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Clin Path > Test Two > Flashcards

Test Two Flashcards

1
Q

Microcytic, hypochromic, non-regenerative, fragmentation morphology

A

Iron deficiency anemia

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2
Q

Where is the patient normally bleeding from in iron deficiency anemia?

A

GI Tract

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3
Q

Severe regenerative anemia with many polychromataphils/aggregate reticulocytes, macrocytic, hypochromic, spherocytes, inflammatory leukogram, microagglutination, ghost cells

A

IMHA

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4
Q

IMHA treatment

A

Prednisone and a transfusion

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5
Q

Mild, non-regenerative anemia, normochromic, normocytic

A

Anemia of chronic inflammatory disease- body thinks you have bacterial infection so it hides iron

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6
Q

What is a keratocyte

A

Two horns on RBC

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7
Q

What is an acanthocyte

A

Uneven spicules

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8
Q

What is a schistocyte

A

Sickle

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9
Q

What conditions may lead to fragmentation morphology

A

Hemangiosarcoma, iron deficiency anemia, DIC, liver disease

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10
Q

How does liver disease lead to fragmentation morphology

A

Cell membranes arent sound due to poor cholesterol metabolism

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11
Q

What is bilirubin

A

Breakdown product of hemoglobin

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12
Q

Where is bilirubin metabolized

A

The liver

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13
Q

What does being icteric mean and indicate

A

Jaundiced appearance, Liver isnt working well or you are lysing RBCs too fast and bilirubin is overwhelming the liver

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14
Q

What type of hemolysis is bilirubinemia associated with

A

Intravascular and extravascular

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15
Q

What is an indicator of intravascular hemolysis?

A

Hemoglobinemia (build up of hemoglobin in the blood)

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16
Q

How long do platelets last in circulation

A

10 days

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17
Q

What causes thrombocytosis

A

Increased platelets- caused by:

Inflammation, Cushing’s, Steroids, rebound from thrombocytopenia, splenectomy, iron deficiency anemia

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18
Q

What three factors increase thrombopoietin production

A

IL6, IL1, TNFa

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19
Q

What mechanism of inflammation causes thrombocytosis

A

Increased IL6, TNFa, IL1- increased thrombopoietin production

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20
Q

What mechanism of Cushings causes thrombocytosis

A

Cortisol inhibits macrophage ability to eat senescent platelets

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21
Q

Will hemorrhage cause thrombocytopenia

A

Not likely, unless most blood volume is lost or DIC is initiated

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22
Q

Why is a purple top tube used for clotting

A

K/EDta inhibits Ca2+ in blood so platelets cant clot

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23
Q

What does EDTA do

A

Chelates Ca2+ so blood doesnt blot

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24
Q

What tube is used in a PT/PTT test and why

A

Blue top- citrate; Citrate sequesters Ca2+ but is gentle enough that adding calcium to the reaction tube will start the clotting process

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25
Q

What role does calcium play in clotting

A

Positive charge mediates the binding of coagulation factor enzyme complexes via their negatively charged residues to the negatively charged phospholipid surface of platelets allowing scaffolding

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26
Q

What are alpha granules

A

In platelets, adhesion proteins like Von Willebrand’s factor

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27
Q

What species is most commonly vWF deficient?

A

Doberman Pinschers

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28
Q

What makes cat blood different

A

Higher MPV (mean platelet volume)- larger; sensitive to activation during blood collection

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29
Q

What kind of blood cells do snakes have

A

Thrombocytes- very large and are full cells

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30
Q

How do you do a platelet estimate

A

Count number of platelets in ten 100x oil immersion fields and average
Dogs- average count x 15,000 mcL
Cats- average count x 20,000 mcL

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31
Q

What is hemostasis

A

The arrest of bleeding

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32
Q

What does hemostasis require

A

Integrated response from the blood vessels, platelets, circulating clotting factors, fibrinogen getting converted to fibrin

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33
Q

What parts of the blood vessels are important in hemostasis

A

Endothelial cells, collagen, smooth muscle cells, fibroblasts

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34
Q

What is primary hemostasis

A

Peripheral vasoconstriction occurring- momentary stoppage before blood flows.

