Small Animal Diseases/Care Flashcards

1
Q

What is vasculitis?

A

(Inflammation of blood vessels)

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2
Q

Is vasculitis localized or systemic?

A

(Could be either)

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3
Q

Is vasculitis primary or secondary?

A

(Could be either, primary rare in animals)

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4
Q

Why do antibodies produced by plasma cells in response to viruses found in blood vessels sometimes instead cross-react to blood vessel walls?

A

(Molecular mimicry)

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5
Q

What two things are released by neutrophils that are triggered by antibodies?

A

(Chemokines that attract more neutrophils and reactive oxygen species)

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6
Q

What occurs subsequently to the narrowing of the affected vessel’s lumen due to occlusion with inflammatory cells, thrombosis, hyperplasia, and/or fibrosis if chronic? Two answers.

A

(Tissue ischemia and organ dysfunction)

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7
Q

What are the common sites for vasculitic lesions in small animals? Six answers.

A

(Limbs, paws, ear pinnae, lips/oral mucosa, tip of tail, and scrotum)

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8
Q

What clinical sign results from increased vascular permeability due to vasculitis?

A

(Edema)

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9
Q

What lung patterns are associated with vasculitis?

A

(Diffuse interstitial to alveolar pattern)

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10
Q

What blood work abnormalities are associated with vasculitis in small animal patients? Four answers.

A

(Anemia, thrombocytopenia, hypoalbuminemia, other changes depending on organs affected)

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11
Q

What two drugs are used for the treatment of less severe cases of vasculitis?

A

(Doxycycline and pentoxifylline)

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12
Q

What drug is used if treatment with doxycycline or pentoxifylline doesn’t work or in more severe cases of vasculitis?

A

(Corticosteroids)

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13
Q

What is the term for the reduction in red blood cell mass?

A

(Anemia)

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14
Q

Anemia leads to a decrease/increase in oxygen delivery to tissues.

A

(Decrease)

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15
Q

One of the physiologic responses to anemia is to increase cardiac output, below are ways that the body increases cardiac output, give the component of cardiac output (heart rate or stroke volume) that they alter:

  • Hypoxia stimulates chemoreceptors
A

(Increases heart rate)

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16
Q

One of the physiologic responses to anemia is to increase cardiac output, below are ways that the body increases cardiac output, give the component of cardiac output (heart rate or stroke volume) that they alter:

  • Catecholamine release increases left ventricular contractility
A

(Increases stroke volume)

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17
Q

One of the physiologic responses to anemia is to increase cardiac output, below are ways that the body increases cardiac output, give the component of cardiac output (heart rate or stroke volume) that they alter:

  • Anemia reduces blood viscosity
A

(Increases stroke volume)

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18
Q

Where does the body redistribute blood flow when responding to anemia? Away from where and towards what.

A

(Away from the periphery and towards cardiac and cerebral)

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19
Q

What do the kidneys excrete in response to anemia that stimulates the proliferation and differentiation of RBC precursors in bone marrow?

A

(Erythropoietin)

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20
Q

How does the body improve oxygen extraction in response to anemia?

A

(Increases production of 2,3 DPG which promotes the release of oxygen from hemoglobin)

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21
Q

The heart rate of an anemic patient will be increased/decreased.

A

(Increased)

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22
Q

The respiratory rate of an anemia patient will be increased/decreased.

A

(Increased)

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23
Q

Why might you hear a heart murmur in a patient with anemia?

A

(Altered blood viscosity)

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24
Q

Do chronic or acute anemia patients have more clinical signs?

A

(Acute)

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25
Q

What are the three causes of anemia?

A

(Hemorrhage, hemolysis, and hypoplasia)

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26
Q

What is the main difference between hematocrit and packed cell volume?

A

(HCT is calculated, PCV is directly measured)

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27
Q

What blood value tells you that your patient has regenerative anemia?

A

(Increased reticulocytes)

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28
Q

What two things do normal or decreased reticulocytes suggest in an anemia patient?

A

(Bone marrow hypoplasia or pre-regenerative anemia)

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29
Q

What is the time period between anemia onset and bone marrow release of reticulocytes?

A

(2-5 days)

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30
Q

How do you get an absolute reticulocyte count when reticulocytes are reported in a percentage?

A

(Multiply reticulocyte % by RBC count)

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31
Q

What is the minimum value of canine reticulocytes that indicates if your patient has regenerative anemia?

A

(>95 thousand cells/microliter)

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32
Q

What is the minimum value of feline reticulocytes that indicates if your patient has regenerative anemia?

