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Clin Path > exam 1 > Flashcards

exam 1 Flashcards

1
Q

How do you calculate your absolute nuke the blood cell differential values?

A

% × total nucleated cell count

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2
Q

How do you calculate your absolute reticulocyte count?

A

% reticulocyte × RBC

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3
Q 
You need to collect blood for a CBC, what color top tube would you use?
A. Red
B. Lavender
C. Blue
D. Gray
E. Green
A

B. Lavender

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4
Q 
What color tube what you use for coagulation test?
A. Red
B. Lavender
C. Blue
D. Gray
E. Green
A

C. Blue

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5
Q 
What color to what you use to separate the serum from rbc's? 
A. Red
B. Lavender
C. Blue
D. Gray
E. Green
A

A. Red

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6
Q

How much blood is approximately needed to run a CBC and a biochemical profile?B

A

Approximately 5 mL of blood

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7
Q

What size needle should you not use any smaller than filling tubes with blood?

A

20gauge needle

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8
Q

How fast do you need to analyze blood for CBC?

A

Within an hour. You can also make a blood film and then refrigerate the tube.
*Don’t refrigerate the blood film.

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9
Q

What happens if you let the blood sent at room for 24 hours?F

A

Erythrocytes will swell resulting in an increase in MCV

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10
Q

What are the steps in doing biochemical profile with blood? (3)

A
  • Blood allowed to clot for 15 to 30 minutes -Centrifuge
  • Separate serum from clot using pipette

*Refrigerate harvested serum until analyzed Freeze if can’t analyze within two days
Some serum enzymes are not stable, but most are.

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11
Q

What are the five basic hematologic techniques? T

A
  • Blood mixing
  • Packed cell volume by centrifugation
  • Plasma protein estimation by refractometry
  • Preparation of blood film
  • Differential leukocyte count
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12
Q

What is another name packed cell volume (PCV)?

A

Hematocrit

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13
Q

How much should you fill the tube?

A

70 to 90% of its length

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14
Q

Will you find in your buffy coat? (3)

A

– Leukocytes
– nucleated erythrocytes
– platelets

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15
Q

If you see a yellow pigmentation in your plasma what would you think will cause this?

A

Icterus, where in March and was it may be due to carotene pigments associated with diet.

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16
Q

What could cause a white/opaque plasma?

A

Lipemia (chylomicrons) which is due to postprandial collection or may be due to diseases associated with abnormalities in lipid metabolism

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17
Q

What could cause a red coloration in plasma?

A

Hemoglobin due to hemolysis
*May be in-vitro due to technique or presence of lipemia. May be in-vivo due to hemolytic anemia (intravascular hemolysis). If PCV not decreased, likely in-vitro.

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18
Q

What can artificially increase a protein estimate done by refractometry?P

A

Lipemia, along with urea, glucose, and cholesterol.

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19
Q

If you have an increased TP and PCV, what does it suggest?

A

Dehydration

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20
Q

If you have a decreased TP and PCV, what does it suggest?

A

Blood loss

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21
Q

What is mean cell hemoglobin concentration (MCHC)?
How/why would it be increased?
How can it be decreased?

A

– it counts the hemoglobin in your blood.
– It could be increased by many reasons including: hemolysis, lipemia, or Heinz bodies (is an artifact/issue from collection)
– decreased may be due to an iron deficiency, or due to the presence of many reticulocytes (associated with regenerative anemia)., L

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22
Q

What is red cell distribution width (RDW)?

A

It describes the relative width of the size distribution.O

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23
Q

What stain causes reticulocytes to be polychromatic?

A

Wrights stain

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24
Q 
Which of the animals below do not release reticulocytes?
A. Cats
B. Dogs
C. Horses
D. Cows
A

C. Horses

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25
Q

What the monocytes become?

A

Macrophages

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26
Q

What is the purpose of the eosinophils?

A

Modulation of immune complex reactions, modulation of allergic inflammation, defense against parasites, etc.

