Blood Flashcards

1
Q

What is Type 1 Von Willebrand disease characterized by?

A

Presence of all multimers but in reduced concentrations

Bleeding precipitated by surgery, trauma, or concomitant hemostatic defect

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2
Q

Which dog breeds are overrepresented in Type 1 Von Willebrand disease?

A
  • Doberman Pinschers
  • Standard Poodles
  • Shetland Sheepdogs
  • German Shepherd Dogs
  • Airedale Terriers

These breeds have a higher incidence of Type 1.

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3
Q

What characterizes Type 2 Von Willebrand disease?

A

Disproportionate loss of high-molecular weight multimers

This type is associated with severe bleeding.

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4
Q

What is the hallmark of Type 3 Von Willebrand disease?

A

Almost complete absence of vWF (<0.1%)

This is the most severe form with life-threatening hemorrhage, often occurring within the first year of life.

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5
Q

True or False: Type 1 Von Willebrand disease is the most common type.

A

True

It is the most frequently occurring form of the disease.

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6
Q

Fill in the blank: Type 3 Von Willebrand disease is characterized by _______.

A

[almost complete absence of vWF (<0.1%)]

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7
Q

What platelet count is at risk for spontaneous hemorrhage?

A

50k

A platelet count below 50,000 cells per microliter increases the risk for spontaneous bleeding.

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8
Q

Formula to estimate total platelet count per hpf?

A

Avg Number/hpf x 15,000

This formula is used to estimate the total platelet count from a microscopic examination.

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9
Q

What is the normal range for Buccal Mucosal Bleeding Time?

A

<3 minutes

A bleeding time of less than 3 minutes is considered normal.

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10
Q

Which conditions can prolong Buccal Mucosal Bleeding Time?

A
  • Thrombocytopenia
  • Thrombopathia
  • Vasculopathy (non-specific)

These conditions affect the ability of blood to clot properly, leading to prolonged bleeding times.

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11
Q

What do Prothrombin Time (PT) and Activated Partial Thromboplastin Time (APTT) test for?

A

PT -> Extrinsic and/or common pathway
APTT -> Intrinsic and/or common pathway

These tests assess different pathways of the coagulation cascade.

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12
Q

What percentage decrease in a single factor can lead to prolongation in PT or APTT?

A

25 to 30%

A decrease of this magnitude indicates potential bleeding disorders.

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13
Q

What condition is the PT particularly sensitive to?

A
  • vitamin K deficiency
  • liver disease
  • deficiencies in clotting factors like VII, X, V, and II

Due to the short half-life of factor VII, PT is affected quickly by vitamin K status.

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14
Q

What does Activated Clotting Time (ACT) evaluate?

A

Intrinsic and common pathways

ACT is used to monitor anticoagulation therapy and surgical bleeding risks.

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15
Q

How does the sensitivity of ACT compare to APTT?

A

Less sensitive

ACT is not as responsive as APTT in detecting minor coagulation issues.

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16
Q

What are Fibrin Split Products generated from?

A

When plasmin lyses fibrinogen, soluble fibrin, or cross-linked fibrin

This process indicates increased fibrinolysis in the body.

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17
Q

What do elevated concentrations of Fibrin Split Products indicate?

A fibrin degradation product (FDP), also known as a fibrin split product, is a small protein fragment that remains in the bloodstream after a blood clot dissolves, essentially a byproduct of the body breaking down a clot through a process called fibrinolysis; elevated levels of FDPs can indicate a potential clotting disorder or excessive clot breakdown.

A

Increased fibrinolysis and/or fibrinogenolysis

While they may be elevated in DIC, they are not specific to it.

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18
Q

What are d-Dimers a specific degradation product of?

A

Cross-linked fibrin

d-Dimers are particularly useful in diagnosing thrombotic conditions. Cross-linked fibrin is a protein polymer that forms clots and stabilizes platelet plugs. It’s created when activated coagulation factor XIII (FXIIIa) cross-links fibrin molecules.

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19
Q

What conditions are d-Dimers sensitive indicators of?

A
  • Disseminated intravascular coagulation
  • Thromboembolism

d-Dimers are more sensitive to thrombosis than fibrin split products.

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20
Q

What is the endpoint of all clotting assays?

A

Fibrin clot

The formation of a fibrin clot is the final step in the coagulation cascade.

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21
Q

At level concentration does fibrinogen typically become prolong on test?

A

<50 to 100 mg/dL

Significant prolongation of clotting tests usually occurs only after fibrinogen levels drop below this range.