A

(>60 thousand cells/microliter)

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33
Q

What two blood smear findings indicate the presence of reticulocytes?

A

(Polychromasia and anisocytosis)

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34
Q

What are classic RBC indices changes that are seen with reticulocytosis?

A

(Macrocytosis and hypochromasia)

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35
Q

Nucleated RBCs on a blood smear are called what term that when present without reticulocytosis is associated with bone marrow disease or injury, splenic diseases, or lead poisoning?

A

(Metarubricytosis)

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36
Q

You have a patient that has non-regenerative anemia and the following RBC indices changes, give the disease/deficiency that can cause these changes (some have multiple):

  • Macrocytic and normochromic
A

(FeLV and B12 or B1 deficiency)

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37
Q

You have a patient that has non-regenerative anemia and the following RBC indices changes, give the disease/deficiency that can cause these changes (some have multiple):

  • Microcytic and hypochromic
A

(Iron deficiency)

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38
Q

You have a patient that has non-regenerative anemia and the following RBC indices changes, give the disease/deficiency that can cause these changes (some have multiple):

  • Microcytic and normochromic
A

(Portosystemic shunt)

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39
Q

Of the gastrointestinal tract sources of blood loss (melena, hematochezia, and hematemesis) which is more likely to result in anemia?

A

(Melena)

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40
Q

What are the three common causes of acute blood loss?

A

(Trauma, coagulopathy, and neoplasia)

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41
Q

What are the four common causes/locations of chronic blood loss?

A

(GI tract, fleas, urinary tract, and respiratory tract)

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42
Q

Describe the pulse of a dog with acute blood loss and associated hypovolemia.

A

(Weak and thready)

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43
Q

Why will your externally hemorrhagic anemic patient also have a decreased total protein?

A

(Plasma protein is being lost with the RBCs)

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44
Q

Why can chronic external hemorrhage cause non-regenerative anemia?

A

(Loss of iron leads to non-regenerative anemia)

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45
Q

What RBC cell types are the results of RBC fragmentation? Three answers.

A

(Keratocytes, acanthocytes, and schistocytes)

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46
Q

A blood transfusion should be given to an anemic patient when there are signs of poor _____________________ such as weakness and/or depression, tachycardia, tachypnea, and bounding or weak femoral pulses.

A

(Tissue oxygenation)

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47
Q

What are the two indications for the use of fresh whole blood prior to refrigeration?

A

(Blood loss anemia and coagulopathy)

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48
Q

Why are packed red blood cells more appropriate for hemolytic or hypoplastic anemias?

A

(Those patients tend to have normal plasma proteins so don’t need that from whole blood)

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49
Q

What is the formula for determining the amount of blood you should administer when doing a blood transfusion?

A

(((Patient body weight in kgs multiplied by blood volume in ml/kg)*(Desired PCV - patient PCV))/Donor PCV)

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50
Q

What is the most clinically relevant dog blood type?

A

(DEA 1.1)

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51
Q

A DEA 1.1 negative dog who has never received a blood transfusion before can be given DEA 1.1 + blood for their first transfusion but will no longer be able to receive DEA 1.1 + blood in the future, why is that?

A

(They will develop antibodies to the DEA 1.1 + blood from the first transfusion, will have to use DEA 1.1 - blood for any future blood transfusions)

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52
Q

What type of blood should type A cats receive only?

A

(Type A)

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53
Q

What type of blood should type B cats receive only?

A

(Type B)

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54
Q

What substances do you use for cross-matching between a patient and a donor?

A

(Patient → serum; donor → RBCs)

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55
Q

When should you perform a cross-match? Two scenarios.

A

(When transfusion hx is unknown and when it has been greater than three days since their last transfusion and you want to give them another)

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56
Q

What are the clinical signs of volume overload induced by transfusion associated circulatory overload?

A

(Tachypnea, serous nasal discharge, and pulmonary crackles)

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57
Q

Patients receiving a transfusion can commonly show signs of a nonhemolytic febrile reaction to the blood, what can be done to minimize this reaction?

A

(Slow the transfusion rate)

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58
Q

What is done to treat hemolytic transfusion reactions after stopping the transfusion? Four answers.

A

(IV fluids, oxygen, corticosteroids, and vasopressors if they have hypotension)

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59
Q

What is the term for the form of hemolysis that occurs by phagocytosis of RBCs by macrophages in the spleen, liver, and bone marrow?

A

(Extravascular)

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60
Q

What substance being abnormally present in the blood and urine is a result of and indicative of extravascular hemolysis?

