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Duncan and Prasse > Chapter 1: Erythrocytes > Flashcards

Chapter 1: Erythrocytes Flashcards

1
Q

Describe the structure of hemoglobin.

A

Tetramer of 4 hemes and 4 globins (2 a and B dimers)
Each heme has an iron atom in the 2+ state
Globin is attached to each heme

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2
Q

Heme synthesis is controlled at the first step by _____.

A

delta-aminolevulinic acid synthase

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3
Q

What are 2 compounds that inhibit heme synthesis?

A

Lead and chloramphenicol

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4
Q

What are porphyrins?

A

intermediates of heme biosynthesis

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5
Q

How do the porphyrias occur?

A

enzyme deficiencies in the heme synthesis pathway–> accumulation of porphyrias and their precursors

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6
Q

Iron is inserted into protoprophyrin to form heme by what enzyme?

A

ferrochelatase

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7
Q

How does hepcidin control plasma iron concentrations?

A

it inhibits iron export by ferroportin from RBCs and macs by degrading ferrorotin

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8
Q

Increased hepcidin–> increased or decreased iron availability?
Decreased hepcidin–> increased or decreased iron availability?

A

Increased hepcidin–> decreased iron availability

Decreased hepcidin–> increased iron availability

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9
Q

How is iron transported in the blood?

A

by the gamma-globulin transferrin

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10
Q

Is a serum iron measurement a reliable measure of total body iron stores?

A

no

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11
Q

What are 5 conditions with decreased serum iron?

A
  1. iron deficiency
  2. acute and chronic inflammation/disease
  3. hypoproteinemia
  4. hypothyroidism
  5. renal disease
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12
Q

What are 5 conditions with increased serum iron?

A
  1. hemolytic anemia
  2. hemolysis during sampling
  3. glucocorticoid excess in the dog (decreased in cattle with glucocorticoid excess)
  4. iron overload (acquired or hereditary)
  5. nonregenerative anemia
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13
Q

What is total iron-binding capacity (TIBC)?

A

an indirect measurement of the amount of iron that transferrin will bind

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14
Q

What is the unit of TIBC?

A

% saturation

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15
Q

What is the unbound iron-binding capacity represent?

A

the numeric difference between TIBC and SI

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16
Q

Hepcidin is made in the ___ and transported in the blood by ____.

A

Hepcidin is made in the liver and transported in the blood by a2-macroglobulin.

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17
Q

What 2 proteins are necessary for transfer of iron from intestinal epithelium and macs to serum transferrin?

A

ferroportin 1 and DMT1 (divalent metal transporter 1)

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18
Q

Iron is stored in macrophages as ____ and ____.

A

Iron is stored in macrophages as ferritin and hemosiderin.

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19
Q

When is serum ferritin concentration decreased?

A

iron deficiency

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20
Q

What conditions cause an increase in serum ferritin? (6)

A
  1. hemolytic anemia
  2. iron overload
  3. acute and chronic inflammation
  4. liver disease
  5. some neoplastic disorders (LSA, malignant histiocytosis)
  6. malnutrition (cattle)
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21
Q

Which is a more stable storage form of iron, ferritin or hemosiderin? Which is more available?

A

Hemosiderin is more stable but less available

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22
Q

What is the Embden-Meyerhof pathway?

A
  • important in RBC metabolism
  • anaerobic pathway where glycolysis makes ATP and NADH
  • ATP is essential for membrane function and integrity
  • NADH is used to reduce methemoglobin
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23
Q

Which enzyme deficiencies in the Embden-Meyerhof pathway can lead to hemolytic anemia?

A

PK and PFK

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24
Q

PK deficiency impairs ___ production–> what kind of anemia?

A

PK deficiency impairs ATP production–> macrocytic hypochromic anemia with 15-50% reticulocytes, myselofibrosis, hemochromatosis, decreased RBC lifespan, and accumulation of PEP and DPG

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25
Q

PFK deficiency results in decreased ____ concentration and what other lab abnormalities?

A

decreased erythrocytic 2,3 DPG concentration, normal or decreased Hct, persistent reticulocytosis, alkalemia which leads to hemolysis

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26
Q

What enzyme is the rate limiting enzyme in the pentose phosphate pathway?

A

G-6-P dehydrogenase

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27
Q

The pentose phosphate pathway produces what, which is important to RBCs how?

A

NADPH which is a major reducing agent in the RBC
It’s a cofactor for reduction of oxidized glutahione (neutralizes oxidants that can denature Hg)

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28
Q

What happens in G6P dehydrogenase deficiencies?

A

hemolytic anemia under mild oxidative stress (Heinz bodies, eccentrocytes)

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29
Q

Hemoglobin is maintained in the ____ state which is necessary for transport of oxygen.

A

Hemoglobin is maintained in the reduced (Fe2+, oxyhemoglobin) state which is necessary for transport of oxygen.

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30
Q

Enzyme deficiencies in what enzyme lead to methemoglobin accumulation? Why?

A

Methemoglobin reductase– because hemoglobin needs to stay in the reduced state to transport oxygen

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31
Q

What is the Rapoport-Luebering pathway?

