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ACVIM General Exam > Respiratory > Flashcards

Respiratory Flashcards

1
Q

What are the two conformations of hemoglobin?

A

T-State: Low oxygen affinity

R-State: High oxygen affinity

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2
Q

What stabilizes hemoglobin into the T-state?

A
  1. H+
  2. CO2
  3. 2,3-DPG

*Due to products of processes occurring in the tissues → in the tissues we want to offload oxygen (low affinity)

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3
Q

What stabilizes hemoglobin in the R-state?

A
  1. O2

2. CO

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4
Q

What happens in carbon monoxide poisoning?

A

The R-form of hemoglobin is stabilized. CO binds to hemoglobin with a higher affinity than oxygen

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5
Q

How does the O2-hemoglobin curve shift in acidemia

A

Right

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6
Q

How does the O2-hemoglobin curve shift with increased CO2 concentrations?

A

Right

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7
Q

How does the O2-hemoglobin curve shift in decreased temperatures?

A

Left

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8
Q

How does the O2-hemoglobin curve shift in increased 2,3-DPG?

A

Right

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9
Q

What is the Bohr effect?

A

The effect of CO2 and H+ on the affinity of hemoglobin for O2

  1. Increased CO2 and H+ → decreases affinity/promotes offloading
  2. Decreasing CO2 and H+ → increases affinity/enhances loading
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10
Q

How does the O2-hemoglobin curve shift at the pulmonary capillary bed?

A

Left

  • Decreased p50
  • Increased O2 affinity and uptake
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11
Q

What forms does CO2 exist in the blood?

A
  1. HCO3 - 70%
  2. Hemoglobin - 23%
  3. Dissolved in plasma (pCO2) - 7%
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12
Q

How does CO2 interact with the red blood cells?

A

It is brought into the red blood cell and interacts with carbonic anhydrase → ultimately results in the dissociation of carbonic acid into H+ and HCO3 → HCO3 diffuses out of the red blood cell and Cl shifts in (Chloride shift)

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13
Q

What is the Haldane effect?

A

O2 + hemoglobin = stronger acid

  1. Less tendency to combine with CO2 to form carbaminohemoglobin
  2. Release an excess of H2 ions
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14
Q

What is the difference between the Bohr and Haldane effects?

A
  1. Bohr → increase in CO2 in blood causes O2 to be displaced from oxygen (tissues)
  2. Haldane → binding of O2 with hemoglobin causes CO2 to be displaced from the hemoglobin (lungs)
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15
Q

What determines the excretion of CO2?

A

Minute ventilation (TV x RR)

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16
Q

What are the regulators of respiration (what and where)?

A
  1. Central chemoreceptors - CO2
    - 2/3 of CO2 regulation (slow)
  2. Peripheral chemoreceptors - CO2
    - 1/3 of CO2 regulation (fast)
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17
Q

Where are the peripheral chemoreceptors?

A

Aortic and carotid bodies

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18
Q

How do peripheral chemoreceptors detect decreases in PO2? What happens when decreased PO2 detected?

A

Glomus cells → O2 sensitive K channels

Decreased O2 → K efflux → calcium influx → depolarization → dopamine release → respiratory stimulation via cranial nerve IX

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19
Q

Why does CO2 have a more potent effect in stimulating the central chemoreceptor neurons than hydrogen ions?

A

The blood brain barrier is not very permeable to hydrogen ions, but CO2 passes easily through the BBB

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20
Q

Where are the central chemoreceptors located?

A

Chemosensitive area bilaterally of the medulla oblongata

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21
Q

How do the central chemoreceptors work?

A

Excited more easily by hydrogen ions → problem because H does not easily pass the BBB

CO2 passes through the BBB and interacts with carbonic anhydrase to form H+ and HCO2 → the H+ then interacts with the central chemoreceptor

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22
Q

Where is the respiratory center located?

A

Bilaterally in the medulla oblongata and the pons

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23
Q

What are the different groups in the respiratory center? What do they control?

A
  1. Dorsal respiratory group → Inspiration
  2. Ventral respiratory group → Expiration (and inspiration), inactive during normal quiet respiration
  3. Pneumotaxic center → rate and depth of breathing, the inspiratory “off-switch”
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24
Q

What disease is associated with dysfunctional cilia?