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22
Q

What role does fibrinogen play during inflammation?

A

Elevated concentrations occur with inflammation

Fibrinogen is an acute phase protein and can reflect inflammatory states.

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23
Q

What do Viscoelastic Testing methods like Thromboelastography (TEG) and Rotational Thromboelastometry (ROTEM) assess?

A

the hemostatic process

Providing a real-time, holistic view of clot formation, strength, and dissolution in whole blood.

These tests evaluate the interplay between plasma and cellular components in coagulation.

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24
Q

What is edema?

A

Presence of abnormally large amounts of fluid in the intercellular tissue spaces of the body

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25
Q

What are the two types of edema?

A

Localized and systemic

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26
Q

What can cause localized edema?

A

Venous obstruction, lymphatic obstruction, or increased vascular permeability

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27
Q

What conditions can lead to systemic edema?

A

Heart failure or renal disease

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28
Q

What is ascites?

A

Fluid accumulation in the peritoneal cavity

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29
Q

What is hydrothorax?

A

Fluid accumulation in the pleural cavity

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30
Q

What is hydropericardium?

A

Fluid accumulation in the pericardial sac

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31
Q

What is massive generalized edema called?

A

Anasarca

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32
Q

What is a contributing factor that can lead to increased hydrostatic pressure?

A
  • Impaired venous return
  • Small-caliber arteriolar dilation
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33
Q

Name a specific clinical syndrome associated with increase hydrostatic pressure due to imparied venous return?

A
  • Congestive heart failure CHF
  • Pericardial disease (pericardial effusion, constrictive pericarditis, pericardial cyst or neoplasm)
  • Portal hypertension
  • Venous obstruction or compression (thrombosis, external pressure, extremity inactivity)
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34
Q

Name a specific clinical syndrome associated with increase hydrostatic pressure due to small-caliber arteriolar dilation?

A
  • Heat
  • Neutohumoral dysregulation

Neutohumoral dysregulation is dysregulation of hormones affecting vascular tone and fluid balance

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35
Q

What can cause small-caliber arteriolar dilation?

A

Heat

This can lead to increased blood flow and subsequent edema.

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36
Q

What is neurohumoral dysregulation?

A

Dysregulation of hormones affecting vascular tone and fluid balance

It can contribute to fluid retention and edema.

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37
Q

What is a contributing factor that reduces plasma oncotic pressure?

A

Hypoproteinemia

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38
Q

Specific Clinical Syndromes assoicated with hypoproteinemia leading to reduced onctic pressure?

A
  • Protein-losing nephropathy (amyloidosis, glomerulonephritis)
  • Synthetic failure (chronic liver disease)
  • Malnutrition
  • Protein-losing gastroenteropathy
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39
Q

What is a contributing factor of lymphatic obstruction?

A

Decreased lymphatic draingage of interstitium

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40
Q

Specific Clinical Syndrome assoicated with decreased lymphatic draingage of interstitium leading to lymphamitic obstruction?

A
  • Various inflammatory conditions
  • Congenital (lymphedema)
  • Neoplastic
  • Postsurgical
  • Postirradiation
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41
Q

What is a contributing factor of sodium retention?

A
  • Excess dietary intake with renal insufficiency
  • Increased tubular sodium resorption
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42
Q

Specific Clinical Syndrome assoicated increased tubular sodium resorption leading to sodium retention?

A
  • Renal hypoperfusion
  • Increased renin-angiotensin-aldosterone secretion
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43
Q

What is a contributing factor of inflammation?

A
  • Acute inflammation
  • Chronic inflammation
  • Angiogenesis

These factors can lead to fluid overload and hypertension.

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44
Q

True or False: Acute inflammation can lead to angiogenesis.

A

True

Angiogenesis is the formation of new blood vessels, which can occur during inflammatory processes.

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45
Q

What is the lifespan of neutrophils?

A

10-15 hours

Production takes approximately 6 days, with 2-3 days in both mitotic and post-mitotic pools.

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46
Q

What is the lifespan of platelets?

A

5-7 days

None.

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47
Q

What is the lifespan of reticulocytes?

A

1-2.5 days

The regenerative response takes approximately 2-3 days and is not seen in acute anemia.

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48
Q

What is the lifespan of canine erythrocytes?

A

4 months

21 days with compatible transfusion, minutes to 12 hours for incompatible transfusions.

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49
Q

What is the lifespan of feline erythrocytes?