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27
Q

What can you find it in basophils?

What would it increase in concentration of these mean?

A

Histamine, heparin, and numerous other proteins.

It’s related to a parasitic infestation.

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28
Q

What does penia mean?

A

Decreased concentration of cells

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29
Q

What does philia/cytosis it mean?

A

Increased concentration

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30
Q

What does a left shift referred to in blood?

When would you see this?

A

An increase in concentration of immature neutrophils in the blood.

Neutrophilia, normal concentration of neutrophils, or neutropenia. If neutropenia more severe inflammatory response.C

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31
Q

What does orderly maturation mean?

What happens if it’s not orderly?M

A

– Concentration of each cell increases with the degree of maturity. In other words, if a left shift is orderly, there should be more bands than metamyelocytes, and more segmented neutrophils than bands.

–IF it is disorderly, consumption is very severe, or a neoplastic process is present (leukemia).

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32
Q

What is leukemia?

A

Presence of neoplastic cells in the blood or bone marrow.

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33
Q

What can cause a neutrophil toxic change?

A
  • Due to accelerated rate of production seen with inflammation, which results in persistence of ribosomes.
  • Increased basophilia of cytoplasm
  • Presence of Dohle bodies
  • Cytoplasmic vacuolation
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34
Q

True or false: you are more likely to see an excitement leukogram in a dog than a cat.

A

False. It is seldom seen in dogs.

*Lymphocytosis is the most prominent feature of feline excitement response.S

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35
Q

A lack of steroid response in a sick animal should trigger what consideration?

A

Hypoadrenocorticism

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36
Q

What will distinguish information from excitement and stress?

A

A left shift

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37
Q

What could cause lymphopenia? (Gen.) (3)

A

Steroid response, acute viral infections, immunodeficiency (rare)

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38
Q

What could cause monocytosis? (2)

A

Information, stress response

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39
Q

What could cause eosinophila? (3)

A
  • Parasitism
  • Hypersensitivity
  • Lesions producing eosinophil chemoattractants, such as mast cell tumor

*basophilia usually accompanies eosinophilia.

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40
Q

If you see a Schistocyte, what would you expect the disease to be?

A

DIC, or iron deficiency anemia

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41
Q

What can cause Heinz body anemia in small animals?(6)

A

-ACETAMINOPHEN (CATS)
-PROPYLENE GLYCOL (CATS)
-ILLNESS (CATS)
(lymphoma, hyperthyroidism, diabetes)
-ONIONS (ALL SPECIES), garlic powder
-CEPHALOSPORINS (DOGS)
-Zinc toxicosis (penny ingestion)

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42
Q

What can cause Heinz body anemia in large animals? (horses, cattle, sheep)

A 
Horses:
-Phenothiazine
-Wilted red maple leaves
Cattle:
-Kale
-Onions
Sheep:
Copper toxicosis
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43
Q

If you see a significant amount of Basophilic stippling in small animals you should consider what?

A

Lead poisoning

*normal to see in ruminants. May see with very regenerative anemia in cats and dogs.

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44
Q

What are the five red blood cell parasites of dogs and cats that we need to worry about? N

A
  • MYCOPLASMA HAEMOFELIS
  • CYTAUXZOON FELIS -MYCOPLASMA HAEMOCANIS
  • BABESIA CANIS & GIBSONI
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45
Q

What are the three ways you can have anemia?

A

– Increase loss (hemorrhage)
–increased destruction (hemolysis)
– decreased production by bone marrow

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46
Q

Define anemia.

A

Decrease in red blood cell mass, resulting in decreased oxygenation of tissues.

*Decreased oxygenation results in numerous clinical signs.

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47
Q

What are some clinical signs associated with one destruction? (3)

A

– Splenomegaly
– icterus (jaundice)
– hemoglobinuria

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48
Q

Which is more severe for clinical signs, slow onset or rapid onset?

