?

A

Average of erythrocytic volume

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33
Q

What is MCH?

A

Average [Hgb] per average sized erythrocytes

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34
Q

How are nucleated erythrocytes counted?

A

Per 100 leukocytes and if they are present, it is necessary to correct the leukocytes count

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35
Q

How are nRBCs usually reported?

A 
#/100 WBC
So, if nRBC= 50/100 WBC that could be a lot or very few
If WBC= 500 μL, nRBC would be 250/μL
If WBC= 50,000 μL, nRBC would be 25,000/μL
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36
Q

What is the reticulocyte concentration?

A 
#/μL or L
RC= RP x [RBC]
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37
Q

What is the reticulocyte percentage or reticulocyte count?

A 
# of reticulocytes per 100 erythrocytes
Percentage of erythrocytes that are reticulocytes in the blood
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38
Q

What is the corrected reticulocyte percentage?

A

Calculated number if RP if animal was not anemic but had the same RC
CRP= RP x (patient’s Htc/avg Hct for species)

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39
Q

What are dicocytes?

A

Mature normal erythrocytes

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40
Q

What is rouleaux caused by?

A

Charges interactions

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41
Q

What does agglutination occur in?

A

Immune hemolytic anemia

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42
Q

How is agglutination different from rouleaux?

A

Will not form stacks of cells

Cannot use a saline dispersion test

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43
Q

What is rubricytosis?

A

Increased number of nRBCs in the blood

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44
Q

When is rubricytosis appropriate?

A

Response to EPO stimulus

With reticulocytosis

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45
Q

When is rubricytosis inappropriate?

A 
Loss of control of nRBC release from BM
BM damage
Extramedulary hematopoiesis
Splenic contraction
Splenectomy
Lead poisoning in dogs
BM dyscrasia in poodles with macrocytosis
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46
Q

What is central pallor?

A

Central area of an erythrocytes that is more clear because it is thinner
Increased is hypochromasia
Decreased is abnormal shape

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47
Q

What is a ghost cell?

A

Complement mediated intravascular hemolysis

Artifact

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48
Q

What is a hypochromic erythrocyte?

A

Hyperchromasia: increased number of hypochromic erythrocytes
Decreased MCHC and CHCM
Decreased RBC [Hgb]
Fe deficiency

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49
Q

What is a polychromatophil?

A

An erythrocyte with enough RNA to stain basophilic with Wright stain

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50
Q

What reflects accelerrated erythropoiesis?

A

Polychromasia and reticulocytosis

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51
Q

What is the preferred method for evaluating marrow response to anemia?

A

Reticulocyte concentration

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52
Q

Describe anaplasma marginale in erythrocytes

A 
0.5 μm small coccus in the internal margin of the erythrocyte
Usually one, but possibly multiple per cell
Causes hemolysis (immune mediated)
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53
Q

Describe anaplasma centrale in erythrocytes

A

0.5 μm small coccus within the erythrocyte
Usually one, but possibly multiple per cell
Causes hemolysis (immune mediated)

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54
Q

Describe Babesia in erythrocytes

A

Intracellular, oval to teardrop trophozoites
Variable sizes
Pale blue with a darker outer membrane and a purple eccentric nucleus
Hemolus: immune mediated, protease activity, decreased cell pliability, oxidative damage

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55
Q

Describe Cytauxzoon felix in erythrocytes

A

Intacellular, oval, 0.1 to 2 μm with outer thin rim and eccentric nucleus
One to several per cell
Anemia: inflammation, BM damage, hemolysis

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56
Q

Describe distemper (dogs) in erythrocytes

A

Round to variably shaped, pale blue to pink, homogeneous inclusions
0.3 to 3 μm
Diff-quick is better to see than Wright stain
Active distemper infection

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57
Q

Describe Mycoplasma (cattle) in erythrocytes

A

Rind, rod, or cocci on erythrocytes’ surface
0.3 to 3 μm
Immune hemolysis

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58
Q

Describe Mycoplasma hemocanis in erythrocytes

A

Thin chain of cocci

Immune hemolysis

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59
Q

Describe Mycoplasma hemofelis in erythrocytes

A

Thin chain of cocci, small rings, pale blue to purple
Less than 0.1 μm
Immune hemolysis

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60
Q

Describe Candidatus Mycoplasma haemominutum in erythrocytes

A

Coccie 0.1 to 0.2 μm, individual or short chains

Immune hemolysis

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61
Q

Describe Theileria in erythrocytes

A

Pleomorphic piroplasm: cocci. rings, rods, pears, and maltese crosses
Anemia: immune, protease, decreased cell pliability, and oxidative damage

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62
Q

What are causes of basophilic stippling?