A

2 months

29-39 days in matched transfusions.

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50
Q

What is respiratory acidosis?

A

A condition caused by hypoventilation leading to hypercapnia (increased PaCO2) and decreased pH

Respiratory acidosis occurs when the lungs cannot remove enough carbon dioxide (CO2) produced by the body.

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51
Q

What happens to pH and CO2 levels in respiratory acidosis?

A

↓pH, ↑CO2

This indicates an acidic environment due to excess CO2 in the bloodstream.

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52
Q

What compensatory mechanism occurs in respiratory acidosis?

A

↑HCO3

The kidneys may retain bicarbonate to help buffer the excess acid.

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53
Q

What are some causes of respiratory acidosis?

A

Cervical compression, pleural space disease, airway obstruction

These conditions can hinder proper ventilation, leading to increased CO2 levels.

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54
Q

What clinical signs are associated with respiratory acidosis?

A

Tachyarrhythmias, ↑ BP, ↑ CO, vasodilation, and ↓ vascular resistance

Patients may also exhibit signs of restlessness and anxiety.

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55
Q

What is the primary treatment for respiratory acidosis?

A

Treat underlying problem and augment ventilation

Addressing the root cause is crucial for effective management.

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56
Q

Are you more likely to die from hypoxemia or acidosis

A

hypoxemia

Hypoxemia refers to low levels of oxygen in the blood, which can occur alongside acidosis.

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57
Q

What should be done regarding oxygen supplementation in respiratory acidosis?

A

Supplement O2 unless chronic

In chronic cases, oxygen may become the ventilatory drive, so caution is needed.

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58
Q

What is the primary cause of Respiratory Alkalosis?

A

Hyperventilation leading to hypocapnia

Hypocapnia is a state of reduced carbon dioxide in the blood, often resulting from increased respiratory rate or depth.

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59
Q

What are the main physiological changes in Respiratory Alkalosis?

A

↑pH, ↓CO2

The increase in pH indicates alkalosis, while the decrease in CO2 is due to excessive ventilation.

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60
Q

What is the compensation mechanism in Respiratory Alkalosis?

A

↓ HCO3

The kidneys compensate for alkalosis by decreasing bicarbonate (HCO3) levels.

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61
Q

List the causes of Respiratory Alkalosis.

A
  • Hypoxemia
  • Primary pulmonary disease
  • Direct activation of central respiratory centers
  • Overzealous manual ventilation
  • Pain, anxiety, or fear

Each cause can lead to increased respiratory rate or depth, contributing to hypocapnia.

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62
Q

True or False: CS are common with Respiratory Alkalosis.

A

False

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63
Q

What type of breathing is associated with Respiratory Alkalosis?

A

Thoracic breathing

Thoracic breathing may be more pronounced in conditions leading to hyperventilation.

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64
Q

Alkalosis:
* Elevated HCO3- and increased pH
* Can result from _____ of chloride or gain of exogenous alkali

A

Alkalosis:
* Elevated HCO3- and increased pH
* Can result from loss of chloride or gain of exogenous alkali

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65
Q

HCO3 replacement formula

A

NaHCO3 (mEq) = 0.3 x body weight (kg) x base deficit (mEq/L)

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66
Q

Percentage of body weight:
* Dry matter -> ______
* intracellular -> ______
* extracellular -> ______

A

Percentage of body weight:
* Dry matter -> 40%
* intracellular -> 40%
* extracellular -> 20%

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67
Q

Percentage of body weight:
* Dry matter -> 40%
* Intracellular -> 40%
* Extracellular -> 20%

Extracellular fluids is divided into what and give percentage.

A

Plasma 5%
Interstitial fluid 15%

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68
Q

Percentage of total fluid of:

  • Intracellular -> _____%
  • Extracellular -> _____%
A

Percentage of total fluid of:

  • Intracellular -> 66%
  • Extracellular -> 33%
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69
Q

Extracellular fluid is made of what two parts? what %?

A

Plasma 25%

Interstitial fluid 75%

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70
Q

Explain extracellular edema with SIRS?

A

Loss of the Glycocalyx layer then Cytokine mediated leading to increased vascular permeability —> proteins + osotonic —> Extravascular System (aka interstitial space) —> interstitial edema (nonpitting edema), hypovolemia, hypoproteinemia

In SIRS, this results in interstitial edema, hypovolemia, and hypoproteinemia.

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71
Q

What does an increase in hydrostatic pressure leads to?