A

Rapid onset

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49
Q

What are the two different types of anemia?

A

Regenerative and non-regenerative

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50
Q

Where the two types of regenerative anemia?

A

– Blood loss (acute or chronic)

– blood destruction

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51
Q

In acute blood loss what happens to the protein in relation to PCV?

A

Protein decreases along with PCV.

*Erythrocyte morphologies usually normal (hemangiosarcoma in dogs is an exception)

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52
Q

List some examples of acute blood loss. (4)

A
  • TRAUMA & SURGERY
  • COAGULATION DISORDERS • BLEEDING TUMORS
  • THROMBOCYTOPENIA*
  • BLOOD LOSS DOES NOT CAUSE THROMBOCYTOPENIA
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53
Q

List some examples of chronic blood loss. (3)

A
  • GI ULCER
  • BLEEDING GI TUMOR
  • BLOOD CONSUMING PARASITES(90% has to do this)

*LOSS VIA INTESTINE MOST COMMON

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54
Q

What is the cause of iron deficiency anemia in nursing animals and adult animals?

A

Nursing: inadequate intake

adults: almost always do to chronic blood loss

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55
Q

Review anemia slide set slides 29-31, 34-35, 72-73, 83-87, 90-93, 98, 100, 103, 105, 107, 109-111, 114, 119, 121-126, 131-132, 135-144

A

Look at Them!!!

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56
Q

What are the 2 categories of blood destruction?D

A

Intravascular hemolysis and extravascular hemolysis

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57
Q

What might you see with blood destruction?

A 
– General signs associated with anemia
– splenomegaly
– hyperbilirubinemia, icterus
– hemoglobinemia
– hemoglobinuria
– total protein normal
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58
Q

IMHA is often _____ two other disorders or events. Examples are infection, modified live virus vaccination, neoplasia, drugs, etc.

A

Secondary

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59
Q

What drugs are associated with IMHA? (4)

A

Penicillin, cephalosporins, trimethoprimsulfamethoxazole, levaminsole

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60
Q

What is IMHA associated with horses and cats?

A

Horses: penicillin clostridial infection, and neoplasia.
Katz: Mycoplasma haemofelis, FeLV, neoplasia.

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61
Q

IMHA is more common in dogs than other species (or easier to recognize). List breeds most likely found in.

A

Cocker spaniels, poodles, collies.

*Incidence is slightly higher in females usually middle-aged to old, but also young.

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62
Q

If you see IMHA and thrombocytopenia what might be?

What would you expect the leukogram to be?

A 
Immune mediated (Evans syndrome)
DIC common with IMHA (also pulmonary thrombi)

inflammatory

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63
Q

What are the differential diagnosis for spherocytosis? (5)

What is the prognosis? I

A
  • Previous mismatched blood transfusion
  • Rattlesnake evenomation
  • Heinz body anemia in horses can look like spherocytes
  • Zinc toxicosis
  • Bee stings

Mortality rate:25% to 50%
*usually die of thromboembolism. Recurrence is common.R

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64
Q

What would you expect to see cell wise with IMHA?

A

Secure sites, a agglutination, neutrophilia with left shift, thrombocytopenia

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65
Q

What is neonatal isoerythrolysis?

A

Maternal antibodies against the neonates blood group antigen attached to the neonates RBCs, with subsequent RBC hemolysis.

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66
Q

What parasites cause intravascular hemolysis?

A

Babesia and Theileria cause intravascular hemolysis

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67
Q

What are the clinical signs of M haemfelis? (7)

A 
• Those of anemia
• Splenomegaly
• Fever
• Lethargy
• Sometimes icterus
• Concurrent disease, immunosuppresion, or splenectomy may predispose.
• Regenerative anemia UNLESS
Underlying disease, such as FeLV or severe inflammatory disease.

*FeLV and FIV titers indicated

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68
Q

How do you treat M haemfelis?