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35
Q

What is the mechanism of primary hemostasis

A

Platelets degranulate and release Ca2+ to form platelet plug

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36
Q

When does primary hemostasis occur-

A

Endothelial defect exposes subendothelial collagen

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37
Q

What is secondary hemostasis

A

Stimulation of the coagulation cascade

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38
Q

What is the mechanism of secondary hemostasis

A

Thrombin (factor 2a) converts fibrinogen (factor 1) to active fibrin (factor 1a)

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39
Q

How does fibrin have an effect on secondary hemostasis

A

Once it is cleaved to 1a (active fibrin), it is incorporated into the clot to stabilize

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40
Q

What is coagulopathy

A

Excessive bleedin due to abnormal function or lack of presence of a coagulation factor

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41
Q

Is coagulopathy a more severe feature of primary or secondary homeostasis

A

Secondary- usually leads to a more severe bleeding

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42
Q

What leads to hemoabdomens, hemothoraxes, hemarthrosis, hematuria, petechiae and purpura

A

Coagulopathy

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43
Q

What species have lower platelet counts

A

King Charles and Greyhounds

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44
Q

What condition is often inherited in KCC Spaniels

A

Inherited asymptomatic thrombocytopenia with macrocytic platelets (60-80k/mcL can be normal because their platelets are large)

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45
Q

What is MPV

A

Mean platelet volume

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46
Q

Large MPV indicates what

A

Young platelets - possible attempted bone marrow response to thrombocytopenia

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47
Q

What values will be effected by platelet clumps in blotted samples?

A

Decreased platelet count, increased MPV

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48
Q

What conditions would show an increased MPV

A

Clotted sample; enhanced thrombopoiesis responding to thrombocytopenia

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49
Q

What will cause petechiae, purpura or ecchymoses

A

Thrombocytopenia- platelets less than 50k/mcL

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50
Q

When will spontaneous hemorrhage from thrombocytopenia occur

A

Usually below 20k/mcL

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51
Q

Where should venipuncture occur in thrombocytopenic patients

A

Not the jugular- use peripheral vessels further from heart

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52
Q

What is a hallmark of tick borne illness

A

Thrombocytopenia

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53
Q

What makes up Evan’s syndrome

A

IMHA and ITP (immune mediated thrombocytopenia)

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54
Q

What conditions would lead to a diagnosis of thrombocytopenia

A

Decreased platelet production, increased platelet consumption, increased platelet destruction**

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55
Q

What is the most common differential of thrombocytopenia

A

Increased platelet DESTRUCTION

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56
Q

How can decreased platelet production be confirmed as a source for thrombocytopenia

A

Bone marrow aspirate to see if platelet precursors (megakaryocytes) are present in high enough quantities.

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57
Q

What is the precursor of platelets

A

Megakaryocytes

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58
Q

What could cause a lack of megakaryocytes

A

Myelophthisis, myeloproliferative diseases, aplastic anemia

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59
Q

What is myelophthesis

A
  • space occupying lesion of the bone marrow
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60
Q

What is aplastic anemia

A

bone marrow not making anything (ex. estrogen knocks out bone marrow in ferrets and dogs)

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61
Q

What conditions would lead to increased platelet consumption

A

DIC, thrombosis, vasculitis, hemangiosarcoma in dogs

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62
Q

What changes would be shown on bloodwork if a patient has increased platelet consumption?

A

Changes to PT/PTT

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63
Q

What causes increased platelet destruction

A

The most common cause of thrombocytopenia!!
ITP (primary autoimmune thrombocytopenia)
Secondary immune-mediated thrombocytopenia

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64
Q

What are the causes of secondary immune-mediated thrombocytopenia

A

Drugs, infection, neoplasia, SLE

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65
Q

What clotting factors rely on Vitamin K

A

2, 7, 9, 10 (2 + 7 = 9 , 10)

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66
Q

What are the clotting factors of the intrinsic pathway

A

PTT- 12 11 9 8

common- 10 5 2 1

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67
Q

What are the clotting factors of the common pathway

A

10 5 2 1

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68
Q

What are the clotting factors of the extrinsic pathway

A

7a, TF (tissue factor)

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69
Q

How does rodenticide work

A

Vitamin K antagonist inhibits enzyme K epoxide reductase in the liver to make the K-associated factors (2, 7, 9, 10) less functional

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70
Q

How will bloodwork show in patients with rodenticide poisoning

A

Because 2, 7, 9, and 10 are the factors affected, you would think PT would be delayed by factor 7 inhibition, but often PTT only or both are delayed.