A
  • Arterial dilation
  • Venule contraction
  • Increased venous pressure (e.g., Heart Failure)

These factors contribute to conditions that lead to extracellular edema.

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72
Q

What does an decreased osmotic pressure leads to?

A

It leads to hypoproteinemia, which can contribute to the development of extracellular edema.

Hypoproteinemia is a condition where there is a low level of protein in the blood.

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73
Q

What substances are associated with increased vascular permeability?

A
  • Substance P
  • Histamine and related substances

These substances play a significant role in the development of edema.

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74
Q

What is inadequate lymph flow’s role in extracellular edema?

A

It contributes to the accumulation of interstitial fluid, leading to edema.

Lymphatic obstruction can prevent proper fluid drainage from tissues.

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75
Q

What type of edema is characterized by interstitial fluid accumulation without pitting?

A

Nonpitting edema.

This type of edema does not leave a dent when pressure is applied.

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76
Q

Fill in the blank: In SIRS, the loss of the Glycocalyx layer leads to _______ permeability.

A

vascular

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77
Q

True or False: Hypovolemia is a condition that can result from extracellular edema.

A

True

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78
Q

What is the rapid equilibration time for crystalloid redistribution infusion between the intravascular and interstitial fluid?

A

20-30 min

This is the time it takes for the fluid to equilibrate (steady state) between intravascular and interstitial spaces.

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79
Q

What type of fluids are crystalloid solutions considered?

A

Extracellular-expanding fluids

These fluids expand the extracellular compartments in the body.

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80
Q

What percentage of the volume infused with crystalloids redistributes to the interstitial space?

A

75%

Only 25% of the volume remains in the vascular space.

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81
Q

What is the percentage of crystalloid infusion that remains in the vascular space?

A

25%

This is the portion of the infused volume that stays within the blood vessels.

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82
Q

What is the maintenance dose for crystalloid infusion in dogs?

A

2-4 ml/kg/hr

Larger dogs and obese dogs may require less fluid.

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83
Q

The osmolarity of crystalloid solutions is the same as what?

A

Plasma

This similarity helps maintain osmotic balance in the body.

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84
Q

What are the main contributors to osmolality?

A

Na+, K+, Cl-, HCO3-, glucose, and urea

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85
Q

Is glucose an effective osmole?

86
Q

Is urea an effective osmole?

87
Q

Fill in the blank: Glucose is an effective osmole (not _______).

A

freely movable

88
Q

Fill in the blank: Urea is not an effective osmole (________).

A

freely movable

89
Q

Are maintenance fluids hypertonic or hypotonic?

A

Maintenance fluids are hypotonic.

They have less sodium and more potassium.

90
Q

What is an example of a maintenance fluid?

A

An example includes dextrose (metabolized and free water remains).

91
Q

How fast should hypernatremia be corrected?

A

Decreased as a rate of >0.5 mEq/h
Should not decrease by > 1mEq/h

92
Q

What can happen if hypernatremia be corrected too fast?

A

Cerebral edema

93
Q

What are hypotonic solutions?

A

Solutions with lower osmolarity than ECF

ECF stands for extracellular fluid.

94
Q

What is the characteristic of maintenance hypotonic crystalloids compared to plasma?

A

↓ Na/Cl- and osmolarity but ↑ K+

Maintenance hypotonic crystalloids are not suitable for bolusing.

95
Q

Why should hypotonic solutions not be used for bolusing?

A

Rapid ↓ osmolarity can cause cerebral edema

This is because the solution distributes to all compartments.

96
Q

In which patients are hypotonic solutions most useful?

A

Perioperative patients that are stable but not eating/drinking or with animals with free water deficit/mild hypernatremia

Obligatory fluid losses are hypotonic, with more K compared to ECF.

97
Q

How can severe free water loss be corrected?

A

With D5W

D5W refers to 5% dextrose in water.

98
Q

What is the recommended rate of D5W to slowly decrease sodium concentration?

A

3.7 mL/kg/hr D5W

This is a guideline for managing free water deficits.

99
Q

What is the formula to calculate fluid needs for correcting sodium levels?

A

0.6 x BW (kg) x (Na pt/normal Na -1)

BW stands for body weight and Na pt refers to the patient’s sodium level.

100
Q

What does Base Excess indicate?

A

The level of acid or base in the blood assessing the metabolic component

Base Excess is a blood test result used in clinical assessments.

101
Q

What does a negative base excess indicate?