A
  • Blood transfusion if anemia severe -Prednisone will suppress -RBC destruction -Doxycycline for 3 weeks
  • Enrofloxacin if problems with doxycycline

**(Cats likely remain carriers)*

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69
Q

What transmits Feline cytauxzoonosis? Is a fatal? How do you treat it?

A
  • Transmitted by ticks (common in Missouri)
  • Almost always fatal
  • Rx with diproprionate or diminazine aceturate.
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70
Q

What can cause methemoglobinemia in cats, cows, and horses?

A

Cats: acetaminophen toxicity

cows: nitrite poisoning (rumen bacteria reduce nitrates to nitrites)
horses: red maple leaf ingestion

*congenital deficiency of NADH-methemoglobin reductase

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71
Q

What is methemoglobin?(refers to iron)

A

Iron is in ferric state, incapable of carrying oxygen. oxidative compounds result in excessive formation. Oxidative damage also causes Heinz body formation.

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72
Q

If blood appears to be chocolate brown, what can you assume?

At what concentration of methemoglobin will an animal die?

How can you treat this? A

A

30% of hemoglobin is methemoglobin

90%

use methylene blue to reduce methemoglobin to deoxyhemoglobin (activates methemoglobin reductase)

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73
Q

Where does copper accumulate in with copper toxicosis? Who is susceptible?S

A

It accumulates in the liver. Sheepare susceptible

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74
Q

What Clostridium is responsible for causing hemolytic anemia in lambs and calves? What is another name for this disease?

A

Clostridium perfringins type a

yellow lamb disease

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75
Q

What Clostridium is responsible for red water disease/bacillary hemoglobinuria?

What animal is usually affected?

What is it associated with?

What are the signs?

A

Clostridium hemolyticum

Cattle

Liver fluke migration

anemia, arched back, bloody diarrhea, fever, dyspnea, hemoglobinuria(+/-)

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76
Q

Look at the slides 4, 5, 8, 11, 13, 14-17, 38

slide set number 6 non-responsive bone marrow

A

Look at them

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77
Q

What is helpful in the diagnosis of a non-regenerative anemia?

A

–Biochem profile (anemia of renal disease)
–Bone marrow aspirate
– size (only help for FeLV macrocytosis)
– RBC morphology (usually not helpful)

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78
Q

What can you see if there’s anemia due to bone marrow problems?T

A

If generalized all cell lines will decrease.

RBC production problem only
– hypoplasia: red cell production decreased
– aplasia: no red cell production

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79
Q

What agents can cause aplastic anemia?

A

FeLV, ehrlichia canis, EIA (a lentivirus)

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80
Q

What is immune mediated aplastic?

A

Antibodies directed against stem cells.

*Maybe drug-induced. Maybe idiopathic

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81
Q

What are the intrinsic factors that can cause erythroid hypoplasia? (3)i

A

Myelodysplasia, leukemia, immune mediated destruction of erythroid precursors

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82
Q

What are the extrinsic factors that can cause erythroid hypoplasia? (3)

A

Chronicling the seas, endocrine disorders, inflammatory disease.h

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83
Q

What would you expect to see with anemia of an inflammatory disease?

A

– mild to moderate anemia
– low serum iron
– increased storage iron

*erythroid suppression may be due to unavailability of iron, or inflammatory cytokines

84
Q

What are the types of endocrinopathy related anemias? (2)

A

Hypothyroidism, hypoadrenocorticism (Addison’s disease)

85
Q

What would you see anemia wise with hypothyroidism?

A 
Mild anemia (usually 30%)
decreased metabolic rate
86
Q

What would you see anemia wise with hypoadrenocorticism (Addison’s disease)?W

A

Mild anemia often masked by dehydration.

*Mechanism is unclear

87
Q

Look at the slides 16,

in 7. bone marrow aspiration and interpretation slide set.

A

Look at slides

88
Q

What are the five indications you should do a bone marrow aspiration?