A

Primary cilia dyskinesia (PCD)

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25
Q

What breed is predisposed to primary cilia dyskinesia?

A

Bichon Frise

*Old English Sheepdogs, Alaskan malamutes and English pointers can also be affected

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26
Q

What are the clinical signs associated with primary cilia dyskinesia?

A
  1. Nasal discharge
  2. Recurrent respiratory infections
  3. Male infertility
  4. Hydrocephalus
  5. Sinus inversus
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27
Q

What is the cause of primary cilia dyskinesia?

A

Mutation in microtubule conformations

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28
Q

Parasympathetic ACh causes what effect in the lung?

A

BronchoCONSTRICTION

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29
Q

Sympathetic Epi/Norepi causes what effect in the lung? Via which receptor?

A

BronchoDILATION

- B2 adrenergic receptors

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30
Q

What is the most common form of canine fungal rhinitis? How is this treated?

A

Aspergillus

Tx: Clotrimazole infusion

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31
Q

What is the most common form of feline fungal rhinitis? How is this treated

A

Cryptococcus

Tx: Fluconazole

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32
Q

What compose the conducting airways?

A

Trachea and bronchi

*Anatomic dead space

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33
Q

What are the basal cells in the respiratory epithelium?

A
  1. Lie underneath the columnar cells
  2. Stem cell producing new epithelial and goblet cells
  3. ABSENT in bronchioles and beyond
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34
Q

What cells secrete secrete surfactant?

A

Type II alveolar epithelial cell (granular pneumocytes)

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35
Q

Which alveolar epithelial cells are most abundant?

A

Type 1 - 95%

Type 2 - 5%

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36
Q

What are the roles of type 1 alveolar epithelial cells (pneumocytes)

A
  1. Line alveoli
  2. Function in gas exchange
  3. Do not divide in vivo

*Exposed to the highest concentration of oxygen - can. have oxygen toxicity damage

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37
Q

What are the roles of type 2 alveolar epithelial cells (pneumocytes)

A
  1. Stem cells from which type 1 cells arise
  2. No gas exchange
  3. Produces/Stores surfactant in the cytoplasm
  4. Resistant to oxygen toxicity damage
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38
Q

What is surfactant composed of?

A
  1. 80% phospholipids
  2. 5-10% neutral lipids
  3. 8-10% proteins
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39
Q

What muscle(s) plays a role in the process of inspiration?

A
  1. Diaphragm → contracts and flattens, causes intrapleural space to become more negative
  2. External intercostals → make diaphragm contraction more efficient, little role at rest, greater role during exercise
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40
Q

What muscle(s) plays a role in the process of expiration?

A
  • Typically a passive process*
    1. Abdominal muscles push diaphragm up → increase the intrapleural pressure
    2. Internal intercostals → oppose action of external intercostals, pull ribcage down and in
    3. Accessory muscles → laryngeal muscles, act as “breaks”
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41
Q

What components determine lung compliance?

A
  1. Elastic forces of the lung → 1/3, composed of elastin and collagen fibers
  2. Elastic forces caused by surface tension of the fluid that lines the inside of the alveoli → 2/3, surfactant
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42
Q

What decreases lung compliance?

A
  1. High lung volume
  2. Surfactant deficiency
  3. Pulmonary edema
  4. Atelectasis or alveolar collapse
  5. Pulmonary fibrosis
  6. Smooth muscle constriction in the small airways (asthma)
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43
Q

What increases lung compliance?

A
  1. Age
  2. Emphysema
  3. Body size
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44
Q

Which breed is predisposed to idiopathic pulmonary fibrosis?

A

Westies!

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45
Q

What is tidal volume?

A

Volume of air inspired or expired with each normal breath

10-15 ml/kg

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46
Q

What is the inspiratory reserve volume?

A

The extra volume of air that can be inspired OVER the normal tidal volume

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47
Q

What is the inspiratory capacity?

A

Tidal volume + inspiratory reserve volume

The total amount of air that an individual can breathe in

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48
Q

What is the expiratory reserve volume?

A

The extra volume of air that can be expelled by an active expiratory effort AFTER passive expiration

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49
Q

What is the the residual volume?

A

The volume of air remaining in the lungs after the most forceful expiration

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50
Q

What is the functional residual capacity?