A

Base deficit = nonrespiratory = Metabolic acidosis

This indicates an excess of acid in the blood.

102
Q

What condition is indicated by a positive base excess?

A

Metabolic alkalosis

This indicates an excess of base in the blood.

103
Q

What is hypertonic saline?

A

A solution with higher osmolarity than extracellular fluid (ECF)

Hypertonic saline is often used in medical settings to manage specific conditions.

104
Q

What is the typical concentration of hypertonic saline used?

A

7-7.5% NaCl

This concentration is specifically administered for therapeutic purposes.

105
Q

What is the recommended dosage of hypertonic saline?

A

4-6 mL/kg administered over 10-20 minutes

106
Q

What happens if the administration rate exceeds 1 mL/kg/min?

A

Leads to osmotic stimulation of pulmonary C-fibers, resulting in vagally mediated hypotension, bradycardia, and bronchoconstriction

It is crucial to avoid exceeding this rate.

107
Q

What are the benefits of administering hypertonic saline?

A
  • Reduces endothelial swelling
  • Increases cardiac contractility
  • Causes mild peripheral vasodilation
  • Modulates inflammation
  • Decreases intracranial pressure (ICP)

These effects make hypertonic saline useful in critical care settings.

108
Q

In which conditions is hypertonic saline used?

A
  • Head trauma
  • Cardiovascular shock (GDV)

Its use is especially critical for rapid intravascular volume expansion.

109
Q

What is the duration for intravascular volume expansion when using hypertonic saline?

A

Less than 30 minutes

After this period, it is necessary to maintain volume with additional fluid therapy (requires a large amt of fluid resuscitation)

110
Q

What are some risks associated with hypertonic saline administration?

A
  • Increased sodium chloride (NaCl)
  • Decreased potassium (K) and bicarbonate (HCO3)
  • Interstitial dehydration
  • Phlebitis/hemolysis if a peripheral vein is used

These risks highlight the importance of careful monitoring during treatment.

111
Q

True or False: Hypertonic saline should be used in dehydrated animals.

A

False

It is contraindicated in dehydrated animals due to the risk of interstitial dehydration.

112
Q

What is the Starling law of capillary?

A

It describes the movement of fluid across capillary membranes based on hydrostatic and oncotic pressures.

113
Q

What generates hydrostatic pressure?

A

The volume of blood, specifically blood pressure (BP) and systemic vascular resistance (SVR).

114
Q

What is the role of capillary and interstitial colloid osmotic pressure?

A

It determines the oncotic pressure gradient affecting fluid movement.

115
Q

What determines the oncotic pressure gradient?

A

The ratio of proteins in the blood and interstitial fluid.

116
Q

Fill in the blank: Hydrostatic pressure is generated by the volume of blood, including _______ and systemic vascular resistance.

A

blood pressure

117
Q

True or False: Oncotic pressure is generated by proteins.

118
Q

What is osmotic pressure?

A

The pressure generated by proteins in the blood and interstitial fluid.

119
Q

What are the anaphylactoid reactions observed in healthy animals receiving human albumin?

A

V+, facial edema, tachypnea, collapse hypotension

These reactions can include delayed hypersensitivity reactions occurring 5-13 days after initial transfusion.

120
Q

What type of hypersensitivity is associated with human albumin transfusions in healthy animals?

A

Type III hypersensitivity

This involves antigen-antibody complex deposition in various tissues.

121
Q

What prolonged immune response can occur in healthy dogs after receiving human albumin?

A

Prolonged IgE immune response

This response can lead to complications in healthy dogs.

122
Q

What were the findings of Matthews et al. regarding facial edema in critically-ill dogs receiving human albumin?

A

2 out of 64 had facial edema

This indicates a low incidence of side effects in critically-ill dogs.

123
Q

What percentage of critically-ill dogs showed minor reactions after human albumin transfusion in a study of 73 dogs?

A

27%

Minor reactions included tachypnea, tachycardia, body temp changes, peripheral edema, and ventricular arrhythmias.

124
Q

Why do critically-ill dogs experience fewer side effects from human albumin compared to healthy dogs?

A

Critically-ill dogs cannot mount a good immune response

Healthy dogs produce IgG in 10-14 days post-infusion, while ill dogs take 4-6 weeks.

125
Q

In what situation is human albumin considered for use in small animals?

A

Only in severely compromised small animals with no other option

This indicates the seriousness of the condition when using human albumin.

126
Q

What are colloids recommended for?