A
  1. Non-regenerative anemia
  2. Neutropenia
  3. Thrombocytopenia
  4. Suspected neoplasia or monoclonal gammopathy
  5. To better classifyleukemia
89
Q

Where should you take a bone marrow aspirate from?

A

Trochanteric fossa or humorous.

90
Q

True or false: local or general anesthesia is needed before doing a bone marrow aspirate.

A

True

91
Q

What size needle do you need to do a bone marrow biopsy?

A

16 to 22gauge needle

92
Q

What should you do when trying to take a bone marrow biopsy?

A

Avoid diluting with blood

93
Q

True or false: if you don’t use EDTA and are doing a bone marrow aspirate you need to make the slide (film) very quickly.

A

True

*you have about 30 seconds to make a film.

94
Q

After you place the bone marrow aspirate on the slide what should you do?

A

Are dry and use Wright’s stain

95
Q

If you are unable to obtain a bone marrow aspirate what should you do?

A

Take a core biopsy for histopathology.

96
Q

What is the normal ratio for the number of granulocytes to nucleated erythrocytes?

What is another name for this ratio?

A

1:1 up to 3:1 is normal

M:E ratio

97
Q

What does an increased M:E ratio mean? (4)

A

Erythroid hypoplasia or achalasia and/or granulocytic hyperplasia, granulocytic leukemia

98
Q

What does a decreased M:E ratio mean?

A

Lack of production of neutrophils, or an increase in RBC production.

99
Q

What other cells might you see in a bone marrow aspirate? (6)

A

Plasma cells, lymphocytes, macrophages, mast cells (common in dogs), osteoblasts and osteoclasts (rare to see in bone marrow aspirate)

100
Q

What microorganisms might you see in the bone marrow aspirate? (4)

A

Histoplasma capsulatum Toxoplasma gondii Leishmania donovani Red cell parasites

101
Q

What does homeostasis mean?

A

Stoppage of blood

102
Q

How do you achieve the goal of homeostasis without obstructing blood flow?

A

You need interaction of: (blood vessels, platelets, coagulation factors) = fibrin formation and fibrinolysis. Or thrombus formation (blood clot)

103
Q

Look at slide number 12 slide set number 8

A

.

104
Q

How long does the platelet last? (It’s lifespan)

A

3 to 5 days

105
Q

How much the spleens mass is taken up my plate?

A

1/3

106
Q

What are macro platelets suggestive of and what’s their size?

A

They are about the size of a red blood cell and they suggest an increase in the production

107
Q

Look at slide 15 – 17 in set 8

A

.

108
Q

What is the maturation time of a megakaryoblast to platelet release?

A

4 to 5 days

109
Q

Where is thrombopoietin(TPO) made? (List 2)

A

Liver and endothelium

*look at slide 18

110
Q

What are the functions of platelets? (3)

A

Increase metabolic activity, primary homeostasis, support secondary homeostasis.

111
Q

What happens during the formation of a primary and metastatic plug (primary homeostasis)?(KNOW THESE)

A 
– 3-5 minutes
– PLTs adhere to subendothelium
– Undergo activation (including shape change) 
– Secrete their granules
– Aggregate to form a platelet plug
112
Q

What is necessary for adhesion of the platelets?(4)

A 
*1. Von Willebrand factor (vWF)
– binds to GPIb on PLT surface 
– bridge b/w PLTs and collagen*
2. ADP
3. Ca2+
4. Serotonin
113
Q

What is one of the main things that happen during activation?

A

Shape change

114
Q

Why is shape change so important when it comes to the activation step of primary hemostasis?

A

• From smooth discs to spheres with many filopodia
• Occurs in response to thrombin
• ↑ surface area
*can increase surface area by 3 to 5 times. This will create a bigger area for secondary hemostasis to occur.

115
Q

What are the different steps during the activation stage of primary hemostasis? (4)

A

–Shape change
– flip the membranes
– carry a negative charge on the outer membrane surface
– the creation of granule products(look at slide 30 for more information on this step)

116
Q

What do the granule contents made during primary hemostasis stimulate?