A

Regenerative anemia

Plumbism

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63
Q

What is the pathogenesis of regenerative anemia?

A

Persistence of ribosomal RNA

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64
Q

What is the pathogenesis of plumbism?

A

Inhibition of pyrimidine 5’-nucleotidase

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65
Q

How does a Heinz body develop?

A

Exposure to oxidants

Pathogenesis: oxidized Hgv precipitates

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66
Q

How does a Howell-Jolly body develop?

A

Increased erythropoiesis, decreased splenic function

Pathogenesis: nuclear remnant free in the cytoplasm

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67
Q

How do siderotic granules develop?

A

Excess Fe in the body, plumbism in dogs, myeloproliferative diseae
Pathogenesis: Fe accumulates in damaged mitochondria or in autophagocytic vacuoles

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68
Q

How does an acanthocyte develop?

A

Hemangiosarcoma; splenic, hepatic, and renal disorders
Pathogenesis: not known how it is formed in domestic mammals, possible changes in membrane lipids or erythrocyte fragmentation

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69
Q

How does a codocyte (mexican hat cell) develop?

A

Regenerative anemias; hepatic, renal, and lipid disorders

Pathogenesis: excess membrane relative to Hgb content, possibly membrane lipid changes

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70
Q

How does a dacrocyte develop?

A

Marrow diseases such as myelofibrosis and neoplasia (pathogenesis: unknown formation mechanism)
Artifact (pathogenesis: stretching during film preparation

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71
Q

How does an eccentrocyte form?

A

Exposure to oxidants, G6PD or FAD deficiencies

Pathogenesis: fusion of damaged membranes

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72
Q

What are the different types of echinocytes?

A

Irregularly shaped cells (type I)
Regularly spaced blunt projections (type II)
Regularly spaced pointed projections (type III)

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73
Q

What is the pathogenesis of echinocytes?

A

Erythrocyte dehydration, strenuous exercise, doxorubicin toxicosis, antonic in dogs, PK deficiency in dogs, rattlesnake and coral snake envenomation

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74
Q

What are crenated erythrocytes?

A

Always an artifact
Features of types I, II, and III echinocytes
All echinocytes should be considered artifact until proven otherwide

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75
Q

How does a keratocyte develop?

A

Vasculitis, intravascular coagulation, hemangiosarcoma, caval syndrome, endocarditis
Pathogenesis: trauma, oxidative injury, vesiculation have been proposed

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76
Q

How does an ovalocyte develop?

A

Protein band 4.1 deficiency in dogs, myelofibrosis, idiopathic in cats, iron deficiency
Pathogenesis: abnormal membrane proteins in hereditary forms, otherwise unknown

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77
Q

How do pyknocytes develop?

A

Exposure to oxidants

Pathogenesis: likely formed from eccentrocytes

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78
Q

How does a schistocyte develop?

A

Intravascular coagulation, vasculitis, hemagiosarcoma, caval syndrome, endocarditis
Pathogenesis: trauma

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79
Q

How do spherocytes develop?

A

Immune hemolysis, fragmentation hemolysis, envenomation, clostridial infections
Pathogenesis: membrane loss due to macrophages partial phagocytosis, trauma

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80
Q

How does a stomatocyte develop?

A

Young erythrocytes, herediatry stomatocytosis in dogs

Pathogenesis: folding of excess membrane

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81
Q

What is the pathogenesis of torocytes?

A

Artifact

Do not confuse these with hypochromia

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82
Q

What is anemia?

A

Decreased Hct, [Hgb], [RBC]

Pathological state, not a disease

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83
Q

What are causes of anemia?

A

Loss
Destruction
Lack of production

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84
Q

What is a regenerative anemia?