A

ARDS or Sepsis with severe hypoalbuminemia (1.3 g/dL)

Severe hypoalbuminemia is defined as a serum albumin level below 1.3 g/dL.

127
Q

What is Canine Albumin?

A

Hyperosmotic solution 16% (for hypotension, causes acute volume expansion) or iso-osmotic 5% preparation

Canine Albumin is used in veterinary medicine to manage fluid balance.

128
Q

What is the purpose of a hyperosmotic solution like Canine Albumin?

A

To treat hypotension and cause acute volume expansion

Hyperosmotic solutions draw water into the bloodstream, increasing blood volume.

129
Q

Fill in the blank: Colloids are recommended for ARDS or Sepsis with severe _______.

A

hypoalbuminemia

130
Q

True or False: Canine Albumin is available in a 10% preparation.

A

False

Canine Albumin is available in 16% and 5% preparations.

131
Q

What is the serum albumin level indicating severe hypoalbuminemia?

132
Q

True or False: Synthetic colloids are large molecules and take longer to break down?

133
Q

List some negative effect of synthetic colloids?

A
  • Decrease in factor VIII and vWF
  • Impairs PLT function
  • Interference with fibrin clot stability (susceptible to fibrinolysis)
134
Q

True or False: Synthetic colloids can impair platelet function.

135
Q

Fill in the blank: VetStarch is also known as _______ starch.

A

Hydroxyethyl starch

136
Q

What is an advantage of hydroxyethyl starch (VetStarch) over other synthetic colloids?

A

More rapidly cleared and less side effects (less coagulopathies).

137
Q

What is the normal value of Central Venous Pressure (CVP) using a water manometer?

A

0 to 8 cm H2O

138
Q

What is the normal value of Central Venous Pressure (CVP) using a pressure transducer?

A

0 to 5 mm Hg

139
Q

What does a decrease in CVP to less than 0 cm H2O indicate?

A

Hypovolemia/ vasodilation

140
Q

List conditions that can cause an increase in CVP greater than 10 cm H2O.

A
  • Cardiogenic shock
  • Right Congestive Heart Failure (R-CHF)
  • Caval obstruction
  • Iatrogenic volume overload
  • Pericardial effusion
  • Pleural space disease
  • Increased intrathoracic pressure (IPPV, tension pneumothorax)
141
Q

What effect does a fluid bolus have on CVP?

A

Increases CVP by 4 - 5 cm H2O for very slow return to baseline (takes 30 to 60 minutes)

142
Q

How long does it take for CVP to return to baseline after a fluid bolus?

A

30 to 60 minutes

143
Q

True or False: A CVP of less than 0 cm H2O indicates hypervolemia.

144
Q

Fill in the blank: The normal range for CVP measured in mm Hg is _______.

A

0 to 5 mm Hg

145
Q

How does positive pressure ventilation affect venous return?

A

It impedes venous return

This then decreases diastolic filling then decrease stroke volume

146
Q

What is the effect of decreased diastolic filling on stroke volume after PEEP impedes venous return?

A

It decreases stroke volume

147
Q

What are the consequences of decreased cardiac output in order?

A
  • Decrease in heart rate or Decrease in stroke volume —>
  • Backing up of blood to venous circulation (decrease venous volume)
  • Increase in thoracic blood volume
  • Increase in central venous pressure
148
Q

What might patients with low intravascular volume display during positive-pressure breaths?

A

Attenuation of the arterial blood pressure waveform

149
Q

How does heart disease lead to an increase in CVP?

A

Heart disease leading to poor perfusion and fluid overload

150
Q

What does PEEP stand for?

A

Positive End-Expiratory Pressure

151
Q

What is the typical range for PEEP in cm H2O?

A

4-5 cm H2O

152
Q

What is the primary purpose of PEEP?

A

To prevent end-expiratory alveolar collapse

153
Q

What effect can PEEP have on systemic venous return?

A

It can decrease systemic venous return

154
Q

What complication can arise from PEEP due to hyperinflation?

A

Pulmonary barotrauma

155
Q

What are the acid-base effects associated with PEEP?

156
Q

What does PEEP help to improve in mechanically ventilated patients?

A

Oxygenation

157
Q

Fill in the blank: PEEP maintains positive pressure in the airways at the end of _______.

A

exhalation

158
Q

True or False: With a high PEEP you can compromise CO via compression the the great vessels.

159
Q

What is the storage time for Fresh Whole Blood?

A

Best before 8 hours; not good after 24 hours

160
Q

What happens to clotting factors in stored whole blood?