A

allows formation of 2,3 DPG which is a regulatory protein in O2 transport

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32
Q

How is 2,3 DPG a regulatory protein in O2 transport?

A

increased 2,3 DPG favors O2 release to tissues by lowering the O2 affinity of Hg

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33
Q

What is the difference in mammal and bird erythropoiesis and where is occurs?

A

mammals- extravascularly in the bone marrow parenchyma
birds- in the vascular sinuses of the bone marrow

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34
Q

What are 3 characteristic morphologic changes that take place during maturation from the rubriblast to mature erythrocyte?

A
  1. cells get smaller
  2. nuclei get smaller and chromatin gets more aggregated
  3. cytoplasmic color changes from blue to orange as Hg is formed and RNA is lost
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35
Q

In what stage does cell division stop in erythroid maturation?

A

late rubricyte stage

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36
Q

In what stage is the nucleus extruded in erythroid maturation?

A

metarubricyte (forms a reticulocyte)

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37
Q

Reticulocytes in most species remain in the BM for __-__ before release and ultimately mature in the blood or spleen. What species have their reticulocytes mature in the BM completely and release mature RBCs?

A

Reticulocytes in most species remain in the BM for 2-3 days before release and ultimately mature in the blood or spleen.

Horses and cattle

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38
Q

The time from stimulation of erythropoietic progenitor cell until reticulocytes are released is ___.

A

The time from stimulation of erythropoietic progenitor cell until reticulocytes are released is 5 days.

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39
Q

How can an increase of erythrocytes delivered to the blood occur?

A
  1. mainly by increased SC input
  2. shortened maturation time
  3. earlier reticulocyte release
  4. skipped cell divisions
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40
Q

Most Epo is made by what cells? What other organ can make it?

A

mainly made by peritubular interstitial cells of the kidney in response to hypoxia
10-15% made by liver (specific hepatocytes and Ito cells)

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41
Q

What are 3 major actions of Epo?

A
  1. inhibition of apoptosis of newly formed progenitor cells and prorubricytes (allows them to mature)
  2. stimulation of Hg synthesis in already dividing erythroid cells
  3. switching of Hg synthesis in sheep from one adult type to another
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42
Q

Identify the normal hematopoietic cells and leukemic cells in BM.

A

A- myeloblast
B- promyelocyte
C- neutrophil myelocyte
D- neutrophil metamyelocyte and segmenters
E- neutrophil metamyelocyte, band, and segmenter
F- rubriblast, rubricyte, metarubricyte, 2 neut metamyelocytes, and a neut segmenter
G- 2 prorubricytes, 4 rubricytes, and an eos
H- 5 rubricytes
I- 5 rubricytes, a metarubricyte, and a polychromatophilic erythrocyte with an HJ body
J- immature megakayocyte with blue, granular cytoplasm
K- mature megakaryocyte with granular, pink cytoplasm
L- promyelocytes in canine myeloblastic leukemia
M- poorly differentiated mast cells in feline mast cell leukemia
N- plasma cells in canine plasma cell myeloma
O- lymphoblasts in canine ALL

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43
Q

What 3 things work with Epo to stimulate multiplication of BFU-E and its differentiation into CFU-E?

A

IL-3, GM-CSF, G-CSF

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44
Q

Model of hematopoiesis.

A
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45
Q

What are the average erythroid lifespans in circulation of these species:
Cow-
Sheep-
Horse-
Dog-
Pig-
Cat-
Bird-

A

Cow- 160 days
Sheep- 150 days
Horse- 145 days
Dog- 110 days
Pig- 86 days
Cat- 70 days
Bird- 35 days

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46
Q

What are the 2 routes that senescent erythrocytes are removed from the circulation in health?

A
  1. Phagocytosis by macs (major route)
  2. Intravascular lysis with release of Hg into plasma (minor route)
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47
Q

What happens to the RBC components once they are phagocytized by macs to be destroyed?

A

Erythrocytes release their Hg in the phagosome and it is split into heme and globin

Globin breaks down into its aas which are utilized

Heme in the iron is cleaved by heme oxygenase which forms CO and biliverdin

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48
Q

Describe iron breakdown in macs.

A

Iron released from Hg–> Heme cleaved off by heme oxygenase–> CO and biliverdin–> biliverdin reduced by biliverdin reductase to bilirubin–> bilirubin excreted in blood and goes to liver with albumin

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49
Q

Why are avian bruises green?

A

They lack biliverdin reductase so they can’t form bilirubin from biliverdin (which is green and is the end product)

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50
Q

When Hg is free in the plasma, it binds ____ (which is a ___). This is then cleared by the ___.

A

When Hg is free in the plasma, it binds haptoglobin (which is an a2-globulin). This is then cleared by the liver.

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51
Q

Enough haptoglobin is available in the plasm to bind ___ of hemoglobin. Plasma appears pink/red when ___ to ___ of hemoglobin is present.