A 
• Aggregation
– Irreversible process
– Fibrinogen binds activated PLTs and bridges adjacent PLTs
– Ca2+ is required
• Platelet plug formation
117
Q

Look at slide 32 of set8

A

.

118
Q

What are the important tests to find completely concentration and morphology (size)?

A

Blood smear and hematology analyzers

119
Q

What’s a good test to find out the production of platelets?

A

Bone marrow aspirate (BMA)

120
Q

Look at the slides 35 – 48. Set 8

A

.

121
Q

During your hematology analyzer test you see an increased MPV, what can this suggest?

A

Increased thrombopoiesis

122
Q

KNOW slides 50 – 66 set 8 this will be all over the exam.S

A

.

123
Q

Is there any disease specifically associated with thrombocytopenia?

A

Diagnostic problem, not a specific disease

124
Q

What are the clinical features of thrombocytopenia? (5)

A

– Mucosal bleeding
– Petechiation
– Ecchymosis
– Spontaneous hemorrhage: PLT count <20,000/μL – +/- Hemorrhagic anemia

125
Q

What are the mechanisms of thrombocytopenia? (6)

A 
– Loss(hemorrhage)
– consumption
– destruction
– decreased production
– abnormal distribution
– Pseudothrombocytopenia
126
Q

Can hemorrhage cause significant thrombocytopenia on its own? Any exceptions?E

A

Hemorrhage alone does not usually cause significant thrombocytopenia. an exception is acute severe hemorrhage may result in mild thrombocytopenia.

127
Q

What is meant by consumption as a mechanism of thrombocytopenia?A

A

Utilization of plates coagulation

128
Q

What are some of the causes of consumption (thrombocytopenia)?(3)

A

–Disseminated intravascular coagulation (DIC)
– vasculitis (Rickettsial disease, FIP)
– viral infection

129
Q

What is the degree of thrombocytopenia caused by consumption?

A

Mild to moderate

130
Q

When can hemorrhage occur during the consumption mechanism of thrombocytopenia?O

A

Hemorrhage occurs if there are coagulation defects (DIC) or leakage of blood from vessels (vasculitis).

131
Q

If you see a low number of platelet count to the point where you can have instant bleeding, what should you think? (Can be exam question)

A

Immune mediated thrombocytopenia (ITP)

132
Q

What are your primary and secondary causes of ITP?

A

Primary/idiopathic
secondary: drugs, viruses, sepsis, neoplasia

*LOOK AT SLIDE 57

133
Q

Look at slide 58

A

.

134
Q

Where the clinical signs of thrombocytopenia due to destruction? (2)

A

– associated with thrombocytopenia

– +/- anemia

135
Q

LOOK AT SLIDE 60

WILL BE ON EXAM

A

.

136
Q

If destruction is causing thrombocytopenia and you do a bone marrow aspirate, what would you expect to see?D

A

Increased megakaryocytes

  • look at slide 61
137
Q

In thrombocytopenia what could cause the decreased production? (3)

A

– Bone marrow hypoplasia
– neoplasia
– myelonecrosis or myelofibrosis

*look at slide 63

138
Q

Look at slide 65 & 66.

A

.

139
Q

What are the two major mechanisms of thrombocytosis?

A

Increased production and increased distribution plasma

140
Q

What are some diseases associated with thrombocytosis?

A

*– chronic inflammatory disease
– iron deficiency anemia
– chronic hemorrhage
– IMHA

*look at slide 69

141
Q

Look at slide 70.

A

.

142
Q

What are the two things you see in animals that are suspect for qualitative disorders?

What are the two causes?