A

Clotting factors don’t work as they degrade (factor V and VIII)

161
Q

What is the shelf life of pRBS at 4°C?

A

20 days; extended to 35 days with additives

162
Q

What are the additives that can extend the shelf life of pRBS?

A
  • Adsol
  • Nutricel
163
Q

What does Fresh Frozen Plasma contain?

A
  • Plasma proteins
  • Clotting factors (rich in labile factors V & VIII and vWF)
164
Q

How soon must Fresh Frozen Plasma be frozen after collection and temperature?

A

Within 6 hours; Below 20°C

165
Q

What is the maximum storage duration for Fresh Frozen Plasma for liable clotting factors?

A

Less than 1 year

166
Q

What happens to frozen plasma after one year?

A

Becomes Frozen Plasma and sources of clotting factors V, VIII, and vWF not liable

167
Q

What does Cryoprecipitate contain?

A
  • Factor VIII
  • vWF
  • Fibrinogen
168
Q

What is the lifespan of Platelets?

169
Q

What does a rightward shift in the oxygen saturation curve indicate?

A

Decreased affinity of hemoglobin for oxygen

This means oxygen is more actively unloaded at the tissues.

170
Q

List the factors that cause a right shift in the oxygen saturation curve.

A
  • ↓ pH
  • ↑ Temp
  • ↑ CO2
  • ↑ 2,3-DPG
171
Q

What is the effect of a rightward shift on oxygen release?

A

More oxygen is released at the tissues

This facilitates oxygen delivery to metabolically active tissues.

172
Q

What does a leftward shift in the oxygen saturation curve indicate?

A

Increased hemoglobin affinity for oxygen

This results in a reluctance to release oxygen.

173
Q

What is the effect of a leftward shift on oxygen availability to tissues?

A

Reduces oxygen availability to the tissues

174
Q

Fill in the blank: A rightward shift of the curve indicates that hemoglobin has a _______ for oxygen.

A

decreased affinity

175
Q

Fill in the blank: A left shift of the oxygen saturation curve indicates an increase in hemoglobin’s _______.

A

oxygen affinity

176
Q

Major source of lactate

A

Muscle and GI tract

177
Q

What causes hyperlactatemia?

A

Lack of perfusion

Can increase despite normal O2 due to the lack of perfusion

Hyperlactatemia is often a result of inadequate oxygen delivery to tissues.

178
Q

True or False: Trends in lactate levels more useful than a single value.

A

True

Monitoring changes in lactate levels can provide better insight into a patient’s condition.

179
Q

What is considered a normal lactate level?

A

Normal = <2 (>6 is severe hyperlactatemia)

Lactate levels above 2 mmol/L indicate hyperlactatemia, with levels above 6 being classified as severe.

180
Q

What are the pitfalls of using lactate as a marker of hypoperfusion?

A
  • Kidney are great at clearing even with low perfusion
  • Artifactually increased due to poor sample handling
  • There is type A and B lactic acid
181
Q

Artifact increase in lactate levels once sample id collected?

A

Artifactual ↑ in lactate with poor sample handling

Improper collection or handling of blood samples can falsely elevate lactate readings.

182
Q

What does Type A lactic acid indicate and what does Type B lactic acid inddicate?

A

Type A lactic acid = poor perfusion (GDV)

Type B lactic acid = mitochondrial dysfunction (drugs/toxin/sepsis/DM)

Type A lactate elevation is primarily associated with conditions that reduce tissue perfusion.

Type B lactate elevation is linked to metabolic issues unrelated to perfusion.

183
Q

What did GDV hyperlactatemia predict regarding gastric health?

A

GDV hyperlactatemia predicted gastric necrosis but base excess did not

This finding suggests that lactate levels may be a more reliable indicator of gastric necrosis than base excess.

184
Q

What is the first phase of clotting?

A

Initiation phase

In this phase, tissue factor creates thrombin through the extrinsic pathway.

185
Q

What occurs during the amplification phase of clotting?

A

PLT become active and release factors

IIA activates vWF, which then activates VIIIa and releases vWF.
IIA amplifies the initial signal by activating PLT and cofactors (Va and VIIIa) on the PLT surface.

186
Q

What is the role of IIA in the amplification phase?

A

Amplifies the initial signal by activity PLT and cofactors on PLT surface

IIA is crucial for activating factors that enhance the clotting process.

187
Q

What happens during the propagation phase?