A

Enough haptoglobin is available in the plasma to bind 150 mg/dL of hemoglobin. Plasma appears pink/red when 50 to 100 mg/dL of hemoglobin is present.

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52
Q

When will you be able to detect Hg dimers in the urine?

A

When the plasma haptoglobin is saturated beyond the 150 mg/dL limit

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53
Q

With time, free Hg in the plasma is oxidized to ____, which dissociates to free ___, which complexes with the B-globulin, ____.

A

With time, free Hg in the plasma is oxidized to methemoglobin, which dissociates to free ferriheme, which complexes with the B-globulin, hemopexin.

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54
Q

What 2 complexes keep Hg from being lost in the urine?

A

heme-hemopexin complex
Hg-haptoglobin complex

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55
Q

What happens to Hg that passes into the glomerular filtrate?

A

It is either absorbed by the proximal tubules and catabolized to iron, bilirubin, and globin or if goes through unabsorbed, causes hemoglobinuria.

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56
Q

What is Hct?

A

percent of blood comprised of RBCs

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57
Q

What cells are in the buffy zone?

A

leukocytes and platelets

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58
Q

What is the Hct% formula?

A

Hct %= (RBC/uL) x MCV (fL)

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59
Q

Between PCV and Hct, which has the greater potential for error and why?

A

Hct because only dogs have RBC volume comparable to human RBCs

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60
Q

What methodology is used to determine Hg concentration?

A

colorimetric determination by the cyanmethemoglobin technique or the newer cyanide-free hemoglobinhydroxylamine complex method

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61
Q

What may falsely increase Hg concentration measurements? (4)

A

Heinz bodies, hemolysis, lipemia, Oxyglobin

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62
Q

Which measurement is the most direct indication of oxygen transport capacity of the blood?

A

Hb conccentration

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63
Q

Hb should be __ the Hct if RBCs are of normal size.

A

1/3

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64
Q

What is the value in the RBC count?

A

allows you to determine the MCV and MCH

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65
Q

Which types of dogs and breeds in this group have higher Hct/PCV normally?

A

Sighthounds- greyhound, saluki, whippet, afghan

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66
Q

What is the formula for MCV?

A

MCV (fL)= (PCV x 10)/RBC count (millions)

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67
Q

Why does iron deficiency cause microcytosis?

A

An extra cell division occurs before the critical cytoplasmic concentration of Hg is reached that is needed to stop DNA synthesis and cell division

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68
Q

Greyhounds normally have a higher/lower MCV?

A

higher

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69
Q

Why does cobalamin (vit B12) deficiency cause a macrocytic anemia?

A

There is an interference with nucleic acid synthesis that causes an inhibition of cell division–> larger cells

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70
Q

Congenital macrocytosis occurs in which breed?

A

Poodles

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71
Q

What are some causes of macrocytosis?

A

reticulocytosis
being a greyhound
cobalamin deficiency
congenital in poodles
hereditary in alaskan malamutes, drentse-partrijshond, and min schnauzers
FeLV cats
RBC agglutination

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72
Q

What does MCH represent and what are the units?

A

how much Hb is in an average RBC in picograms

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73
Q

What is the formula for MCH?

A

MCH (picograms)= (Hb concentration x 10)/RBC (millions)

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74
Q

How is MCH related to MCV?

A

smaller RBCs have less Hb–> lower MCH
bigger RBCs have more Hb–> higher MCH

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75
Q

Why is MCHC a better determinant for cell Hb than MCH?

A

it corrects for cell volume

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76
Q

What does MCHC represent?

A

the average Hb concentration per average RBC in grams of Hb/100 mL of erythrocytes

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77
Q

What is the formula for MCHC?

A

MCHC (g/dL)= [Hb concentration (pg) x 100]/Hct (%)

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78
Q

Why would you have an increased MCHC?

A

in vitro or vivo hemolysis or treatment with oxyglobin

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79
Q

What is the formula for RDW?

A

RDW= (SDmcv/MCV) x 100

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80
Q

What does RDW tell you?

A

it’s an index of the degree of anisocytosis or variation in the size of RBCs

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81
Q

What might cause an increased RDW?

A

reticulocytosis or anemias with significant microcytosis or macrocytosis

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82
Q

How big are normal canine erythrocytes?

A

7 um diameter

83
Q

How big are normal cat erythrocytes?

A

5.8 um

84
Q

How big are normal bovine erythrocytes?

A

5.5 um

85
Q

How big are normal equine erythrocytes?

A

5.7 um

86
Q

How big are normal porcine erythrocytes?

A

6 um

87
Q

How big are normal ovine erythrocytes?

A

4.5 um

88
Q

How big are caprine erythrocytes?

A

<4 um

89
Q

What is the average size of bird erythrocytes?

A

12 x 6 um

90
Q

Why does hyperfibrinogeniemia or hyperglobulinemia cause rouleaux?

A

normal negative surface charge is masked and decreases the repelling nature of the RBCs

91
Q

The degree of rouleaux correlates positively with ___.

A

erythrocyte sedimentation rate

92
Q

What are causes of microcytosis?