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71
Q

What clotting factor has the shortest half life

A

7a

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72
Q

Why would PT be prolonged in rodenticide poisoning?

A

7a has the shortest half life, even though some species would have PT/PTT both or sometimes PTT only delayed

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73
Q

What are teh anti-coagulation proteins

A

Anti-thrombin and alpha-2 macroglobulin

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74
Q

What is the action of antithrombin

A

Stops thrombin from converting fibrinogen to fibrin

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75
Q

What action does heparin take

A

Keeps thrombin and antithrombin together

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76
Q

What are the signs of a PLN

A

Low albumin only

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77
Q

What does low albumin only indicate

A

PLN - protein losing nephropathy

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78
Q

What does low albumin and low globulin indicate

A

PLE- protein losing enteropathy

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79
Q

What indicates a PLE

A

low albumin and globulin

80
Q

What will low anti-thrombin cause

A

Hypercoagulable state, DIC, PLN, PLE

81
Q

What are the phases of clotting

A

Vascular and platelet

82
Q

Describe the first phase of clotting

A

Vascular- exposure of subendothelial matrix and exposure of tissue factor

83
Q

Describe the second phase of clotting

A

Platelet- adhesion, activation, shape change, secretion/degranulation, aggreggation

84
Q

What factor induces adhesion in platelets to each other and vasculature

A

vWF

85
Q

What stimulated release of vWF? For what?

A

Desmopressin stimulates their release from endothelial cells for adhesion in the platelet phase of coagulation

86
Q

What is the source of vWF

A

Synthesized and released from endothelial cells and platelets

87
Q

Name a major platelet agonist

A

PAF- platelet activating factor

88
Q

Where is PAF made

A

Platelet activating factor is made my the cells of the immune system

89
Q

How are coagulation and inflammation linked

A

PAF (platelet activating factor) is made by the cells of the immune system

90
Q

Is DIC a primary or secondary concern

A

Secondary

91
Q

What conditions can lead to DIC

A

Pancreatitis, IMHA, neoplasia, extreme enteritis, vasculitis

92
Q

Why can IMHA cause DIC

A

Fragmentation morphology damaging vasculature

93
Q

What change in clotting cascade must be seen to indicate prolonging of clotting

A

70% decrease in factors

94
Q

How do you evaluate platelet function

A

BMBT- buccal mucosal bleeding test

95
Q

What does it mean when both PT and PTT are prolonged

A

Disorder in common

96
Q

What can cause platelet function disorder

A

vWFd

97
Q

What kind of blood is in a blue top

A

Citrated PLASMA

98
Q

What is the function of factor 8a

A

Cross-linking of fibrin

99
Q

What causes cross linking of fibrin

A

Factor 8a

100
Q

What effect does eastern diamondback rattlesnake venom cause

A

fibrinogenolysis

101
Q

What is contained in cryoprecipitate

A

vWF, fibrinogen, factors 8 and 13

102
Q

Whats up with cat platelets?

A

Largest and most activated

103
Q

What is thrombocytosis

A

Increased platelets

104
Q

What is thrombocytopenia

A

Decreased platelets

105
Q

What is the most common cause of thrombocytosis

A

Inflammation

106
Q

How does inflammation lead to thrombocytosis

A

IL6 increases thrombopoietin (TPO)

107
Q

What effect is seen after a splenectomy

A

Within one week, thrombocytosis **?

108
Q

What can cause hypercoagulable state

A

Inflammation, initial reaction to thrombosis and DIC, antithrombin deficiency

109
Q

Why would mast cells be in circulation in a dog

A

IMHA, inflammation, parvo (not tumor!)