A

Expiratory reserve volume + residual reserve volume

The amount of air that remains in the lungs at the end of normal expiration

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51
Q

What is the vital capacity?

A

Tidal volume + inspiratory reserve volume + expiratory reserve volume

The maximum amount of air an individual can expel from the lungs after filling the lungs to the maximum extent and then expiring to a maximum extent

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52
Q

What is the total lung capacity?

A

Vital capacity + residual volume

The maximum amount of air the lungs can be expanded with the greatest amount of effort

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53
Q

What factors affect diffusion in the lung?

A
  1. Thickness of membranes
  2. Surface area
  3. Diffusion coefficient of gas
  4. Partial pressure difference
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54
Q

What happens to the blood vessel if the concentration of O2 in an alveoli decreases?

A
  1. Adjacent blood vessels constrict → increase vascular resistance
  2. Distributes blood flow to where the lungs are better aerated
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55
Q

What occurs to V/Q in the following scenarios?

  1. Without ventilation
  2. Without perfusion
A
  1. V/Q = 0

2. V/Q = infinity

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56
Q

What diseases can lead to a low V/Q (poor ventilation, decreased PaO2)

A
  1. Chronic bronchitis
  2. Asthma
  3. Pulmonary edema

*Ventral lungs have slightly lower V/Q

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57
Q

What diseases can lead to a high V/Q (poor perfusion, increased PaCO2)

A
  1. Pulmonary thromboembolism

* Dorsal lungs have high V/Q

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58
Q

Which intestinal worms have pulmonary migration?

A
  1. Ancylostoma

2. Toxocara

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59
Q

How do you treat intestinal worm associated pulmonary disease?

A
  1. Glucocorticoids

2. Fenbendazole - 2 doses, 2 weeks apart

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60
Q

Lung worms are (easy/difficult) to diagnose based on fecal flotation or sedimentation. Why?

A
  1. Difficult
  2. Intermittent shedding

*Treat with empiric fenbendazole if suspected

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61
Q

What is the most common feline lungworm? Where (geographically) is it most prevalent?

A
  1. Aelurostrongylus

2. Southern US

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62
Q

Where do Aelurostrongylus reside in the lungs?

A

Terminal bronchioles and alveoli

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63
Q

How are Aelurostrongylus transmitted?

A
  1. Fecal-oral transmission
    * They are coughed up and then passed in the feces
  2. Eating encysted larvae in the tissue of mice and birds
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64
Q

What are the clinical signs associated with Aelurostrongylus infection?

  1. Mild
  2. Severe
A
  1. Typically asymptomatic - Hard to differentiate from feline lower airway disease!
  2. Severe eosinophilic bronchopneumonia with bronchointerstitial to alveolar infiltrates
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65
Q

How is Aelurostrongylus diagnosed?

A

BAL or Baerman

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66
Q

How do you treat an Aelurostrongylus infection?

A
  1. Fenbendazole or macrocyclic lactone
  2. Anti-inflammatory glucocorticoids
  3. Bronchodilators
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67
Q

What are the lung flukes? Where are they present geographically?

A
  1. Paragonimus kellicoti and westermani

2. Great Lakes, midwest, and South

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68
Q

What do paragonimus sp. cause in the lungs of dogs and cats?

A

Cysts

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69
Q

What clinical signs are common with paragonimus sp.

A
  1. Eosinophilic pleurites and cough (common)
  2. Nodules, bullae, and atelectasis can occur in the RIGHT MIDDLE LUNG LOBE
  3. Hemoptysis and pneumothorax can occur when adults emerge
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70
Q

How are paragonimus sp. diagnosed?

A
  1. Ova often present on BAL

2. Intermittently present on sedimentation

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71
Q

How are animals infected with paragonimus sp.?

A

Eating raw crabs or crayfish

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72
Q

How are paragonimus sp. treated?

A

Fenbendazole or praziquantel

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73
Q

What are the canine lungworms?

A
  1. Filaroides hirthi and milksi

2. Crenosoma vulpis

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74
Q

What population acquires filaroides spp.?

A

Research colonies

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75
Q

Adult filaroides live in which part of the lung?

A

Terminal bronchioles and alveoli

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76
Q

How are filaroides sp. treated?

A

Fenbendazole or ivermectin

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77
Q

Where is crenosoma vulpis located geographically?