A

iron and pyridoxine deficiency, remnants of Heinz body and fragmentation anemias, PSS, hyponatremia, healthy Asian breeds of dogs

93
Q

Hyponatremia can affect red blood cell size how?

A

Makes RBCs microcytic (when put back into a normocytic solution like saline, they will swell and can get macrocytosis on the CBC)

94
Q

What causes hypochromasia?

A

iron deficiency and lead toxicosis (from inhibition of Hg synthesis)

95
Q

Describe echinocytes and what causes them?

A

evenly spaced spicules
Type 1- on periphery only; in vitro artifact (drying, temp, pH)
Type 2- all over cell; altered electrolytes with expansion of the outer layer; uremia, electrolyte depletion, lymphoma, doxorubicin, glomerulonephritis

96
Q

Describe keratocytes (helmet cells) and what causes them?

A

1 or 2 projections that form a ruptured vesicle

oxidative damage to the membrane (same reasons as Heinz bodies)

97
Q

Describe acanthocytes and what causes them?

A

spiculated RBCs with irregular, blunted projections

altered lipid:cholesterol ratios; HSA, gloemrulonephritis, lymphoma, liver disease

98
Q

Describe schistocytes and what causes them?

A

irregular fragments from shearing by IV fibrin or turbulent blood flow

DIC, HSA, glomerulonephritis, CHF, myelofibrosis, chronic doxorubicin toxicosis, vasculitis, etc

99
Q

Describe fusocytes and what animals have them normally?

A

elongated erythrocytes

healthy Angora goats

100
Q

Describe elliptocytes and in what cases are they seen?

A

oval cells seen in healthy camelids

4.1 band deficiency in the RBC membrane in dogs causes them

occasionally seen in iron deficiency

101
Q

What hereditary condition in dogs may cause elliptocytes?

A

4.1 band deficiency

102
Q

Describe dacrocytes and when are they seen?

A

tear-drop shaped
if tails in the same direction, may be artifact
may be in llamas with iron deficiency anemia

103
Q

Describe leptocytes and when are they seen?

A

thin cells with increased membrane:volume ratio; may look folded

have been seen in PSS

104
Q

Describe target cells and when are they seen?

A

are actually leptocytes that are bell-shaped but look like targets on the smear; from increasing the amount of membrane via lipid and cholesterol insertion or by decreasing cytoplasmic volume like in hypochromia

may be from liver disease, iron deficiency, and reticulocytosis

105
Q

Describe stomatocytes and when are they seen?

A

type of leptocyte that is bowl-shaped with oval areas of central pallor from expansion of the inner layer of the cell membrane

hereditary stomatocytosis in alaskan malamutes, drentse partrijshond, and min schnauzers

can be artifacts in thick areas

106
Q

What represents basophilic stippling and when is it seen?

A

punctate aggregation of residual RNA

seen as a part of a regenerative response

anemia sheep and cattle and sometimes in feline anemia

can be seen in lead toxicosis (with metarubricytosis and minimal polychromasia)

107
Q

What are Heinz bodies?

A

precipitated Hg

108
Q

Up to __% of feline erythrocytes can have Heinz bodies in health.

A

10%

109
Q

Describe eccentrocytes and when are they seen?

A

Hg is condensed in one portion of the cell and leads a clear blister-like area in the remaining portion of the cell

from oxidative injury with lipid per oxidation and cross-linking of the membrane

110
Q

In what situation may you see elevated numbers of nRBCs without anemia as an appropriate response?

A

hypoxia (Epo induced)

111
Q

What conditions might have an inappropriate release of metarubricytes?

A

lead toxicosis, iron deficiency, copper deficiency, HSA, EMH, myelopthisis, IVD, hereditary macrocytosis of poodles, endotoxemia, bone marrow trauma, metastatic neoplasia of the marrow, myelofibrois, FeLV, MDS, leukemia (especially of erythremic myelosis in cats)

112
Q

Nucleated RBCs have been reported in what breed of dog?

A

Miniature Schnauzers

113
Q

What are erythroplastids?

A

anucleated fragments of erythrocyte cytoplasm occasionally found in bird smears

114
Q

What are hematogones?

A

free erythrocyte nuclei in bird smears

115
Q

The dog has up to ___% of aggregate type reticulocytes in health.

A

1%

116
Q

What 2 types of reticulocytes occur in the cat?

A

Aggregate reticulocytes
Punctate reticulocytes

117
Q

Which type of reticulocyte in the cat is used in the retic count and why?

A

Aggregate retics because punctate retics stay in circulation for 2-3 weeks.

118
Q

Birds can have __-__% of reticulocytes in health.

A

4-5%

119
Q

Why is the reticulocyte percentage a potential overestimate of bone marrow response to anemia?

A

retics released from the bone marrow into the blood of anemic animals are mixed with fewer mature erythrocytes–> higher relative % of reticulocytes

larger, more immature retics are released earlier (shift retics) in response to anemia–> they last longer in blood because they take longer to mature–> higher % of retics

120
Q

What’s the formula for correcting retics?