A

(Bilirubin)

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61
Q

What is the term for the form of hemolysis that occurs within the blood vessels?

A

(Intravascular)

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62
Q

What substance being abnormally present in the blood and urine is a result of and indicative of intravascular hemolysis?

A

(Hemoglobin)

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63
Q

(T/F) Extravascular hemolysis is always present in cases of intravascular hemolysis.

A

(T)

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64
Q

What can the partial phagocytosis by macrophages of an RBC result in that be seen on a blood smear for an extravascular hemolytic patient?

A

(Spherocytes)

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65
Q

What type of cell do you see on the cytology of blood from an intravascular hemolytic patient?

A

(Ghost cells)

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66
Q

Hemolytic patients will have weak/thready or bounding pulses?

A

(Bounding)

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67
Q

What is the most common cause of extravascular hemolysis in dogs and cats?

A

(Immune mediated hemolytic anemia)

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68
Q

The activation of what system causes the concurrent intravascular hemolysis in some cases of IMHA?

A

(Complement system activation)

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69
Q

Is primary or secondary IMHA more common?

A

(Primary aka idiopathic)

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70
Q

What are the four potential triggers for secondary IMHA?

A

(Drugs, vaccination, infections, and neoplasia)

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71
Q

What three things are considered strong evidence for IMHA?

A

(Autoagglutination, spherocytosis, and positive Coombs test)

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72
Q

What is the first line treatment for IMHA?

A

(Prednisone/prednisolone)

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73
Q

What is the immunosuppressive dose of prednisone/prednisolone?

A

(2 mg/kg/day)

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74
Q

In what two situations would you consider secondary immunosuppressants in combination with corticosteroids?

A

(If the patient is refractory to corticosteroid tx and/or if the patient may not tolerate corticosteroids well long term)

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75
Q

Does azathioprine have a slower or faster onset of action when compared to prednisone?

A

(Slower)

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76
Q

What are the three side effects of azathioprine?

A

(Bone marrow suppression, hepatotoxicity, and pancreatitis)

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77
Q

Why should azathioprine not be used with mycophenolate?

A

(They have similar mechanisms of action → worse side effects)

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78
Q

What are the two side effects of mycophenolate?

A

(GI → diarrhea, vomiting, and anorexia; bone marrow suppression)

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79
Q

Does cyclosporine have a slower or faster onset of action when compared to prednisone?

A

(Faster)

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80
Q

Is the vegetable oil based Sandimmune formula of cyclosporine recommended or not recommended? What about the ultra micronized Atopica formula?

A

(Sandimmune → not recommended; Atopica → recommended)

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81
Q

Should cyclosporine be administered with a full meal or on an empty stomach?

A

(Empty stomach)

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82
Q

Immunosuppressants exacerbate risk of infection but cyclosporine increases the risk for what type of infection particularly?

A

(Fungal)

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83
Q

What two drugs can be used to prevent systemic thromboembolisms, a common complication of IMHA?

A

(Low dose aspirin or clopidogrel)

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84
Q

What is the bacterial agent for infectious anemia in cats?

A

(Hemotropic mycoplasma)

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85
Q

Of laboratory findings, what might be present in infectious anemia cases that is not typically present with IMHA (so you can potentially use this to differentiate between the two)?

A

(Thrombocytopenia)

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86
Q

What are the feline risk factors for hemotropic mycoplasma infections? Three answers.

A

(Male, outdoor access, FeLV/FIV positive)

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87
Q

What is the highly sensitive diagnostic test for hemotropic mycoplasma?

A

(PCR)

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88
Q

What two drugs are used for treatment of hemotropic mycoplasma?

A

(Doxycycline or fluoroquinolones)

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89
Q

What dog breed has a high seroprevalence of B. canis vogeli but that also often lacks clinical signs?

A

(Greyhounds)

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90
Q

What dog breed has a high prevalence of B. gibsoni but that also often lacks clinical signs?

A

(American pit bull terriers)

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91
Q

Which of the babesia species is considered the small one?

A

(Babesia gibsoni)

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92
Q

What are the two forms of cytauxzoonosis clinical disease?

A

(Tissue phase and erythrocyte phase)

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93
Q

What antioxidant does the intracellular systems that reverse hemoglobin oxidation utilize?

A

(Glutathione)

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94
Q

(T/F) All patients with hemolysis should have abdominal radiographs performed.

A

(T)

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95
Q

How is zinc toxicity diagnosed?

A

(Take a radiograph)

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96
Q

What type of hemolytic anemia does zinc toxicity induce in animals?