A

With reticulocytosis (increased number of reticulocytes)
Following blood loss or erythrocyte destruction (hemolysis); erythroid neoplasia in cats; resolution of nonregenerative anemia
Show active erythropoiesis
May be blunted by other concurrent conditions

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85
Q

What is a nonregenerative anemia?

A

Without reticulocytosis (normal or decreased numbers of reticulocytes)
Defective or reduced erythrocyte production
Persistent status shows that BM is not able to produce cells

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86
Q

When does reticulocytosis occur?

A

3-4 days after EPO stimulus and will peak at 7-10 days

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87
Q

What is normocytic?

A

Based on MCV

Maturation is not defective

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88
Q

What is macrocytic?

A

Based on MCV

Presence of reticulocytes or defective cells

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89
Q

What is microcytic?

A 
Based on MCV
Extra mitosis (Fe deficiency); fragments
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90
Q

What is normochromic?

A

Based on MCHC/CHCM

Hgb synthesis is complete

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91
Q

What is hypochromic?

A

Based on MCHC/CHCM

Hgb synthesis is incomplete (young cells or defective synthesis)

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92
Q

What is hyperchromic?

A

Based on MCHC/CHCM

RBCs were not produced hyperchromic. Either lost volume in vitro or artifact

93
Q

What is normocytic normochromic?

A

Blood smear has uniform erytrocytes
Most anemias begin as normocytic normochromic
Most anemias in the horse are this

94
Q

What is macrocytic hypochromic?

A

Expect anisocytosis and polychromasia on the blood smear (do not see hypochromic cells, see polychromatophils)
Anemia probably due to blood loss or hemolysis

95
Q

What is macrocytic normochromic?

A

Anisocytosis and possibly polychromasia on the blood smear
Common in blood loss and hemolysis
Occasionally defective erythopoiesis (FeLV, Folic acid and Cobalamin, Erythroleukemia)
Artifact (erythrocyte agglutination, cell swelling during storage, In vivo hyperosmolar state, too little blood and too much K-EDTA)

96
Q

What is microcytic hypochromic?

A

Microcytosis, codocytosis, hypochromasia, and anisocytosis on blood smear
Defective Hgb synthesis (Fe deficiency, Copper deficiency, Possibly Vit B6 deficiency

97
Q

What are causes of microcytic normochronic anemias?

A

Hepatic failure: hepatic disease, or portosystemic shunt
Foals and kittnes (lower MCV); Akitas and Shibas
Hereditary disease

98
Q

What is normocytic hypochromic?

A

Uncommon: likely inaccurate data, or inadequate reference interval
Possible with Fe deficiency

99
Q

What is macrocytic hyperchromic?

A

Falsely increased MCHC

Compare to CHCM

100
Q

What is normocytic hyperchromic?

A

Flasely increased MCHC

Compare to CHCM

101
Q

What is microcytic hyperchromic?

A

Hypoosmolar plasma cell (cell shrinkage)

If MCHC is flasely increased, think of other causes for microcytic anemias

102
Q

What is the problem with a increased MCHC or CHCM?

A

It is not physiologically possible: Hgb production stops when optima [Hgb] is reached
Mostle falsely increased with falsely increased MCH

103
Q

What are causes of increased MCHC or CHCM?

A

CHCM is not affected
Hemolysis
Oxyglobin
Interferences on Hgb tests: lipid droplets, markedly icteric sample, extreme leukocytosis, precipitated IgA

104
Q

What are examples of true cases of increased MCHC?

A

Eccentrocytosis and pyknocytosis; spherocytosis

105
Q

What are the most common cause of nonregenerative anemias?

A

Decreased RBC production

Defective erythopoiesis

106
Q

What is the life span of erythrocytes?

A

2-5 months: dogs- 100 days, cats- 70 days, cattle and horses-150 days

107
Q

What will most diseases do to the production of erythrocytes?

A

Slow down production, but will not stop completely

108
Q

What determines the severity of nonregenerative anemia?

A

Duration of disease
Degree of erythropoiesis decrease
Presence/absence of processes that shorten the RBC life span

109
Q

What is the most common cause of nonregenerative anemia in domestic mammals?

A

Inflammatory disease (AID: anemia of inflammatory disease)

110
Q

What type of anemia

morphology usually occurs with inflammatory disease?

A

Normocytic normochromic

111
Q

What is the pathogenesis of nonregenerative anemia caused by inflammatory disease?