110
Q

Why would mast cells be in circulation in a cat

A

Mast cell tumor in spleen, liver or intestines (visceral organs)

111
Q

What do snake venoms do

A

Degrade fibrinogen

112
Q

What signs would you see in venom poisoning

A

Increased FDPs but not D dimers

113
Q

Increased FDPs but normal D dimers, some spheroechinocytes would indicate what

A

Venom

114
Q

Increased FDPs could be from what

A

Venom or breakdown of fibrin monomers by plasmin before crosslinking

115
Q

How are FDPs usually removed

A

Liver

116
Q

Decribe the breakdown of FDPs

A

Plasmin breakdown of fibrin monomers before crosslinking by factor 13a

117
Q

What does the presence of D dimers indicate

A

Active breakdown of covalently cross-linked (by 13a) fibrin - active coagulation and clot breakdown

118
Q

If increased D dimers are seen, what does that indicate

A

Active coagulation, thrombus formation

119
Q

Why are increased D dimers a sign of thrombus formation

A

Because thrombus formation only occurs when 13a cross links soluble fibrin and plasmin cleaves it to form D dimers

120
Q

Name a positive acute phase protein

A

Fibrinogen

121
Q

What is the only early sign of thrombosis in large animals

A

Fibrinogen

122
Q

If a large animal is inflamed, what should be seen

A

Fibrinogen

123
Q

What could a lack of fibrinogen indicate

A

Liver failure leading to lack of fibrinogen production or fibrinogen converting to fibrin and throwing clots- now look for DIC

124
Q

What are signs of DIC

A

Low fibrinogen, increased D dimers and increased FDPs, platelet consumption (thrombocytopenia), fragmentation morphologies

125
Q

First action when DIC noticed

A

Plasma transfusion

126
Q

What is the cause of hemophilia A

A

Factor 8 deficiency

127
Q

What is the cause of hemophilia B

A

Factor 9 deficiency

128
Q

What would normal Pt, platelets, BMBT but prolonged PTT indicate

A

Missing factor 12- doesnt actually cause bleeding disorder, just increased PTT in tube

129
Q

What factor is not necessary for secondary hemostasis in vivo

A

Factor 12 (missing in some cats and other species)

130
Q

What does missing factor 12 cause

A

Prolonged PTT (all others normal) in clotting test- not in vivo

131
Q

PT/PTT both prolonged indicates

A

Common pathway 10, 5, 2 and 1

132
Q

What does factor 2 do

A

Common pathway - prothrombin to thrombin

133
Q

What does factor 1 do?

A

Fibrinogen to fibrin

134
Q

What is a normal leukocyte number for cats and dogs

A

5,000 to 15,000

135
Q

What is a leukmoid response

A

50,000 leukocytes/mcL

136
Q

What does leukmoid response indicate

A

50,000 leukocytes/mcL - indicated acute inflammation

137
Q

What could cause leukmoid response

A

Infection (pyothorax, pyelonephritis, pyometra, etc), Immune mediated disorders like IMHA, glomerulonephritis)

138
Q

What species will most show leukmoid response and why

A

Dogs bcause huge neutrophil reserves in bone marrow

139
Q

Increased leukocytes can be attributed to what artifact

A

Metarubricytes (nRBCs) counted by machine

140
Q

Cats/dogs/horses neutrophil-lymphocyte-monocyte proportions

A

NLM - 70-30-5

141
Q

Cattle/ruminant neutrophil-lymphocyte-monocyte proportions

A

NLM 50/50

142
Q

Where are neutrophils stored

A

Bone marrow

143
Q

Who has the most neutrophils and who has the least

A

[Dogs >= cats >= horses] >= cows/sheep

144
Q

What caution must be taken when reading leukocyte values

A

Do not look at %, may be artifact- always look at absolute numbers

145
Q

What indicated hypersegmentation in neutrophils

A

5 or more distinct nuclear lobes

146
Q

What can cause hypersegmentation in neutrophils

A

endo/exo glucocorticoids (older neuts stay in circulation because macrophages arent eating them after 10 hours), old blood samples

147
Q

What re basophils, eosinophils and neutrophils

A

Granulocytes

148
Q

What is chediak higashi

A

Neutrophil function problem- unable to form phagolysosome

149
Q

What causes neutrophils not to form phagolysosome?