A

(Heinz body anemia)

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97
Q

What type of hemolytic anemia does acetaminophen ingestion induce in animals?

A

(Methemoglobinemia)

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98
Q

Why is methemoglobinemia called a ‘physiologic anemia’?

A

(RBCs are present and not decreased, just unable to carry oxygen appropriately)

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99
Q

What does N-acetylcysteine do to intracellular glutathione levels that makes it useful in treatment for oxidant-induced hemolytic anemia?

A

(Increase intracellular levels of glutathione)

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100
Q

What is another term for microangiopathic hemolytic anemia?

A

(Fragmentation hemolytic anemia)

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101
Q

What is the RBC fragmentation due to in a case of fragmentation hemolytic anemia?

A

(RBC contact with abnormal vasculature)

102
Q

Is the hemolysis due to fragmentation hemolytic anemia mild or severe?

A

(Mild)

103
Q

Cytokines associated with the primary disease that causes fragmentation hemolytic anemia can suppress bone marrow, this means the patient may present with that type of anemia?

A

(Non-regenerative anemia)

104
Q

What are the two blood smear findings associated with fragmentation hemolytic anemia?

A

(Schistocytes and acanthocytes)

105
Q

Hypoplastic anemia should be regenerative or non-regenerative?

A

(Non-regenerative)

106
Q

What cell lines are impacted in a case of primary failure of erythropoiesis?

A

(RBC cell line only)

107
Q

Listed below are the different types of primary failure of erythropoiesis and regenerative IMHA, identify which induce erythroid hypo or hyperplasia:

  • Pure red cell aplasia
A

(Erythroid hypoplasia)

108
Q

Listed below are the different types of primary failure of erythropoiesis and regenerative IMHA, identify which induce erythroid hypo or hyperplasia:

  • Non-regenerative immune-mediated anemia
A

(Erythroid hyperplasia)

109
Q

Listed below are the different types of primary failure of erythropoiesis and regenerative IMHA, identify which induce erythroid hypo or hyperplasia:

  • Regenerative IMHA
A

(Erythroid hyperplasia)

110
Q

How do you tell the difference between non-regenerative immune-mediated anemia and regenerative IMHA on a bone marrow sample?

A

(Non-regenerative → +/- RBC maturation arrest; regenerative → normal maturation)

111
Q

What can bone marrow be replaced by in chronic aplastic anemia?

A

(Fat cells)

112
Q

What is the term for displacement of bone marrow tissue?

A

(Myelophthisis)

113
Q

What is myelofibrosis?

A

(Displacement of bone marrow tissue by collagen)

114
Q

What is the most common cause of deficient hemoglobin synthesis?

A

(Iron deficiency)

115
Q

What is the CBC progression in iron deficient patients? Four steps, give the RBC indices and reticulocytes.

  • Beginning of blood loss, 12-24 hours
A

(Normocytic, normochromic, no retics)

116
Q

What is the CBC progression in iron deficient patients? Four steps, give the RBC indices and reticulocytes.

  • Has been losing blood for 2-5 days
A

(Macrocytic, hypochromic, +++ retics)

117
Q

What is the CBC progression in iron deficient patients? Four steps, give the RBC indices and reticulocytes.

  • Has been losing blood for >7 days
A

(Normocytic, normochromic, ++ retics)

118
Q

What is the CBC progression in iron deficient patients? Four steps, give the RBC indices and reticulocytes.

  • Has been losing blood for > 14 days, total body iron deficiency
A

(Microcytic, hypochromic, +/- retics)

119
Q

What is the most common cause of non-regenerative anemia in cats and dogs?

A

(Anemia of chronic/inflammatory disease)

120
Q

Is the anemia mild, moderate, or severe in relation to anemia of chronic disease?

A

(Mild to moderate)

121
Q

Should the RBC indices be changed or normal with anemia of chronic disease?

A

(Normal –> normocytic, normochromic)

122
Q

Can anemia of chronic diseases be resolved; if so, how?

A

(Yes with resolution of underlying disease)

123
Q

What portion of total body water is in the intracellular fluid compartment?

A

(⅔ of total body water)

124
Q

What is the other (so besides intracellular) fluid compartment of the body?

A

(Extracellular fluid compartment)

125
Q

The extracellular fluid compartment is made up of two additional fluid compartments, what are those two compartments?

A

(Interstitial and intravascular)

126
Q

What are the three categories of dehydration?

A

(Hypotonic, isotonic, and hypertonic)

127
Q

What are the two most common categories of dehydration?