A
  1. Northeastern US

2. Canada

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78
Q

Where are crenosoma vulpis adults located in the lung?

A

Terminal bronchioles and alveoli

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79
Q

How are crenosoma vulpis treated?

A

Fenbendazole or macrocyclic lactones

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80
Q

Where is angiostrongylus vasorum located geographically?

A
  1. Canada
  2. Europe

*“French heart worm”

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81
Q

Bacterial pneumonia is most commonly secondary to what?

A
  1. Immune suppression

2. Aspiration

82
Q

What are empiric therapy options for bacterial pneumonia?

A
  1. Potentiated penicillin or 3rd gen cephalosporin
  2. Fluoroquinolone

*Used in patients with disease too severe to wait for culture results

83
Q

Cough suppressants are (indicated/contraindicated) in bacterial pneumonia

A

contraindicated

84
Q

What are causes of fungal pneumonia?

A
  1. Histoplasmosis
  2. Blastomycosis
  3. Coccidiomycosis
  4. Aspergillosis
85
Q

How is fungal pneumonia diagnosed?

A
  1. Urine antigen testing

2*. Cytology is possible for pulmonary aspergillosis

86
Q

How is fungal pneumonia treated?

A
  1. Histo, blasto, cocci: Itraconazole
  2. Asper: Itraconazole (pulmonary) or voriconazole (systemic)

*Pulmonary aspergillosis may require a lung lobectomy

87
Q

What can cause pulmonary edema (general)?

A
  1. Increased hydrostatic pressure
  2. Decreased oncotic pressure
  3. Failure of lymphatic drainage
  4. Increased vascular permeability
88
Q

What is the mechanism behind cardiogenic pulmonary edema?

A

Increased hydrostatic pressure from heart failure related fluid overload

89
Q

What kind of fluid is associated with heart failure?

A

Modified transudate with low protein

90
Q

How is cardiogenic pulmonary edema treated?

A
  1. Diuretics
  2. Reduction in after load
  3. +/- positive inotropes
91
Q

What is the mechanism behind non-cardiogenic pulmonary edema?

A

Vascular permeability increases due to lung injury - the fluid is relatively protein rich

92
Q

What are causes of non-cardiogenic pulmonary edema

A
  1. Neurogenic
  2. Respiratory obstruction (lar par, brachycephalic airway, and pneumothorax)
  3. Acute lung injury or ARDS secondary to severe systemic inflammation
  4. Direct pulmonary injury
  5. Severe hypoalbuminemia
93
Q

What kind of heart rhythm is associated with:

  1. Cardiogenic pulmonary edema
  2. Non-cardiogenic pulmonary edema
A
  1. Sinus tachycardia

2. High vagal tone and sinus arrhythmia

94
Q

What is a finding on the CBCs of dogs with idiopathic eosinophilic pneumonia/bronchitis?

A
  1. 50% have eosinophilia
95
Q

How is idiopathic eosinophilic pneumonia treated in the dog?

96
Q

What is the prognosis of eosinophilic pneumonia/bronchitis?

97
Q

What causes lipid pneumonia?

A

Accumulation of lipid in the airways - often secondary to administration of petroleum medications used for the treatment of hairballs or constipation

98
Q

Which secondary condition is often associated with pulmonary fibrosis? How is this treated?

A
  1. Pulmonary hypertension

2. Sildenafil

99
Q

What is the most common cause of pulmonary contusions?

A
  1. Hit by car or bite wound
100
Q

What is the most common (non-traumatic) cause of pulmonary contusions?

A

Rodenticide toxicity

101
Q

What are causes of pulmonary hypertension?

A
  1. Primary (Idiopathic)
  2. Left heart failure
  3. Pulmonary disease or hypoxia
  4. Thromboembolic disease
  5. Compressive mass lesions
102
Q

How does chronic hypoxia cause pulmonary hypertension?

A

Causes inappropriate vasoconstriction

*Altitude, pulmonary fibrosis, chronic bronchitis, neoplasia

103
Q

How is pulmonary hypertension diagnosed?

A

Tricuspid regurgitation velocity > 2.8

*Indicates pressure difference of >31

104
Q

How is pulmonary hypertension treated? What is the mechanism behind this therapy?