A
  1. Clinical signs of thrombocytopenia (mucosal bleeding, petechiation, ecchymosis
  2. Normal platelet count

acquired causes and inherited causes (many intrinsic platelet defects identified)

143
Q

What are the required causes of qualitative disorders? (4)

A

Urania, drugs, fibrinogen degradation products (FDPs), paraproteins(slide 73 for this)

144
Q

What are some examples of drugs in acquired qualitative disorders?

A

Aspirin, Phenylbutazone, acetaminophen, NSAIDS, Some anesthetics, xanthine derivatives, and calcium
channel blockers.

145
Q

How does fibrin degradation products (FDPs) work?

A

Inhibit PLT function in disease process ( e.g.DIC)

146
Q

What are the inherited causes of qualitative disorders? (4)

A

– Absence of glycoprotein receptors
– Absence or reduction in platelet granules
– Signal transduction defects
– Von Willebrand’s disease

147
Q

KNOW SLIDE 75, 78-80.

A

.

148
Q

vWF is a carrier for what factor?

A

VIII

know slide 78

149
Q

What are the 2 types of coagulation factors in secondary hemostasis, and where are they made?

A

Enzymatic and non-enzymatic
synthesized in the liver

*look at slide seven set number nine

150
Q

What is required for the initiation of secondary hemostasis?

A

tissue factor

151
Q

Look at slide 21 and 23 in set number 9.

A

.

152
Q

What are the vitamin K dependent cofactors/proenzymes ? (4) know these for example

A

Factors/Proenzymes II, VII, IX, X. Is all done in liver.

*hint to help remember (2+7 = 9, which is close to 10)

153
Q

What is the key factor that promotes amplification of secondary hemostasis?

A

Thrombin

154
Q

What can inhibit the production of fibrin?

A

Antithrombin (AT)

155
Q

What is the drug that works to activate antithrombin, thus inhibiting fibrin formation?

A

Heparin

156
Q

What are the two primary test used for procoagulation activity?

A

Activated partial thromboplastin time (aPTT, PTT), and prothrombin time (PT)

157
Q

Look at slides for set 10.

A

.

158
Q

What are the two types of anticoagulant tests

A

Fibrinolytic activity, and inhibitor consumption.

159
Q

What does the fibrinolytic activity test?

A

Fibrin degradation products (FDPs) and D – dime

160
Q

What does inhibitor consumption test?

A

Anti- thrombin (AT)

161
Q

How the citrate plasma differ from what?

A

No RBCs, no WBCs, no PLT’s. Also decreased calcium (show latest by citrate)

162
Q

Look at slide eight on set 10

A

.

163
Q

What are the two intrinsic/common pathway test?
What did both tests test?
What is the significance of prolonged time?

A

Activated partial thromboplastin time (aPTT) and activated clotting time (ECT)

they both test for time

1) Deficiency or inhibition of any intrinsic or common pathway factor
2) Heparin therapy

164
Q

What does the activated partial thromboplastin time measure time for?

what percent efficiency is needed before you detect anything?

A

Fibrin clot formation inCitrate plasma plus contacted activator plus calcium plus PLT phospholipid substitutes

70%

165
Q

What does ACT measure?

What percent deficiency is needed before section?

A

Time for fibrin clot formation in non-anticoagulated whole blood

95%

166
Q

What does prothrombin time test?

A

Fibrin clot formation in citrated plasma plus tissue factor plus calcium plus late with Oslo lipid substitutes
(slide 18/10 )

167
Q

Look at slide 23/10

A

.

168
Q

When what you see an increase with FDPs?

A

Increased fibrinolysis, severe internal hemorrhage with fibrinolysis, decreased clearance of FDP by liver

169
Q

Look at slide 26/0

A

.

170
Q

Look at slide 29/10

A

.

171
Q

Look at slide 34-58/10

A

.

172
Q

What are some clinical features you would see with vitamin K deficiency?

A

Anemia, weakness, hypovolemia, shock, lameness, neurological signs, and even death.

173
Q

How would you treat vitamin K deficiency/warfarin toxicity?