A

(Hypotonic or isotonic)

128
Q

What are the two sides of fluid balance?

A

(Intake versus loss)

129
Q

What changes to the two sides of fluid balance cause dehydration?

A

(Intake → decreased; loss → increased)

130
Q

What two cases will make skin turgor/pliability difficult to assess?

A

(Chunky animals → excessive subq fat; emaciated or older patients → lack of subq fat and elastin)

131
Q

What action of the patient can affect the moistness of oral mucous membranes and make them difficult to assess for hydration status?

A

(Panting → dries mucous membranes)

132
Q

What position of the eyes in their orbits indicates dehydration?

A

(Sunken position → dehydration of the fat layer behind the eyes)

133
Q

Will HCT and/or PCV increase or decrease with non-hemorrhagic dehydration?

A

(Increase)

134
Q

Will TP increase or decrease with non-hemorrhagic dehydration?

A

(Increase)

135
Q

What should the urine specific gravity value be higher than to indicate normal renal function?

A

(> 1.045)

136
Q

When you are administering fluids to maintain a patient, what type of fluids will you reach for?

A

(Hypotonic crystalloid fluid)

137
Q

What two fluid compartments do crystalloid fluids exert their effects on?

A

(Interstitial and intracellular compartments)

138
Q

What type of case is hypertonic saline used for?

A

(When you desire a rapid increase in intravascular volume)

139
Q

The primary effect of colloids is on which fluid compartment?

A

(Intravascular compartment)

140
Q

Which vein is used for delivery of large volumes of fluids?

A

(Jugular vein)

141
Q

Is volume overload more or less likely when administering subcutaneous fluids?

A

(Less likely when compared to intravenous)

142
Q

Only use of what type of fluids is recommended for the subcutaneous route?
A - Isotonic
B - Hypertonic
C - Hypotonic
D - Colloids

A

(A)

143
Q

What is the rate of administration of fluids determined by in terms of fluid loss? Two answers.

A

(Magnitude and rapidity of fluid loss)

144
Q

What is the fluid rate per day for maintenance?

A

(40-60 mL/kg/day)

145
Q

How do you calculate a patient’s fluid deficit?

A

(Body weight in kgs multiplied by % dehydration as a decimal will equal deficit in liters)

146
Q

What is the difference in administration times between chronic and acute loss of fluids?

A

(Chronic → replace fluids over 24 hour period; acute → replace fluids over 6-8 hours)

147
Q

Which of the below options can answer the question ‘What is shock?’?

A - A momentary pause in the act of death
B - Reduced effective tissue perfusion
C - A syndrome resulting from imbalance of cellular substrate supply and demand
D - Inadequate cellular energy production

A

(All of them)

148
Q

Listed below are the four classifications of shock, give their causes:

Hypovolemic
Cardiogenic
Obstructive
Maldistributive

A

Hypovolemic (Low circulating volume)
Cardiogenic (Pump failure)
Obstructive (Blocked venous return to the heart)
Maldistributive (Blood pooling in the peripheral vasculature)

149
Q

Where does the body pull blood/fluid from into the intravascular space to maintain volume as a compensatory mechanism against shock?

A

(Interstitial and intracellular compartments)

150
Q

The mechanisms by which the body reduces urinary losses to maintain volume as a compensatory response to shock are listed below, give if they are decreased or increased to accomplish this:
Increase or decrease glomerular filtration rate?
Increase or decrease aldosterone?
Increase or decrease vasopressin?

A

Increase or decrease glomerular filtration rate? (Decrease)
Increase or decrease aldosterone? (Increase)
Increase or decrease vasopressin? (Increase)

151
Q

The mechanisms by which the body reduces venous capacitance to maintain pressure as a compensatory response to shock are listed below, give if they are decreased or increased to accomplish this:
Increase or decrease circulating epinephrine?
Increase or decrease angiotensin?
Increase or decrease vasopressin?

A

Increase or decrease circulating epinephrine? (Increase)
Increase or decrease angiotensin? (Increase)
Increase or decrease vasopressin? (Increase)

152
Q

What is the equation for blood pressure?

A

(Blood pressure is equal to cardiac output multiplied by systemic vascular resistance)

153
Q

What is the equation for cardiac output?

A

(Cardiac output is equal to heart rate multiplied by stroke volume)

154
Q

What two mechanisms are used to increase the contractility and rate of the heart to maintain/improve cardiac performance as a compensatory mechanism to shock?

A

(Sympathetic surge and adrenal stimulation)

155
Q

What are the two possible differential causes for white gums?