A

Large-scale IIa production on the surface of the activated PLT

This phase leads to the conversion of fibrinogen to fibrin.

188
Q

Fill in the blank: In the propagation phase, _______ is converted to fibrin.

A

Fibrinogen

189
Q

Fill in the Blank: During the initiation phase of clotting, tissue factor creates ______ through the extrinsic pathway.

190
Q

Fill in the Blank: During the initiation phase of clotting, tissue factor creates thrombin through the ___________ pathway.

A

Extrinsic pathway

191
Q

Fill in the Blank: During the initiation phase of clotting, ______ _________ creates thrombin through the extrinsic pathway.

A

Tissue Factor

192
Q

What is Antithrombin?

A

A circulating α2-globulin produced by the liver that inactivates Thrombin (IIa) and FXa

Antithrombin plays a crucial role in regulating blood coagulation.

193
Q

How does Activated Protein C function?

A

It is activated by the thrombin-thrombomodulin complex, which inactivates factors Va and VIIIa, slowing the rate of IIa formation

Activated Protein C requires protein S as a cofactor for its action.

194
Q

What role does thrombomodulin play in coagulation?

A

It binds free IIa (not bound to antithrombin) on the endothelial surface, leading to the activation of protein C

Thrombomodulin is essential for the activation of the protein C pathway.

195
Q

What is the function of Tissue Factor Pathway Inhibitor?

A

It binds with and inactivates Xa, forming a tetramer with VIIa-TF that inactivates VIIa-TF

This mechanism is important for regulating the extrinsic pathway of coagulation.

196
Q

True or False: Antithrombin inactivates only Thrombin (IIa).

A

False

Antithrombin also inactivates FXa.

197
Q

Fill in the blank: Activated Protein C inactivates factors _____ and _____ to slow IIa formation.

A

Va and VIIIa

This action is crucial for controlling the coagulation process.

198
Q

True or False: More complex surgeries have a higher chance of bleeding complications.

199
Q

What should be giving Greyhound for surgery due to there delayed post-op bleeding associated with altered/ enhanced fibrinolysis?

A

Aminocaproic acid

200
Q

What factors do vW dz effect?

A

vW factor

Is a protein that helps platelets stick together and form a clot, and also stabilizes clotting factor VIII.

201
Q

How do you diagnoses vW dz?

202
Q

What are the types of vW disease?

A

Type 1: The most common type, characterized by a reduced amount of vWF.
Type 2: Some vWF is present, but it’s abnormal in structure.
Type 3: Very little or no vWF is present.

203
Q

What is the treatment for VW disease?

A

Treated by cryoprecipitate

Cryoprecipitate elevates vWf within 30 minutes of transfusion and lasts for 4 hours.

204
Q

What prophylactic treatment can be used for Type 1 VW disease?

A

Desmopressin

Desmopressin is also known as de-amino D-arginine vasopressin (DDAVP).

205
Q

What is the mechanism of action of Desmopressin?

A

Synthetic Vasopressin analog → via V2 receptors, releases subendothelial vWf stores, fVIII and plasminogen

This mechanism helps in increasing levels of von Willebrand factor and factor VIII.

206
Q

When should Desmopressin be administered prophylactically?

A

30 minutes before surgery

The effect of Desmopressin lasts for 2 hours.

207
Q

For which type of vWF is Desmopressin effective?

A

Only effective for type 1 vWF

Type 1 vWF is characterized by reduced concentrations of all multimers.

208
Q

What is the risk associated with having less than 20% vWf?

A

Spontaneous bleed

Reduced levels can lead to bleeding disorders.

209
Q

Which dog breeds are overrepresented in VW disease?

A

Dobermans, Standard Poodles, Shetland Sheepdogs, German Shepherd Dogs, Airedale Terriers

These breeds are more likely to be affected by VW disease.

210
Q

What is VW disease?

A

VW disease is platelet dysfunction disease

VW disease refers to von Willebrand disease, which affects the blood’s ability to clot.

VWF binds to platelets and helps them adhere to the damaged blood vessel wall, initiating the clotting process.
VWF carries and stabilizes factor VIII, a clotting protein.

211
Q

What is the normal time from incision to cessation of bleeding in dogs?

A

1.7 - 4.2 min <3min

The cessation of bleeding time is a critical measure in evaluating hemostasis.

212
Q

What is the normal time from incision to cessation of bleeding in cats?

A

1.4 - 2.4 min

This time frame is essential for assessing bleeding tendencies in feline patients.