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clinical pathology > Lecture 4 > Flashcards

Lecture 4 Flashcards

1
Q

What species are reticulocytes NOT released in response to anemia

A

Horses

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2
Q

What are 2 ways to correct the reticulocyte percent

A

Calculate Absolute Reticulocyte count

Calculate corrected reticulocyte percent

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3
Q

How do you calculate the absolute reticulocyte count?

A

RBC count X uncorrected reticulocyte count as a decimal = absolute reticulocytes

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4
Q

How do you calculate the corrected reticulocyte percent?

A

(patient’s PCV/ mean norm. PCV for species) X uncorrected reticulocyte as a % = corrected reticulocyte percent

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5
Q

What are two causes of regenerative anemia?

A

Hemorrhage

Hemolysis

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6
Q

What are the 2 types of hemorrhage

A

External and internal

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7
Q

What are the features of external hemorrhage

A

RBC’s are lost
Iron is lost
Blood proteins are lost
If chronic, iron loss can be so severe RBC production stops
IF iron deficiency, non-regenerative anemia may develop

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8
Q

What are some causes of external hemorrhage

A

Trauma
Bleeding GI or UG lesions
Blood sucking parasites
some hemostatic disorders

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9
Q

What are the features of internal hemorrhage

A

RBC’s are NOT lost
Iron is CONSERVED and available to make new RBC’s
Blood proteins are NOT LOST
autotransfusion may occur from a hemoabdomen or hemothorax

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10
Q

What are some causes of internal hemorrhage

A

Trauma
Bleeding tumors of intra-abdominal or thoracic organs
some hemostatic disorders

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11
Q

What happens initially with acute hemorrhage?

A

Blood cells and blood fluid are both lost in equal amount
total blood volume is decreased
At first, PCV remains the same because relative proportion of blood cells to blood fluid is unchanged

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12
Q

What are the initial protective responses that occur to preserve oxygen delivery with acute hemorrhage?

A 
Heart rate and blood pressure increase
Splenic contraction (releases stored RBC's)
Body tissue fluids (interstitial fluid) slowly moves from tissues to blood vessels  so remaining RBC's and TP are diluted
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13
Q

What are 2 classic findings after hemorrhage?

A

anemia and panhypoproteinemia

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14
Q

What are the laboratory findings with acute hemorrhage

A

Initial findings may not reveal anything
Fluid shift starts 3 hrs post hemorrhage and continues for 2-3 days post hemorrhage

Decreased PCV and total protein will show up ~ 12-24 hours post hemorrhage

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15
Q

What are some factors that may influence the lab findings with acute hemorrhage?

A

Splenic contraction - increases PCV acutely
Autotransfusion - increases PCV slowly
Fluid therapy prior to transfusion can dilute the PCV and TP even more along with the interstitial fluid shift

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16
Q

How long does it take the regenerative response to anemia to appear in the blood

A

3-4 days

1 week in old or debilitated animals

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17
Q

When does the peak regenerative response occur

A

1 week post hemorrhage

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18
Q

is the regenerative response more or less dramatic in ruminants

A

less but more basophilic stippling

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19
Q

Because equids do not release reticulocytes what do we need to do evaluate the regenerative response?

A

Check PCV every few days

Check bone marrow

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20
Q

What are some things to remember when assessing regenerative anemia in horses?

A

Splenic contraction happens readily
Do not release reticulocytes or exhibit polychromasia
Freshly matured RBC’s are larger than older RBC’s so:
- MCV, RDW, and anisocytosis will be increased

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21
Q

What is the lifespan of RBC’s in circulation?

A

~100 days

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22
Q

How are old RBC’s removed

A

As RBC’s age, damage to the membrane occurs and the receptors on the membrane begin to trimerize which the macrophage recognizes and then engulfs the RBC

23
Q

What happens when RBC’s are broken down

A

Hemoglobin –> Heme + globin
Heme –> iron + unconjugated bilirubin

Useful nutrients from dead RBC’s are recycled ie. iron, amino acids
liver metabolizes bilirubin which is excreted in urine and feces

24
Q

What are the two classifications of hemolytic anemia

A

congenital and acquired

25
Q

Which classification of hemolytic anemia is more common

A

Acquired

26
Q

What is hemolysis?