A

(Anemia and vasoconstriction)

156
Q

Tachycardia and vasoconstriction are the two physiological responses to shock that can be noted on PE, what clinical signs indicate vasoconstriction? Three answers.

A

(Pale pink/white mm, prolonged CRT, cool extremities/low rectal temperature)

157
Q

Which of the consequences of shock below is incorrect?
A - Weakness
B - Poor mentation
C - Organ dysfunction
D - Pain
E - Increased lactate

A

(D)

158
Q

What is often the earliest recognizable sign of shock in a patient?

A

(Increased heart rate expect in cardiogenic shock d/t bradyarrhythmias)

159
Q

Listed below are the different classifications of shock, give their treatment:
Hypovolemic
Cardiogenic
Obstructive
Maldistributive

A

Hypovolemic (Fluids)
Cardiogenic (No fluids, help heart)
Obstructive (Relieve obstruction)
Maldistributive (Increase vascular tone)

160
Q

What are the two drugs commonly found in a crash cart?

A

(Epinephrine and atropine)

161
Q

What two issues arise from delays in initiating CPR?

A

(Neurologic impairment and reduction in survival rates)

162
Q

Is the initiation of CPR in patients not in cardiopulmonary arrest associated with any adverse outcomes? If yes, what adverse outcomes?

A

(No CPR on a patient not in cardiopulmonary arrest is not associated with any adverse outcomes)

163
Q

Once you have a patient in cardiorespiratory arrest intubated, you should begin manual breathing and listed below are parameters pertinent to manual breathing, answer the questions:

How many breaths per minute should you administer?

A

(8-10 bpm)

164
Q

Once you have a patient in cardiorespiratory arrest intubated, you should begin manual breathing and listed below are parameters pertinent to manual breathing, answer the questions:

What should be the inspiratory time of the breath you administer?

A

(1 second)

165
Q

Once you have a patient in cardiorespiratory arrest intubated, you should begin manual breathing and listed below are parameters pertinent to manual breathing, answer the questions:

How many mls of air should be administered per kg of body weight?

A

(~10 ml/kg, enough to cause the chest to visibly rise)

166
Q

For mouth to snout breathing, what is the ratio of chest compressions to breaths administered that should be performed until you can get to a veterinary hospital?

A

(30 compression for every 2 breaths)

167
Q

What is the body weight in kgs cutoff for thoracic versus cardiac pump model?

A

(10 kgs, <10kgs → cardiac pump model; >10kgs → thoracic pump model)

168
Q

(T/F) The best way to perform CPR is to flex and extend your elbows while keeping the rest of your body still.

A

(F, keep elbows locked and use rest of body)

169
Q

What is the depth that you should aim for when performing CPR in percentage of the chest wall?

A

(30% of the chest wall)

170
Q

Why is CPR performed in 2 minutes cycles, so someone switches off every 2 minutes? Two answers.

A

(To avoid leaning and to minimize interruptions)

171
Q

What is the rate that chest compressions should be administered at?

A

(100-120 bpm)

172
Q

What are the two rhythms that can be defibrillated?

A

(Ventricular fibrillation and pulseless ventricular tachycardia)

173
Q

If you cannot get an IV catheter in a patient you are performing CPR on, some emergency drugs can be administered intratracheal, name the five drugs.

A

(Naloxone, atropine, vasopressin, epinephrine, lidocaine)

174
Q

What is the main difference between epinephrine and vasopressin?

A

(Epinephrine has chronotropic/inotropic effects, vasopressin does not)

175
Q

Of epinephrine and vasopressin, which works better in acidotic patients (which CPR patients become as CPR is prolonged)?

A

(Vasopressin)

176
Q

Is atropine a…
A - Parasympatholytic
B - Parasympathomimetic
C - Sympatholytic
D - Sympathomimetic

A

(A)

177
Q

(T/F) Asphyxia induced pulseless electrical activity is more likely to be resuscitated when you administer atropine in a canine patient.

A

(T)

178
Q

Is lidocaine routinely indicated in cardiac arrest?

A

(No)

179
Q

Is sodium bicarbonate administration useful in early or prolonged CPA/CPR?

A

(Prolonged)

180
Q

(T/F) End title CO2 reflects perfusion, not ventilation in a patient in cardiopulmonary arrest.

A

(T)

181
Q

What type of neoplasm is lymphoma the most common of?

A

(Hematopoietic neoplasia)

182
Q

What is the average survival time for an untreated dog with lymphoma?