A

Sildenafil

*Delays breakdown of cGMP → prolongs the vasodilatory effects of NO

105
Q

What test has a high sensitivity for pulmonary thromboembolism?

A
  1. Elevated D-dimer
106
Q

What are the most common causes of noninfectious tracheitis?

A
  1. Secondary - tracheal collapse, cardiac enlargement, oropharyngeal disease, prolonged barking
107
Q

What is the treatment for noninfectious tracheitis?

A
  1. Bronchodilators - theophylline or terbutaline

2. Cough suppressants - dextromethorphan, hydrocodone, butorphanol

108
Q

What is the most common cause of canine respiratory disease complex?

A
  1. Bordetella bronchiseptica with either canine parainfluenza or canine adenovirus
109
Q

Where does osleuris osleuri reside in the dog?

A

*Tracheal worm - also called filaroides osleuri

Lives in the proximal trachea and large bronchi

110
Q

What kind of lesions does osleuris osleuri form in the dog?

A

Semi-circular mass like nodules along the inside of the trachea as they mature

111
Q

What age of dog is osleuris osleuri infection most common?

A

Young dogs (<2 year)

112
Q

How is osleuris osleuri treated?

A
  1. Fenbendazole

2. Surgical removal of large nodules if breathing is inhibited

113
Q

What is the underlying cause of tracheal hypoplasia? What kind of breed is this most common?

A
  1. Congenital

2. Brachycephalic breeds

114
Q

How is tracheal hypoplasia diagnosed?

A

Radiographs - tracheal lumen is less than 2x the width of the third rib

115
Q

What is the prognosis for dogs with tracheal hypoplasia?

116
Q

What is a common sequelae to tracheal hypoplasia?

A

Bronchopneumonia

117
Q

What else should you look for in dogs with tracheal hypoplasia?

A

Other congenital defects - e.g. cardiac defects

118
Q

What are the causes of tracheal stenosis?

A
  1. Congenital

2. Trauma/Tracheostomy

119
Q

What is the underlying cause of congenital tracheal stenosis?

A

Absence of tracheal rings which leads to focal stenotic regions

120
Q

Which direction is collapsing trachea most common?

A

Dorsoventral

121
Q

What is the underlying cause of tracheal collapse?

A
  1. Progressive cartilage destruction

- Cartilagenous rings are hypocellular and have decreased glycosaminoglycans and glycoprotein levels

122
Q

How does inspiratory/expiratory effort help distinguish location of collapsing trachea lesions?

A
  1. Inspiratory effort → extrathoracic lesion

2. Expiratory effort → intrathoracic lesion

123
Q

What is the definition of canine chronic bronchitis?

A

Inflammatory condition of the upper airway lasting for >2 months

124
Q

What is the underlying type of inflammation in canine chronic bronchitis?

A

Neutrophilic or eosinophilic inflammation

* Also have thickened smooth muscle layer and fibrosis/scarring of the lamina propria

125
Q

Canine chronic bronchitis is most commonly seen in (small/large) breed dogs

126
Q

How is canine chronic bronchitis treated?

A
  1. anti-inflammatory glucocorticoids
  2. Bronchodilators
  3. Cough suppressants at night
127
Q

What is bronchiectasis?

A

Chronic changes to the structure of the airways due to destruction of connective tissue and muscle → leads to permanent dilation and destruction of mucociliary conduction

128
Q

What causes bronchiectasis?

A

Secondary to:

  1. Chronic bronchitis
  2. Primary ciliary dyskinesia
  3. Chronic exposure to inhaled irritants
129
Q

How is bronchiectasis diagnosed?

A

Imaging (CT is best) → lack of appropriate taper at the periphery

130
Q

How is bronchiectasis treated?

A
  1. Often need chronic antibiotics due to damaged mucociliary apparatus
  2. Nebulization/Coupage
  3. Management of underlying chronic bronchitis (glucocorticoids)
  4. AVOID antitussive medications
131
Q

What type of hypersensitivity reaction is feline bronchial disease?

A

Type 1 due to inhaled allergens

132
Q

Pneumomediastinum (does/does not) occur secondary to pneumothorax

133
Q

Pneumothorax, subcutaneous emphysema, or pneumoretroperitoneum (can/can not) occur secondary to pneumomediastinum

134
Q

Non-neoplastic mediastinal masses are typically ____ in origin

A

Infectious

135
Q

What clinical signs are associated with a space occupying mediastinal mass?