A

abnormally increased rate of erythrocyte destruction

erythrocyte lifespan is reduced causing anemia

27
Q

The severity of the hemolytic anemia and clinical signs depend on:

A

how fast the RBC’s are destroyed

clinical signs also depend on the predominant site with in the body the RBC’s are being destroyed

28
Q

Where is the predominate site of Extravascular hemolytic anemia

A

macrophages in the spleen

29
Q

Where does intravascular hemolytic anemia occur

A

blood stream

30
Q

What are the features of Extravascular hemolysis

A

Abnormal RBC death occurs in a normal location (spleen)
Can be acute or chronic
Macrophages remove RBC’s as they pass through the spleen
DIC is possible

31
Q

What are the features of intravascular hemolysis?

A

Abnormal RBC death occurs in an abnormal location (blood stream)
Often acute (very rapid)
Circulating fragments or damaged RBC’s increase risk of DIC and anaphylactic shock

32
Q

Lysed RBC’s from intravascular hemolysis release what into the blood stream?

A

Free hemoglobin

33
Q

What does the circulating free hemoglobin cause?

A

Hemoglobinemia (plasma is pink or red)

34
Q

what protein mops up free hemoglobin and transports it to the liver

A

Haptoglobin

35
Q

What occurs when haptoglobin transport capacity is overwhelmed

A

Not all of the hemoglobin is captured by the haptoglobin and is excreted in the Urine HEMOGLOBINURIA

36
Q

How is bilirubin excretion affected if RBC destruction is severely rapid.

A

bilirubin excretion is first backed up in the urine and feces causing it to turn an orange color (bilirubinuria)
Then it backs up in the plasma causing (bilirubinemia)
Then it can eventually cause icteric mucocutaneous membranes

37
Q

What will you see with Extravascular hemolysis

A

Bilirubinuria
Bilirubinemia
Mucocutaneous icterus

38
Q

What will you see in Intravascular hemolysis that you won’t see in extravascular hemolysis?

A

Hemoglobinemia

Hemoglobinuria

39
Q

What are possible clinical findings with hemolytic anemia?

A

Anemia (low PCV and RBC)
TP - reflects hydration status
RBC morphology may reflect the underlying cause of hemolysis
Clinical signs of anemia
may have fever, organomegaly of spleen, liver, lymph nodes
discolored urine, feces, plasma, or membranes

40
Q

Abnormal RBC shape

A

Poikilcytosis

41
Q

Give the different names of abnormal RBC shapes

A 
Acanthocytes
Schistocytes
Keratocytes
Spherocytes
RBC ghosts 
Eccentrocytes and pyknocytes
42
Q

What are 2 abnormal RBC inclusions?

A

Heinz bodies

Infectious RBC parasites

43
Q

What abnormal RBC shape occurs usually as an artifact

A

Echinocyte

44
Q

What can cause echinocytes

A

IF RBC membrane sits in tube too long it loses ATP causing artifacts
can also be caused by inappropriate ratio of anti-coagulant

45
Q

What RBC shape occurs as a result of fragmentation or liver disease?

A

Acanthocytes

46
Q

What 3 things can cause fragmentation

A

Mechanical injury
Endothelial injury
Thermal injury

47
Q

What RBC shape is seen with DIC and fragmentation

A

Schistocytes

48
Q

What RBC shape is a red flag ofr Immune mediated hemolytic anemia

A

Spherocytes

49
Q

What do spherocytes look like?

A

smaller perfectly round RBC’s with no central pallor

50
Q

What RBC shape occurs as a result of Intravascular hemolysis

A

RBC ghosts

51
Q

How are RBC ghosts formed

A

macrophage undergoes complement mediated lysis of the cells / macrophage basically punches holes in the cell so hemoglobin leaks out into the blood and urine causing hemoglobinemia and hemoglobinuria

52
Q

What blood shape is formed from oxidative damage

A

Eccentrocytes

53
Q

What are the 3 targets for oxidative damage of RBC’s

A

Lipid membrane (becomes oxidized and pushes hemoglobin away)

Heme

Globin molecule

54
Q

What forms when the globin molecule undergoes oxidation and sticks to the cell membrane

A

Heinz bodies

clinical pathology (6 decks)

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