A

Corrected retics= Observed retic % x (patient’s Hct percentage/”normal” Hct percentage)

121
Q

Corrected retic % greater than __% in the dog and greater than __% in the cat indicate bone marrow response to anemia.

A

Corrected retic % greater than 1% in the dog and greater than 0.4% in the cat indicate bone marrow response to anemia.

122
Q

What is the formula for absolute retic count?

A

Absolute retic count/uL= Reticulocyte % (converted to a decimal) x (total RBC count/uL)

123
Q

An absolute retic count greater than ____/uL in the dog and ____/uL in the cat indicates a regenerative response.

A

An absolute retic count greater than 80,000/uL in the dog and 60,000/uL in the cat indicates a regenerative response.

124
Q

What is the formula for reticulocyte production index?

A

RPI= observed retics (%) x [observed Hct (normal Hct)] x [1 + blood maturation time]

125
Q

Between hemolytic and external hemorrhage anemias, which has a more intense reticulocytosis? Why?

A

Hemolytic– because iron from disrupted RBCs is more available for erythropoiesis than iron stored as hemosiderin

126
Q

Reticulocytosis doesn’t become evident until __ to ___ after the occurrence of anemia.

A

48-72 hours

127
Q

Do dogs or cats have a greater reticulocyte response?

A

Dogs

128
Q

What is unique about healthy suckling pigs and the number of retics they have?

A

they normally have high retic counts

129
Q

The M:E ratio is usually determined to assess _____. What count is needed for proper identification of the ratio?

A

The M:E ratio is usually determined to assess the erythropoietic response to anemia. The WBC (specifically the neutrophil count) is needed for interpretation.

130
Q

If the WBC count is within the reference interval, any change in the M:E ratio is due to _____.

A

If the WBC count is within the reference interval, any change in the M:E ratio is due to changes in the erythroid series.

131
Q

A high M:E ratio in an anemic animal with a EBC count within the reference interval suggests what?

A

erythroid hypoplasia

132
Q

A high M:E ratio in an anemic animal with an increased WBC count could be from ___ or ___.

A

this is more difficult to interpret because could be from myeloid (granulocytic) hyperplasia and/or erythroid hypoplasia

133
Q

A low M:E ratio in an anemic animal with a WBC count within or above the reference interval suggests what?

A

early erythroid regeneration of ineffective erythropoiesis

134
Q

Describe the relative percentages of the various stages in the myeloid and erythroid series in health.

A

80% of myeloid are metamyelocytes, bands, and segs
90% of erythroid are rubricytes and metarubricytes

135
Q

What stains can be used to distinguish iron-deficiency anemia (decreased iron stores) from anemia of chronic disease (increased iron stores) by staining hemosiderin but not ferritin?

A

Perl’s or Prussian blue

136
Q

___ mares bred to ___ stallions are at greater risk of having a second foal with neonatal isoerythrolysis.

A

Aa-negative mares bred to Aa-positive stallions are at greater risk of having a second foal with neonatal isoerythrolysis.

137
Q

Which DEA groups in the dog are highly immunogenic and will sensitize recipients?

A

DEA-1.1 (Aa1)
DEA-1.2 (Aa2)
DEA-1.3 (Aa3)

138
Q

What are 3 naturally occurring DEA antibodies in dogs?

A

anti-DEA-3 (Ba)
anti-DEA 5 (Da)
anti-DEA 7 (Tr)

139
Q

Antibodies in mare colostrum to __ and __ blood types are most frequently involved in neonatal isoerythrolysis.

A

Antibodies in mare colostrum to Aa and Qa blood types are most frequently involved in neonatal isoerythrolysis.

140
Q

What happens in type B cats transfused with A blood and type A cats transfused with type B blood?

A

Type B cats with natural anti-A abs can have severe hemolytic reactions when transfused with A blood

Type A cats with natural anti-B abs have early erythrocyte removal when transfused with B blood

141
Q

Describe the major cross match.

A

Donor RBCs
Recipient serum

–detects abs in the recipient that will react with donor cells

142
Q

Describe the minor cross match.

A

Donor serum
Recipient RBCs

–detects abs in the donor blood

143
Q

What signifies an incompatible cross match in the dog and cat? What about the horse and cow?

A

in the dog and cat- agglutination
in the horse and cow- hemolysis

144
Q

What does the direct antiglobulin test (DAT/direct Coombs’) detect?

A

antibody and/or complement attached to the membrane of the patient’s washed RBCs

145
Q

What is the difference in monovalent and polyvalent reagents for the Coombs’?

A

monovalent tests for one antibody or complement
polyvalent tests for multiple

146
Q

What does the indirect antiglobulin test (indirect Coombs’) detect? Describe the test.

A

detects anti-RBC antibody in the serum of the patient

patient serum is tested against washed RBCs of the sire, offspring, or prospective donor (can use supernatant from colostral milk instead of serum to detect reactions against the offspring’s cells)

147
Q

What test can be used to detect antibodies in DAT-negative canine AIHA but is primarily a research tool?

A

DELAT (ELISA based)

148
Q

What 3 things may cause hyperchromia?