A

Chediak higashi

150
Q

When might it be ok to see neutrophilic granules

A

Siamese cats and healthy foals

151
Q

What is a left shift

A

More immature neutrophils out of bone marrow- sign of inflammation

152
Q

What indicates a left shift

A

> = 300 bands/mcL

153
Q

What is an inflammatory leukogram

A

> = 300 bands/mcL

154
Q

1+ toxicity

A

Dohle bodies OR basophilic cytoplasm

155
Q

2+ toxicity

A

Dohle bodies and basophilic cytoplasm

156
Q

3+ toxicity

A

vauolization of cytoplasm, Dohle bodies and basophilic cytoplasm

157
Q

4+ toxicity

A

granulation band neutrophils

158
Q

What are immature and mature neutrophils

A

imm- bands; mature- segmented

159
Q

What is immature about immature neutrophils

A

Not enough time to clean up basophilic RNA in cytoplasm

160
Q

What does toxicity indicate

A

Inflammation

161
Q

Thrombocytopenia and shifting leg lameness indicates

A

Tick borne disease

162
Q

Metamyelocytes, bands, segs (identifty)

A

Metamyelocyte- kidney shaped center

Bands- no segmentation, horseshoe

163
Q

Regenerative left shift

A

segs > bands/metamyelocytes/myelocytes

164
Q

Degenerative left shift

A

bands/metamyelocytes/myelocytes > segs

165
Q

What is pelger huet anomaly

A

Aussies- do not segment neutrophils, still functional

166
Q

Describe horse neutrophils

A

hypersegmented

167
Q

What causes neutrophilia

A

Epinephrine, physiologic, glucocorticoids, inflammation

168
Q

How does epinephrine cause neutrophilia

A

BV and spleen contract and neuts come out

169
Q

What indicates physiologic neutrophilia

A

No left shift/toxicity

170
Q

How do glucocorticoids cause neutrophilia

A

Pred causes lack of regression of old neuts so they stay in blood

171
Q

More immature neutrophils and some toxicity indicated which leukogram

A

Inflammatory

172
Q

300 or more neutrophils/mcL

A

INFLAMMATORY LEUKOGRAM

173
Q

What causes a physiologic leukogram

A

Stress (but not a stress leukogram) due to vasoconstriction and splenic contraction - mature neutrophilia with lymphocytosis

174
Q

Mature neutrophils with lymphocytosis (20k)

A

physiologic leukogram

175
Q

Mature neutrophilia with lymphopenia, eosinopenia, monocytosis

A

Stress leukogram

176
Q

What characterizes a stress leukogram

A

Mature neutrophilia, lymphopenia, eosinopenia, monocytosis

177
Q

What is the only salient feature of a stress leukogram

A

Lymphopenia, because underlying stress leukogram can be present

178
Q

What does lymphopenia indicate

A

Stress leukogram

179
Q

Mixed leukogram

A

bands high (300+) [= inflammatory], lymphopenia [stress leukogram]

180
Q

What is neutropenia caused by

A

Increased utilization or destruction, acute infection, sepsis, endotoxemia, estrogen toxicity, viral (parvo), erlichiosis

181
Q

When neutropenia is seen, what should you check for?

A

Infection- migration into tissues is most common

182
Q

What can estrogen toxicity cause

A

Neutropenia

183
Q

What can cancers like leukemia, mast cell tumors and T cell lymphomas cause

A

Eosinophilia (increased eosinophils)

184
Q

What can cause eosinophilia

A

Cancers like eosinophilic leukemia, mast cell tumors and T cell lymphomas

185
Q

What do granules in eosinophils look like

A

Dogs- round; Cats- rod shaped

186
Q

How can acute infection cause neutropenia

A

Infection takes hold befor granulocytic hyperplasia can occur

187
Q

What can low TP in babies indicate

A

failure of passive transfer of maternal immunity

188
Q

What is leukemia

A

Bone marrow cancer

189
Q

What are the two types of leukemia

A

Lymphoid and myeloid

190
Q

What characterizes acute leukemia

A

Leukoblasts and immature forms in circulation

191
Q

What characterizes chronic leukemia

A

Well differentiated cells

192
Q

Rank leukemias

A

Chronic lymphocytic > chronic myelogenous > acute lymphocytic > acute myelogenous

193
Q

Why would you prefer chronic lymphocytic leukemia?

A

Well differentiated cells in circulation plus presence of neutrophils to fight bacteria

194
Q

What can moderate to severe lyphocytosis in a dog indicate

A

CLL Chronic lymphocytic leukemia- do a bone marrow aspirate!

195
Q

What indicates IMHA

A

Severe regenerative anemia: macrocytic, hypochromic, polychromataphils/aggregate-reticulocytes, spherocytes, inflammatory leukogram, microagglutination, ghost cells

Clin Path (1 decks)

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