A

Shortened RBC survival
Impaired Fe mobilization or utilization
Impaired RBC production

112
Q

What are the ab findings of nonregenerative anemia caused by inflammatory disease?

A 
Normocytic normochromic
Mild to moderate
Hyperproteinemia
BM: normal to mildly decreased erythropoiesis
Hypoferremia
113
Q

What is the anemia severity with chronic renal disease?

A

Mild to moderate

114
Q

What is the pathogenesis of nonregenerative anemia caused by chronic renal disease?

A

Inadequate EPO production
Decreased RBC life span
Decreased BM response to EPO
Possible hemorrhage or nutritional status

115
Q

What are the lab findings for a nonregenerative anemia caused by chronic renal disease?

A

Normocytic normochromic

Evidence of chronic renal disease, such as azotemia, isostenuria, and electrolyte disturbances

116
Q

What are some diseases causing marrow hypoplasia or aplasia of several cell lineages that cause nonregenerative anemia?

A 
Idiopathic
Infectious agents
Toxicosis
Irrafiation
Myelophtisis (marrow replacement)
117
Q

Describe how diseases that cause marrow hypoplasia or aplasia of several cell lineages cause nonregenerative anemias

A

One or more BM components could be affected: blood vessels, sinusoids, reticular adventitial cells, marrow stroma, hematopoietic stem cells
Nonreversible or reversible damage

118
Q

How can infectious agents cause nonregenerative anemia?

A

Direct cell damage; myelitis or secondary effects
Suppression with bacterial septicemias
Ehrlichiosis: disseminated micosis, viral infections, protozoal infections

119
Q

How does cytauxzoonosis cause nonregenerative anemia?

A

Piroplasms in RBCs and schizonts in macrophages

Clinically: rapid progression and highly fatal

120
Q

What is the anemia morphology associaated with nonregenerative anemias caused by cytauxzoonosis?

A

Normocytic normochromic

121
Q

What are diseases causing erythroid hypoplasia or ineffective erythropoiesis that cause nonregenerative anemias?

A 
Pure red cell aplasia
Immune-mediated nonregenerative anemia
FeLV
Nutrient deficiencies (Iron, Copper, Folate, Cobalamin, endocrine disorders (hypothyroidism, hypoadrenocorticism)
Hyperestrogenism
Liver disease or failure
122
Q

What is the pathogenesis of pure red cell aplasia?

A

Humans: viral or immune mediated

Not clear in dogs and cats

123
Q

What are the lab findings with nonregenerative anemia caused by pure red cell aplasia?

A

Normocytic normochromic
Spherocytes
Coomb’s test positive
BM with erythroid severe hypoplasia or aplasia

124
Q

What is immune-mediated nonregenerative anemia?

A

Similar to aplastic anemia, but BM with left shift and maturation arrest, or persistent erythroid hyperplasia and nonregenerative anemia
Coomb’s positive

125
Q

What is the pathogenesis of FeLV for causing nonregenerative anemia?

A

Precursor cell damage and following hypoplasia

Neoplastic transformation caused by mutations, producing a defective cell that may not be able to mature properly

126
Q

What are the lab findings for nonregenerative anemia caused by FeLV?

A

Normocytic normochromic or macrocytic normochromic
Inappropriate rubricytosis
Dysplastic RBCs

127
Q

How does an iron deficiency cause a nonregenerative anemia?

A

Chronic external blood loss or inadequate dietary Fe intake

128
Q

What is the morphology of the nonregenerative anemia caused by Fe deficiency?

A

Microcytic hypochromic, but possible microcytic normochromic

129
Q

What does a deficiency in folate and cobalamin lead to?

A

Abnormal cell production because they are required for DNA synthesis

130
Q

What are the findings with a nonregenerative anemia due to a folate and cobalamin deficiency?

A

Macrocytic (or normocytic) normochromic

131
Q

How does hypothyroidism case nonregenerative anemia?

A

Decreased metabolic rate leading to decreased oxygen need. That causes decreased EPO which leads to anemia

132
Q

What are the lab findings for nonregenerative anemia due to hypothyroidism?

A

Normocytic normochromic

Evidence of thyroid dysfunction

133
Q

What are the lab findings for nonregenerative anemia due to hypoadrenocorticism?