A

hemolysis, Oxyglobin administration, and rare cases spherocytosis

149
Q

What would the M:E ratio look like in a patient with regenerative anemia?

A

it would be decreased because of erythroid hyperplasia

150
Q

Put these species in decreasing order of ability to mount a regenerative response
cat, cow, bird, horse, dog

A

Bird, dog, cat, cow, horse

151
Q

What 2 lab findings on the CBC may suggest regenerative response to anemia in the horse?

A

increased MCV and RDW

152
Q

How many days roughly does it take to start seeing signs of regeneration in the peripheral blood?

A

2-3 days

153
Q

Name 6 examples of conditions where you would expect a nonregenerative anemia.

A

AID, renal failure, iron deficiency anemia, aplastic anemia, pure red cell aplasia, and endocrine disorders

154
Q

Describe some major categories of causes of acute hemorrhage.

A

GI ulcers
Hemostasis defects (including hemophilia, DIC, toxicoses)
Neoplasia
Thrombocytopenia
Trauma
Surgery

155
Q

Describe some major categories of causes of chronic hemorrhage.

A

GI ulcers
Neoplasia
Hemophilia
Parasitism
Vit K deficiency

156
Q

In acute blood loss, describe the laboratory findings directly after the blood loss, within a few hours, and within a few days.

A

Within a few hours, the Hct is normal because all blood components are lost together. The spleen contracts to get high Hct blood into circulation so the Hct may be temprarily high.
Within 2-3 hours the blood volume is restored by addition of interstitial fluid, and you’ll start to see lab signs of anemia and +/- hypoproteinemia.Platelet numbers usually increase. Neutrophilia usually w/i 3 hours.

48-72 hrs polychromasia and reticulocytosis are evident, plasma protein levels increase (return to normalize before Hct, RBC, and Hb conc)

Hemogram back to normal in 1-2 weeks if single hemorrhage

157
Q

What are some lab findings in cases of chronic blood loss?

A

regeneration but less intensely than acute blood loss

hypoproteinemia

peristent thrombocytosis

iron deficiency anemia may develop as iron stores are depleted

158
Q

Are reticulocyte counts typically higher in hemolytic anemias or external hemorrhages? Why?

A

Hemolytic anemias because iron from hemolyzed erythrocytes is more readily available for erythropoeisis than is storage iron or hemosiderin.

159
Q

What are some lab findings that may be found in cases of hemolytic anemia?

A

Reticulocytosis

Normo or hyperproteinemia

Hemoglobinemia if intravascular

Neutrophilic leukocytosis

Hyperbilirubinemia

Hemoglobinuria

Abnormal RBC morphology based on the cause of the hemolysis

160
Q

What are the 3 main RBC membrane antigens that are recognized in antibody/C3b mediated hemolysis?

A

Glycophorins, band 3, and spectrin

161
Q

What are 5 major mechanisms leading to immune-mediated hemolytic anemia?

A
  1. idiopathic (AIHA)
  2. Infectious agents–> alter RBC membrane to expose hidden antigens or from adsorption of immune complexes to the membrane in response to the pathogen
  3. Drugs that adsorb to the RBC membrane and act as a hapten
  4. Alteration in the immune system from lymphoid cell function disturbances or anything that triggers the immune system like infections or cancer
  5. Paraneoplastic response to lymphoma or multiple myeloma
162
Q

What does the direct antiglobulin or Coombs’ test detect?

A

warm-active IgG alone, IgG plus C3, C3 alone, and rarely cold-active IgM on the RBC membrane

163
Q

What is cold agglutinin disease?

A

When cold-reactive IgM on the surface of RBCs fixes complement in the absence of IgG

Associated with autoagglutination, IV hemolysis, acute onset, and severe signs

164
Q

What is the significance of cold agglutinins that bind to RBC membranes below 10 to 15 degrees C?

A

They are usually insignificant and observed in blood specimens from many healthy animals.

165
Q

What are 4 examples of RBC changes resulting in decreased RBC deformability which could lead to extravascular hemolysis?

A
  1. Schistocytes
  2. Spherocytes
  3. Parasitized RBCs
  4. Eccentrocytes or Heinz body-containing RBCs
166
Q

What are 4 situations that may make an RBC susceptible to removal from the circulation?

A
  1. antibody and/or C3b mediated
  2. decreased deformability
  3. reduced glycolysis and ATP content of the RBC (aging)
  4. increased macrophage phagocytic activity
167
Q

What are some lab abnormalities that may be seen with extravascular hemolysis?

A
  1. regenerative response
  2. normal or increased plasma protein
  3. NO hemoglobinemia/uria
  4. hyperbilirubinemia is hemolysis is of great enough magnitude
  5. Hct may be normal if compensated by the bone marrow
  6. neutrophilia, monocytosis, thrombocytosis are common
  7. splenomegaly from EMH and incr mac activity
168
Q

What are 2 examples of hereditary causes of hemolysis? Which breeds are represented in each of these diseases?