A

Supplement with vitamin K, decontaminate, and use plasma and/or blood transfusions.

174
Q

What does DIC cause?

A

Continued activation of coagulation and fibrinolysis

175
Q

Know slide number 46/10

A

.

176
Q

Where the clinical signs associated with DIC?

A

Signs associated with signs of primary disease. Signs of organ dysfunction secondary to thrombosis. Bleeding (mucosal (PLT consumption), hemorrhage (factor consumption)).

177
Q

KNOW SLIDE NUMBER 51/10

A

.

178
Q

Slides 5 – 6/11 are terminology

A

.

179
Q

What are the two major dog blood type systems? (Not the DEA 1.1 and DEA 1.2, they are examples of one system)

A

The two systems are dog erythrocyte antigen (DEA) blood system and the Dal blood system.

180
Q

What are the seven different types of blood in the DEA blood system?

A

DEA 1.1, 1.2, DEA 3 –7

*dogs can have more than 1 RBC antigen (blood type)

181
Q

Which are the most immunogenic blood types of the DEA system?

A

DEA 1.1 (is 45% population) and DEA 1.2 (20% of population)

182
Q

Which blood types are considered to be the universal donors for dogs?

A

DEA 4+ and/or DEA 6+

183
Q

Which of the DEA blood types are expressed in 98% of dogs? (2 types)

A

DEA 4 and 6

184
Q

Look at slides 23-24/11

A

.

185
Q

Which DEA’s is reported in delayed transfusion reaction?L

A

DEA 3, 5, and 7

186
Q

What is the Dal blood system?

A

It’s a blood system with one single antigen (Dal) it is ubiquitous in non-Dalmatians.
*Look at slide 25/10

187
Q

What are the two blood systems for cats?

A

The AB group system and the Mik system.

188
Q

Do cats have a universal donor for blood?

A

No

189
Q

What should you do before giving of blood transfusion to any and all Cats?

A

Blood type

190
Q

In the AB group system what type it is most common?

A

Type A. 95% of cats have this type.

191
Q

What is the antigenic reaction of type A blood to a type B transfusion?

A

Weak

192
Q

What’s the percent you find of type B blood in cats? (brittish breeds in US)

A

25 – 50%

193
Q

What is the type B’s blood antigenic response to a type A transfusion?

A

Very strong. Can be severe and lethal transfusion reactions.

194
Q

What type of blood is the universal recipient in cats?

A

Type AB

195
Q

Look at slide 32-35/10

A

.

196
Q

How many blood systems do horses have?

Do they have in universal donors?

A

They have 7 blood systems

no universal donors
*slide 36/10

197
Q

What two types of blood are highly immunogenic in horses?

What is an implication with these two blood types? (Think of mother and foal)

A

Aa and Qa
Neonatal isoerythrolysis (NI)
*slide 37/10

198
Q

Will you see equine neonatal isoerythrolysis with the first foal?

A

No, it’s associated with the second

* slide 39-40/10

199
Q

What are the clinical signs of equine neonatal isoerythrolysis?

A

Lethargy, weakness, icterus, increased heart rate, increased respiratory rate. (All in foal)

severe cases: hemoglobinemia, hemoglobinuria, severe hypoxia leading to convulsions/coma/death

200
Q

Look at the slides 39-40, 47-50 set 11. equine neonatal isoerythrolysis

A

.

201
Q

What is the purpose of blood typing?

A

Identify specific RBC antigens

slide 52/10

202
Q

What are the different ways to blood type? (2) (slides 51-59 cover this)

A

typing cards and typing dipsticks

203
Q

On a typing card for canine blood what would agglutination mean?

A

Positive

204
Q

On a typing card for cats what would agglutination mean?

A

Type B

no agglutination= Type A

205
Q

On a canine blood typing dipstick, what would a strong line beyond the control mean?

A

DEA 1.1
*weak line= 1.2
no line=not 1.1 or 1.2

Clin Path (4 decks)

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