A

Normocytic normochromic

Evidence of adrenal dysfunction

134
Q

How does hyperestrogenism cause nonregenerative anemia?

A

Excessive production or iatrogenic

135
Q

What is the morphology of the nonregenerative anemia caused by liver disease/failure?

A

Normocytic normochromic

136
Q

What is the pathogenesis of nonregenerative anemia caused by liver disease/failure?

A

AID
Defective amino acids, protein, and lipid metabolism affecting RBC membranes and life span
Dogs: not total Fe deficiency, but possible functional Fe deficiency

137
Q

What are the lab findings for nonregenerative anemia due to liver disease/failure?

A

Normocytic (or microcytic) normochromic

Findings are consistent with hepatic disease

138
Q

What are causes of blood loss anemia?

A

Hemorrhage
Parasitism
Donating blood for transfusions

139
Q

Describe acute blood loss anemia

A

Sudden loss of blood from vessel creates hypovolemia
Shift of ECF into vessels dilutes erythrocytes and causes anemia
Splenic contraction reduces severity of anemia
Few hours after blood loss
Hemothorax or hemoperitoneum
Tissue hypoxia –> EPO production—> reticulocytes in 3-4 days (horses)

140
Q

What are the clinical findings associated with acute blood loss anemia?

A

Observation of blood (gross external hemorrhage; hemothorax, hemoperitoneum)
Regenerative anemia
Hypoproteinemia

141
Q

What can chronic blood loss anemia lead to?

A

Iron deficiency

142
Q

How does chronic blood loss anemia develop?

A

Compensatory erythropoiesis prevents anemia for weeks to months
Fe deficiency diminishes erythropoiesis and causes mild anemia
Full blown Fe deficiency causes microcytic hypochromic anemia

143
Q

What are the clinical findings associated with chronic blood loss?

A

Melena, hematuria, parasites, or their eggs/larvae
Poorly or nonregenerative anemia
Microcytic normochromic or hypochromic anemia
Marrow: erythroid hyperplasia but ineffective erythropoiesis
Mild to moderate hypoproteinemia
Hypoferremia, decreased total body Fe and decreased ferritin

144
Q

Are young or old animals more prone to chronic blood loss? Why?

A

Young

Small Fe storage

145
Q

What causes hemolytic anemia?

A

Increased rate of erythrocytes destruction

146
Q

What is intravascular hemolysis?

A

It occurs in the blood, within blood vessels or heart

147
Q

What is extravascular hemolysis?

A

Occurs outside the vessels, erythrocytes are phagocytized

148
Q

Why should you differentiate between intravascular and extravascular hemolysis?

A

Different diseases cause different hemolytic anemias

Prognosis and treatment

149
Q

Why is the classification of hemolysis a problem?

A

Diseases do not read books
May cause both intravascular and extravascular
May switch from one to another

150
Q

What should you look for when examining a blood smear?

A

Organisms and RBCs morphologic changes

151
Q

What are signs of hemolytic anemia?

A

Icterus
Bilirubinuria
Urobilinogenuria

152
Q

What is the primary mechanism for hemolytic hemoglobinemia/hemoglobinuria?

A

Hgb tetramers–> Hgb dimers –> bind to haptoglobin –> hepatocytes –> (unconjugated –> conjugated bilirubin + Fe)

153
Q

What is the secondary mechanism for hemolytic hemoglobinemia/hemoglobinuria?

A

Hgb tetramers –> Hgb dimers –> bind to hemopexin –> hepatocytes –> (unconjugated –> conjugated bilirubin + Fe)

154
Q

What is the overflow mechanism for hemolytic hemoglobinemia/hemoglobinuria?

A

Hgb tetramers –> Hgb dimers –> glomerular filtration –> hemoglobinuria

155
Q

What causes immune-mediated hemolytic anemias?

A

Animal produces Ig that bind directly or indirectly to RBC surface (erythrocyte surface associated immunoglobulin: ESAIg)
If Ig, fix complement MAC can cause hemolysis

156
Q

What can ESAIg be?

157
Q

What is used to detect ESAIg or complement factors on RBC surface?

A

Coomb’s test

158
Q

What are the clinical findings associated with IMHA (idiopathic immune hemolytic anemia)?