A

Phosphofructokinase deficiency- American Cocker Spaniel, English Springer Spaniel, mixed breeds with Spaniel heritage

Pyruvate kinase deficiency- Basenji, Beagle, Chihuahua, Dachshund, Pug, Miniature Poodle, West Highland White, Eskimo, Cairn Terrier, Abyssinian, Somali, DSH

169
Q

What additional tests can be done in a case of suspected extravascular hemolysis to confirm?

A

Coombs’ (+)

DELAT (+)

170
Q

Which antibody is very affective at fixing complement, making it responsible for many of the cases of complement-mediated hemolysis?

A

IgM

171
Q

If complement is fixed to C3, this promotes ____ and results in extra/intravascular hemolysis.

If complement is fixed to C9, this promotes ____ and results in extra/intravascular hemolysis.

A

If complement is fixed to C3, this promotes phagocytosis and results in extravascular hemolysis.

If complement is fixed to C9, this promotes formation of the MAC and a membrane pore and results in intravascular hemolysis.

172
Q

What are the major mechanisms of intravascular hemolysis?

A
  1. Complement-mediated lysis
  2. Physical injury
  3. Oxidative injury
  4. Osmotic lysis
  5. Other- castor bean, snake venom, bacterial toxins, Babesia infections
173
Q

Oxidants affect the erythrocyte in which 3 ways?

A
  1. denaturation of Hb with heinz body formation
  2. oxidation and cross-linking of membrane proteins with eccentrocyte formation
  3. oxidation of Hg iron (Fe2+) with the formation of metHg (Fe3+)– interferes with O2 transport but doesn’t cause anemia
174
Q

What are the 2 major pathways that protect the RBC from daily exposure to oxidants?

A
  1. reduced glutathione (kept in reduced state by pentose phosphate pathway)
  2. iron is maintained in the reduced state by methemoglobin reductase
175
Q

What would happen in a patient with methemoglobin reductase or glucose-6-phosphate dehydrogenase deficiency?

A

These are enzymes necessary to protect the RBC membrane from oxidant injury so you would get changes indicative of oxidant injury (heinz bodies, metHg, eccentrocytes)

176
Q

What are some ways a cell can become susceptible to IV hemolysis secondary to osmotic lysis?

A

hypophosphatemia (esp in patients with diabetes)

membrane alterations that allow water to leak into the cell

hypotonic IV fluids

cold hemoglobinuria in cattle

177
Q

What are some lab abnormalities that can be seen in cases of IV hemolysis?

A
  1. Hx of drug, plant ingestion, recent transfusion or colostrum ingestion
  2. regenerative response (may not be evident for 2-3 days)
  3. hemoglobinuria**
178
Q

Hemoglobinemia is usually detected by:

  1. ___ discoloration of plasma
  2. Increased/decreased MCHC & MCH
  3. Increased/decreased serum haptoglobin and hemopexin concentrations.
A
  1. Red discoloration of plasma
  2. Increased MCHC & MCH
  3. Decreased serum haptoglobin and hemopexin concentrations
179
Q

When does hyperbilirubinemia first occur in cases of a hemolytic episode?

A

bilirubin isn’t formed until 8-10 hours after the onset of the hemolytic crisis

180
Q

What are the CBC findings in aplastic anemia?

A

Pancytopenia (nonregenerative anemia, granulocytopenia, and thrombocytopenia)

181
Q

Normocytic, normochromic anemia with normal to increased neutrophil and platelet counts and an increased M:E ratio caused by hypocellular erythroid marrow

These general types of anemia include which types of diseases (5)?

A
  1. Anemia of erythropoietin lack (chronic renal disease, endocrinopathies)
  2. AID
  3. FeLV-associated nonregenerative anemias
  4. Pure red cell aplasia
  5. Trichostronglye infection, liver disease, Vit E deficiency (unknown mechanisms)
182
Q

What cells in the kidney make Epo?

A

peritubular interstitial cells

183
Q

What are 4 mechanisms for the development of nonregenerative anemia in cases of chronic renal failure?

A
  1. Epo deficiency from destruction of peritubular interstitial cells
  2. hemolysis from factors in uremic plasma
  3. GI hemorrhage from abnormal platelet function and vascular lesions
  4. inhibitors of Epo in uremic plasma
184
Q

AID is mediated by which peptide?

A

hepcidin

185
Q

What are the mechanisms of nonregenerative anemia in AID?

A

decreased hepcidin, decreased marrow responsiveness to Epo, blunted Epo release, impaired availability of iron to the RBC, shortened RBC lifespan

186
Q

What are 7 lab findings in AID?

A
  1. decreased normal serum iron concentrations
  2. decreased to normal total iron-binding capacity
  3. normal to increased serum ferritin concentration
  4. normal to increased bone marrow macrophage iron stores
  5. mild to moderate anemia that is usually nonprogressive
  6. normocytic, normochromic RBCs
  7. rarely microcytosis and hypochromia (must be very chronic)
187
Q

Normocytic, normochromic anemia with neutropenia (except in myeloproliferative disorders) and/or thrombocytopenia, variable M:E ratio, generalized bone marrow hypocellularity and/or proliferation of abnormal cells

These types of anemia include the following:

A
  1. aplastic anemia or pancytopenia
  2. myelophthisic anemia
  3. nonregenerative anemias from infectious agents
188
Q

Aplastic anemia/pancytopenia is a disease of what type of cell?