A

(1-2 months)

183
Q

What is the treatment of choice for lymphoma?

A

(Chemotherapy)

184
Q

What are the three major types of lymphocytes?

A

(B, T, and natural killer lymphocytes)

185
Q

What is the major event that leads to the malignant transformation of lymphocytes leading to lymphoma?

A

(Immune deregulation)

186
Q

How are dogs exposed to herbicides, which have conflicting results as to whether they play a role in lymphoma in dogs?

A

(Slow, chronic exposure → you walk through grass and bring small amounts of herbicide inside)

187
Q

Why do you want to obtain a urinalysis in your lab evaluation of animals that you suspect have lymphoma?

A

(Immune suppression/dysregulation → more risk of urinary tract infections → don’t want to start chemotherapy on a dog with urinary tract infection)

188
Q

In what two cases would you choose to pursue a bone marrow aspirate when you suspect canine lymphoma?

A

(Presence of cytopenias or circulating neoplastic cells)

189
Q

For a dog to be considered to be in stage four lymphoma, what organs need to be involved?

A

(Liver and/or spleen)

190
Q

For a dog to be considered to be in stage four lymphoma, do they also need the signs of stage III (generalized lymphadenopathy)?

A

(No, just liver and/or spleen = stage IV no matter if there is lymphadenopathy or not)

191
Q

What does it mean if a dog is in stage IIb lymphoma?

A

(Stage II → multiple lymph nodes involved but regionally; b → symptomatic d/t lymphoma)

192
Q

Of T and B cell lymphoma, which is worse in canine patients?

A

(T cell lymphoma)

193
Q

Which substage is a negative prognostic factor?

A

(Substage b → symptomatic d/t lymphoma)

194
Q

What two tests can be used to diagnose T-zone lymphoma, which is Stage V T cell lymphoma but that has a good median survival time and a mild treatment course?

A

(Histopath and flow cytometry)

195
Q

(T/F) Most dogs with lymphoma will go into remission.

A

(T)

196
Q

(T/F) Most dogs will relapse within 1 year from chemo initiation in treatment of lymphoma.

A

(T)

197
Q

Why should you never put a suspected lymphoma patient on prednisone as a therapeutic trial?

A

(Pred will upregulate the expression of the PgP pump → results in multidrug resistance)

198
Q

If you suspect a cat has lymphoma, what should you test them for?

A

(FeLV/FIV)

199
Q

What is the most common presentation of lymphoma in a negative FeLV cat?

A

(Alimentary)

200
Q

What is the most common presentation of lymphoma in a positive FeLV cat?

A

(Mediastinal)

201
Q

What common paraneoplastic related finding in dogs is rare in cats?

A

(Hypercalcemia)

202
Q

Why are clonality assays more useful in cats than in dogs?

A

(Cats tend to get small cell lymphoma, so it can be hard to distinguish between normal inflammatory response (such as IBD) from lymphoma. With a clonality assay, if there are multiple types of lymphocytes → inflammatory, if there is only one type of lymphocyte → lymphoma)

203
Q

What size lymphoma, small cell or large cell, is a negative prognostic factor in cats with lymphoma?

A

(Large cell)

204
Q

Why is it necessary to get a full thickness GI biopsy in cats with suspected alimentary lymphoma?

A

(To differentiate between lymphoma and inflammatory bowel disease)

205
Q

What can you do instead of biopsies of the GI tract that is less invasive and can still be diagnostic in cats with suspected lymphoma?

A

(Upper and lower GI scoping)

206
Q

What size of lymphoma, small or large cell, is typically the culprit in nasal lymphoma?

A

(Large cell)

207
Q

What is the treatment for nasal lymphoma and is it curative?

A

(Radiation +/- chemotherapy; local disease can be cured, may result in disease cure)

208
Q

How do cats with renal lymphoma tend to present to a hospital?

A

(As an emergency in acute renal failure with big kidneys)

209
Q

If _____________ is preserved in a case of renal lymphoma, long term survival is possible.

A

(Kidney function)

210
Q

What are the four steps in the ‘overview’ of hemostasis?

A

(Endothelial injury → primary hemostasis → secondary hemostasis → fibrinolysis)

211
Q

What chemical does injured endothelium release?

A

(Endothelin)

212
Q

What is the purpose of the localized vasoconstriction that occurs after endothelial injury?

A

(Reduces blood loss)

213
Q

What four things are required for platelet plug formation, which is the product of primary hemostasis?

A

(Platelets, healthy endothelium, fibrinogen, and von Willebrand factors)

214
Q

What chemical stimulates platelet production in the bone marrow?