A

Regenerative anemia
Icterus
Possibly hemoglobinuria
Spherocytosis
Positive Coomb’s or flow cytometry for ESAIg
Acute inflammatory leukogran
Lack findings of other immune hemolytic anemia

159
Q

What drugs can induce hemolyic anemia?

A 
Penicillin (horse)
Propylthiouracil (cats)
Cephalosporins (suprapharmological doses in dogs)
TMS (horses)
Lecamisole (dogs)
Pirimicarb (dogs)
160
Q

What can vaccine-induced hemolytic anemia occur in?

161
Q

How does neonatal isoerythrolysis cause alloimmune hemolysis?

A

Colostral Ig –> intestinal absorption –> bind to RBCs paternally inherited antigens
Cats: Anti-A antibodies
Horses: Anti-A or anti-Q antibodies
Dogs: possible anti DEA 1.1

162
Q

How does an incompatible blood transfusion cause alloimmune hemolysis?

A

Donor’s erythrocytes are attacked by recipient’s antibodies

163
Q

What causes feline infectious anemia?

A

Feline hemic Micoplasma spp.
M. hemofelix is more pathogenic and larger
Candidatus M. Haemominuturm is considered opportunistic

164
Q

What can happen during feline infectios anemia caused by Micoplasma?

A

Parasitemia is usually present during hemolysis but may disappear fast
May detach from RBCs

165
Q

How does canine hemic Mycoplasma spp cause hemolytic anemia?

A

M. haemocanis: splenectomized or immunologically compromised dogs
May detach from RBCs

166
Q

What are otehr mycoplasma spp that cause hemolytic anemias?

A

M. haemosuis and M. parvum in pigs
M. wenyonii in cattle
Candidatus M. haemolamae in llamas and alpacas

167
Q

What is the pathogenesis of hemothropic mycoplasma species causing hemolytic anemia?

A

Immune-mediated mechanisms

168
Q

What are the lab findings with hemothropic mycoplasma species causing hemolytic anemias?

A 
Mycoplasma spp on erythrocytes (most numerous when Hct is falling)
Moderate to severe anemia
Reticulocytosis/polychromasia
Hyperbilirubinemia/hyperbilirubinuria
Positive Coomb's test
Spherocytosis
Autoagglutination
PCR positive for Mycoplasma spp
169
Q

What Anaplasma spp can cause hemolytic anemia?

A 
Anaplasma marginale (cattle)
Anaplasma ovis (sheep and goats)
Anaplasma centrale (cattle)
170
Q

What is the pathogenesis of hemolytic anemias caused by Anaplasma spp?

A

Immune-mediated

171
Q

What are the lab findings for hemolytic anemia caused by Anaplasma?

A

Moderate to severe anemia
Reticulocytosis/polychromasia
Mild to marked hyperbilirubinemia/hyperbilirubinuria
PCR positive for Anaplasma spp

172
Q

What Leptospira spp can cause hemolytic anemia?

A

L. interrogans serovars pomona and icterohemorrhagica

173
Q

What do L. interrogans serovars pomona and icterohemorrhagica cause?

A

Do not infect RBCs

Cause vasculitis, infection of liver and kidneys –> hemolytic state in calves, lambs, and pigs

174
Q

What is the pathogenesis of hemolytic anemia caused by Leptospira?

A

Immune-mediated (IgM clod agglutinins or Leptospiral phospholipase)

175
Q

What are the lab findings associated with hemolytic anemia caused by Leptospira?

A

Moderate to severe anemia
Hemoglobinemia/hemoglobinuria
Hyperbilirubinemia/hyperbilirubinuria
Neutrophilia
Leptospiral spirochetes in urine or other fluids
4-fold increase in titers for pomona and icterohemorrhagica serovars
Positive PCR for Leptospira spp

176
Q

What Clostridium spp cause hemolytic anemia?

A

C. haemoliticum
C. novyii type D
C. perfringens type A

177
Q

What do C. haemoliticum and C. novyii type D cause in cattle and sheep?

A

Bacillary hemoglobinuria

178
Q

What is the pathogenesis of hemolytic anemia caused by C. haemoliticum and C. novyii type D?

A

Beta-toxin with phospholipase and lecithinase activity

179
Q

What are the lab findings associated with hemolytic anemia caused by C. haemoliticum and C. novyii?