A

multipotential stem cell in the bone marrow (or it can result from a disrupted bone marrow microenvironment)

189
Q

Does anemia, thrombocytopenia, or leukopenia develop first in cases of aplastic anemia?

A

Leukopenia and thrombocytopenia happen before anemia because of their shorter lifespans

190
Q

What are 5 casues of aplastic anemia?

A
  1. Idiosyncratic drug reactions– late estrogen toxicosis in dogs, chloramphenicol toxicosis in cats, phenylbutazone, TMS, albendazole
  2. Chemicals and plants (bracken fern)
  3. Irradiation
  4. Cytotoxic T cell or antiobdy mediated
  5. Infectious agents (FeLV, ehrlichia)
191
Q

What are 5 examples of myelophthisic anemia?

A
  1. myeloproliferative disorders
  2. myelofibrosis
  3. osteosclerosis
  4. diffuse granulomatous osteomyelitis
  5. metastatic cancer
192
Q

Microcytic, hypochromic anemia with variable neutrophil and platelet counts, and usually a hypercellular marrow with a variable M:E ratio

Causes of this type of anemia include:

A
  1. Iron deficiency
  2. Pyridoxine deficiency
  3. Copper deficiency
  4. Dyserythropoiesis in English Springer Spaniels
  5. Microcytosis without anemia in Asian breeds
  6. Microcytosis with mild anemia in shunts
  7. Drugs or chemical (chlormaphenicol, lead)
193
Q

What does iron deficiency look like in the bone marrow early on? What about when it’s more chronic?

A

Early on iron deficiency is associated with ineffective erythropoeisis and a hyperplastic marrow. With chronicity, the marrow becomes hypoplastic and microcytosis and hypochromia are more evident.

194
Q

What are lab findings in iron deficiency anemia?

A
  1. decreased serum iron concentrations
  2. low percent saturation of transferrin
  3. TIBC is often within the reference interval or increased
  4. decrease/absence of marrow macrophage iron stores
  5. decreased serum ferritin concentration
  6. increased free erythrocyte protoporphyrin
  7. microcytosis
  8. hypochromasia
  9. poikilocytosis
  10. hypercellular BM early on with disporportionate number of late rubricytes and metarubricytes from extra cell divisions
  11. low serum hepcidin concentrations
195
Q

T/F: Hypochromia often precedes microcytosis in cases of iron deficiency.

A

False– Microcytosis often precedes hypochromasia in cases of iron deficiency.

196
Q

What is pyridoxine and how does it lead to an iron-lack anemia?

A

it is a vitamin and is a cofactor in heme synthesis; without it, there is a failure to utilize iron

197
Q

How does copper deficiency lead to iron deficiency?

A

Copper-containing ceruloplasmin and hephaestin are important in iron absorption and transfer between intestine, macrophages, and transferrin.

198
Q

How do the elliptical erythrocytes of members of Camelidae family appear in cases of iron deficiency?

A

they are microcytic and have irregular or eccentric areas of hypochromasia representing irregular Hg distribution

199
Q

Macrocytic, normochromic anemia with variable neutrophil and platelet counts, M:E ratio is usually low because of hypercellular erythroid marrow

Cases of this type of anemia include:

A
  1. ruminants grazing on cobalt-deficienct or molydbenum-rich pastures
  2. Vit B12 and folic acid deficiencies
  3. erythremic myelosis or erythroleukemia
  4. congenital dyserythropoiesis and progressive alopecia of polled Hereford calves
  5. FeLV infection
  6. macrocytosis of Poodles
200
Q

What are some blood smear/bone marrow findings in cases of Vitamin B12/folic acid deficiencies?

A
  1. megaloblastoid erythroid precursors in the BM
  2. enlarged, hypersegmented neutrophils in the blood smear
  3. hypercellular BM indicating ineffective erythropoiesis
201
Q

Common clinical pathology findings in animals with polycythemia vera include:

  1. Epo- increased, normal or decreased?
  2. PO2- increased, normal or decreased?
  3. Platelets and leukocytes- increased, normal, or decreased?
A
  1. Epo- usually in the reference interval or decreased
  2. PO2- within the reference interval
  3. Platelets and leukocytes- sometimes low
202
Q

What is secondary absolute polycythemia?

A

Caused by increased Epo secretion

203
Q

What are causes of appropriate compensatory secondary absolute polycythemia?

A

occurs during chronic hypoxia (low PO2) like in-

  1. high altitude
  2. chronic pulmonary disease
  3. cardiovascular anomalies with right to left shunting of blood
204
Q

When does inappropriate secondary absolute polycythemia occur?

A

in some cases of hydronephrosis or renal cysts, Epo-secreting neoplasms, and endocrinopathies

normal PO2 and no hypoxia

Duncan and Prasse (2 decks)

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