A

(Thrombopoietin)

215
Q

What does secondary hemostasis require, both of which are produced primarily by the liver?

A

(Clotting factors and fibrinogen)

216
Q

What does thrombin convert fibrinogen into?

A

(Fibrin)

217
Q

Thrombin also activates factor XIII, what is the role of factor XIII in secondary hemostasis?

A

(Crosslinks fibrin → makes it more stable)

218
Q

What are the two pathways of blood coagulation activation?

A

(Extrinsic and intrinsic)

219
Q

What do the extrinsic and intrinsic pathways result in the activation of?

A

(The common pathway)

220
Q

Which of the secondary hemostasis pathways is activated by tissue factor release and whose important clotting factor is factor VII?

A

(Extrinsic pathway)

221
Q

The intrinsic pathway is activated by direct collagen contact and involves which four clotting factors, which factors?

A

(Factors XII, XI, IX, and VIII)

222
Q

What are the four clotting factors related to the common pathway?

A

(Factors X, V, II, and I)

223
Q

What degrades the crosslinked fibrin into small fragments in fibrinolysis?

A

(Plasmin)

224
Q

Does increased FDPs (fibrin degradation products) always imply there is a blood clot somewhere in the body?

A

(No, fibrinogen also increases with inflammation)

225
Q

What is the product of plasmin action on cross linked fibrin only, which can be measured and is a true reflection of clot formation?

A

(D-dimers)

226
Q

Primary hemostasis is associated with mucosal surface or body cavity bleeding?

A

(Mucosal surface bleeding)

227
Q

Secondary hemostasis is associated with mucosal surface or body cavity bleeding?

A

(Body cavity bleeding)

228
Q

What test will assess the quantity of platelets?

A

(Platelet count → included in CBC)

229
Q

What test will assess the functionality of platelets?

A

(Buccal mucosal bleeding time)

230
Q

What pathways does prothrombin time [PT] assess?

A

(Extrinsic and common)

231
Q

What pathways does partial thromboplastin time [PTT] assess?

A

(Intrinsic and common)

232
Q

Do animals with congenital macrothrombocytopenia have bleeding tendencies?

A

(No)

233
Q

What are the four main causes of thrombocytopenia?

A

(Destruction, consumption, decreased production/hypoplasia, and sequestration)

234
Q

Is the resulting thrombocytopenia due to immune-mediated thrombocytopenia [IMTP] mild, moderate, or severe?

A

(Severe)

235
Q

What type of infection can cause secondary IMTP?

A

(Rickettsial infections)

236
Q

What is the use of vincristine in the treatment of IMTP?

A

(Shortens platelet count recovery time and hospitalization time when combo’d with corticosteroids)

237
Q

What should you avoid when administering vincristine?

A

(It is a vesicant → avoid extravasation)

238
Q

When should you transfuse an IMTP patient?

A

(When they have clinical signs related to blood loss anemia)

239
Q

If you are presented with a patient that has bleeding but normal platelet counts and normal clotting times (PT and PTT), what should you consider to be the issue?

A

(Thrombocytopathia)

240
Q

(T/F) The buccal mucosal bleeding time test should only be performed in animals with a normal platelet count.

A

(T)

241
Q

What are von Willebrand factors important for?

A

(Platelet adherence to damaged endothelium)

242
Q

What breed is the poster child for von Willebrand disease?

A

(Doberman pinscher)

243
Q

What is the ideal product to use in treatment of von Willebrand disease, treatment being aimed at addressing severe bleeding or preventing hemorrhage prior to invasive procedures?

A

(Cryoprecipitate)

244
Q

What clotting factor deficiency is hemophilia A?

A

(Factor VIII)

245
Q

What clotting factor deficiency is hemophilia B?

A

(Factor IX)

246
Q

What clotting factor time test can be used to determine if a patient has hemophilia A/B?

A

(PTT → will be prolonged)

247
Q

What are the vitamin K dependent coagulation factors?

A

(Factors II, VII, IX, and X)

248
Q

What effect on PT and PTT times does vitamin K coagulopathy have in general?

A

(Prolongs both PT and PTT times)

249
Q

What should be done when monitoring PT times in a patient with vitamin K antagonist rodenticide toxicity and the PT time becomes prolonged?

A

(Start vitamin K therapy)

250
Q

Is PTT or PT prolonged initially with DIC?

A

(PTT)

251
Q

What can you administer to a DIC patient to combat capillary obstructions and restore tissue perfusion?

A

(Administer fluids)