A

Severe anemia

Hemoglobinemia/hemoglobinuria

180
Q

How can you diagnose hemolytic anemia caused by C. haemoliticum and C. novyii postmortem?

A

Bacilli in spleen and liver or fluids

Culture

181
Q

What does C. perfringens type A cause in lambs and calves?

A

Yellow lamb disease

182
Q

What is the pathogenesis of hemolytic anemia caused by C. perfringens type A?

A

Alpha-toxin with phospholipase C activity

183
Q

What are the major lab findings more hemolytic anemia caused by C. perfingens type A?

A

Acute severe cases: anemia; hemoglobinemia/hemoglobinuria; icterus
Less severe: anemia; polychromasia/reticulocytosis; rubricytosis; leukocytosis

184
Q

What is Equine Infectious Anemia Virus?

A

Retrovirus that infect cells from the mononuclear phagocytic system in horses, mules, donkeys, and ponies
Disease: equine infectious anemia

185
Q

What is the pathogenesis of EIA?

A

Production of TNF and other cytokines that decrease RBC production
Hemolysis: immune complexes or complement adhered to RBCs –> extravascular hemolysis

186
Q

What are the lab findings associated with EIA?

A

Acute: intravascular hemolysis, hemoglobinemia
Chronic: extravascular hemolysis
Macrocytosis, thrombocytopenia, neutropenia, neutrophilia, positive Coomb’s test, positive Coggin’s test

187
Q

What is the pathogenesis of FeLV?

A

Decreased RBC production

188
Q

What can FeLV predispose the cat to?

A

Mycoplasma spp infectio or can cause immune hemolytic anemia

189
Q

What is the pathogenesis for hemolytic anemia caused by Babesia?

A

Nonhemolytic and hemolytic processes

Hemolytic: proteases, immune-reaction to parasitized RBCs, oxidative damage to RBCs

190
Q

What are the lab findings for hemolytic anemia caused by Babesia?

A

Chronic: few/rare organisms in RBCs, mild anemia, mild lymphocytosis, seropositive and PCR positive for Babesia spp
Acute or subacute: many organisms in RBCs, moderate to severe anemia, reticulocytosis/polychromasia, macrocytosis, hyperbilirubinemia/bilirubinuria, possiblee hemoglobinuria, possible spherocytosis, and occasionally eccentrocytosis

191
Q

What species of Theileria can cause hemolytic anemia?

A

Theileria buffeli

192
Q

What is the pathogenesis associated with hemolytic anemia caused by Tehileria buffeli?

A

It is not clear

193
Q

What are the lab findings wtih hemolytic anemia caused by Theileria buffeli?

A

Organisms in RBCs, macrocytosis, polychromasia, basophili stippling, lymphocytosis, hyperbilirubinemia/bilirubinuria

194
Q

What are causes of feline heinz bodies?

A

Spleen with closed circulation
Feline Hgb is prone to form oxidized forms
Feline erythrocytes have lower reductive ability

195
Q

How are Heinz bodies hemolytic anemia in cats diagnosed?

A

Presence of anemia
Presence of evidence of hemolysis (hyperbilirubinermia/bilirubinuria)
Presence of Heinz bodies in erythrocytes

196
Q

What is the pathogenesis of eccentrocutic hemolytic anemias?

A

Eccentrocytes are more rigid and are trapped and removed by macrophages in the spleen
Eccentrocytes are more fragile and are prone to lysis

197
Q

What can oxidative insult form?

A

Eccentrocytes or Heinz bodies

198
Q

What is the pathogenesis of postparturient hemoglobinuria in cattle?

A

Decreased phosphate mobilization from bone and increased loss via milk production–> decreased phosphorus plasma concentration –> decreases ATP production in RBCs –> unstable RBCs membrane –> lysis

199
Q

What are the lab findings associated with postparturient hemoglobinuria in cattle?

A

Hypophophatemia
Hemoglobinemia/hemoglobinuria
Moderate to marked anemia

200
Q

What are causes of hypoosmolar hemolysis?

A

Rapid infusion of hypoosmolar fluids IV

Water intoxication in calves

201
Q

What is the pathogenesis of hypoosmolar hemolysis?

A

Infusion of hypoosmolar fluids or large volume of water intake –> hypoosmolar plasma –> rapid movement of water into RBCs –> RBC swelling and lysis

202
Q

What are the lab findings associated with hypoosmolar hemolysis?

A

Anemia

Hemoglobinemia/hemoglobinuria

203
Q

What is the cause of erythrocyte fragmentation?

A

Trauma: presence of rigid structures or rheologic forces

204
Q

What is the pathogenesis of erythrocyte fragmentation?

A

Erythrocyte trauma –> form poikilocytes or lysis
Primary diseases are frequently infectious or noninfectious inflammatory diseases (inflammatory process may be causing anemia)

205
Q

What are the lab findings associated with erythrocyte fragmentation?

A 
Mild to moderate anemia
presence or absence of reticulocytes/polychromasia
Schistocytes
Keratocytes
Acanthocytes
Thrombocytopenia
206
Q

What is erythrocytosis?

A

Increased number of erythrocytes that will increase PCV and Hct

207
Q

What is relative erythrocytosis?

A

When there is an increase in production of cells because there was hemo concentration due to water loss or splenic contraction

208
Q

What is primary absolute erythrocytosis due to?

A

Neoplastic circulation

209
Q

What is secondary absolute erythrocytosis due to?

A

Secondary to something else

210
Q

What occurs with appropriate absolute erythrocytosis?

211
Q

What type of absolute erythrocytosis do you have if things are influencing EPO production and there is no hypoxia?

A

Inappropriate

212
Q

What are causes of hemoconcentration?

A

Dehydration

Endotoxic shock

213
Q

What is the most common cause of erythrocytosis in mammals?

A

Dehydration

214
Q

What are the lab findings associated with hemoconcentration due to dehydration?

A

Hyperproteinemia
Hyperalbuminemia
Hypernatremia
Hypercholremia

215
Q

What is endotoxic shock?

A

Shift of water from intravascular to extravascular space

216
Q

What is the pathogenesis of hemoconcentration due to endotoxic shock?

A

Endotoxins –> endothelial cells damage –> increase permeability to proteins –> decreased oncotic pressure –> plasma fluid migrates from intravascular to extravascular

217
Q

What are the lab findings associated with hemoconcentration due to endotoxic shock?

A

Mild to moderate erythrocytosis
Inflammatory leukogram
Thrombocytopenia

218
Q

What does splenic contraction cause?

A

Physiologic erythrocytosis

219
Q

What is the pathogenesis of physiologic erythrocytosis due to spenic contraction?

A

Physical exercise/fright/excitement –> epinephrine –> splenic contraction –> shift of RBCs from spleen to peripheral blood

220
Q

Why is secondary appropriate erythrocytosis secondary?

A

Because erythropoiesis is stimulated by EPO and not autononmous

221
Q

Why is secondary appropriate erythrocytosis appropriate?

A

Because EPO is increased due to hypoxia

222
Q

What is erythrocytosis caused by?

A

Increased production

223
Q

What are causes of secondary appropriate erythrocytosis?

A

Cardiac diseases
Pulmonary disorders
Hyperthyroidism: increased metabolic rate –> increased oxygen consumption –> increased hypoxia –> increased EPO production
Physiologic (high altitudes, prolonged exercise training)

224
Q

What is the pathogenesis of secondary appropriate erythrocytosis caused by physiologic changes?

A

Hypoxemia or increased oxygen consumption –> sustained renal tissue –> hypoxia –> increased EPO produtcion –> increased erythropoiesis –> erythrocytosis

225
Q

What is the cause of secondary inappropriate erythrocytosis?

A

Inappropriate increased EPO production due to renal cysts, renal neoplasma, or other benign neoplasms that are not renal

226
Q

What is the cause of primary erythrocytosis?

A 
Autonomous erythropoiesis (not dependent on EPO)
Mild to marked erythrocytosis --> increased viscosity of blood --> poor tissue perfusion --> secondary EPO production
227
Q

What disorders are associated with primary erythrocytosis?

A

Neoplastic or nonneoplastic disease that lead to increased RBC production independent of EPO

228
Q

What disorders are associated with polycythemia vera?

A

Neoplastic disease of erythroid, myeloid, and megakacariocytic cell lines

Clinical Pathology (16 decks)

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