A
  1. Horners syndrome
  2. Edema of the head, neck, and forelimbs
  3. Dyspnea or dysphagia
136
Q

Flail chest (does/does not) cause hypoxemia

A

Does not

*Associated contusions can though

137
Q

What is the most common cause of a pyothorax in the dog? The cat?

A
  1. Grass awns

2. Bite wounds

138
Q

What % of patients with a pyothorax will have a fever?

139
Q

What kind of infection do dogs with pyothorax have? Cats?

A
  1. Actinomyces or nocardia
    * Nocardia is partially acid-fast staining
  2. Pasturella
140
Q

What is the treatment for pyothorax?

A
  1. Medical management → Abx for 4-5 weeks (be sure to include anaerobic coverage)
  2. Surgical management → in cases with a mass, foreign body, abscess, or lung lobe torsion. Also in cases where medical management fails to improve patient or if they worsen after 72 hours
141
Q

What is the most common cause of chylothorax?

A

Idiopathic

142
Q

What are the characteristics of the fluid in dogs with chylothorax?

A
  1. Modified transudate or exudate
  2. Small lymphocytes predominate
  3. Pleural fluid triglycerides are higher than serum triglycerides
143
Q

How is chylothorax treated?

A
  1. Medical management - rutin, may take weeks to resolve

2. Surgical - ligate the thoracic duct

144
Q

What is the success rate of thoracic duct ligation in the treatment of chylothorax?

145
Q

What % of idiopathic thoracic effusions resolve spontaneously?

146
Q

What % of traumatic chest injuries in dogs result in a pneumothorax?

147
Q

What is the major site of airway resistance?

A

Medium sized bronchi

*Small airways do not have the largest resistance due to their parallel arrangement

148
Q

Asthma

  1. Obstructive/Restrictive Disease
  2. Inspiration/Expiration Impaired
A
  1. Obstructive

2. Expiration

149
Q

Fibrosis

  1. Obstructive/Restrictive Disease
  2. Inspiration/Expiration Impaired
A
  1. Restrictive

2. Inspiration

150
Q

What is Fick’s Law of Diffusion

A

Diffusion = (Pressure gradient x Surface Area x Solubility)/(Distance x MW^(1/2))

151
Q

What is perfusion limited gas exchange?

A
  • Illustrated by O2
  • The gas equilibrates early along the length of the pulmonary capillary - the partial pressure of the gas in arterial blood becomes equal to the partial pressure in the alveolar air
  • Diffusion of the gas can only be increased with increased blood flow
152
Q

What is diffusion limited gas exchange?

A
  • Illustrated by CO2
  • The gas does not equilibrate by the time the blood reaches the end of the pulmonary capillary
  • The partial pressure of the gas between alveolar air and pulmonary capillary blood is maintained - diffusion continues as long as the partial pressure gradient is maintained
153
Q

What are the causes of hypoxemia? Which will not respond to oxygen therapy?

A
  1. Hypoventilation (Decreased PAO2)
  2. Diffusion Defect
  3. V/Q Mismatch
  4. Shunts
  5. Low FiO2

*Shunt will not respond to 100% O2

154
Q

What are the causes for hypoxia?

A

*Decreased O2 delivery to tissues

  1. Decreased cardiac output
  2. Hypoxemia
  3. Anemia
  4. CO poisoning
  5. Cyanide poisoning
155
Q

In what zone of the lung is blood flow the lowest? The highest?

A
  1. Zone 1

2. Zone 3

156
Q

How is hypoxia different in the lung compared to other tissues?

A

Lung hypoxia (alveolar) causes vasoconstriction to send blood to better aerated areas of the lung whereas it causes vasodilation in other tissues

157
Q

What part of the lung has the highest ventilation?

A
  1. The base
  2. The apex is the lowest

*Due to the effects of gravity

158
Q

Where is the V/Q ratio the highest? The lowest?

A
  1. The apex

2. The base

159
Q

PO2 and PCO2 are (highest/lowest) in which part of the lung?

A
  1. Apex: PO2 is highest, PCO2 is lowest
    - Due to higher V/Q, gas exchange is more efficient
  2. Base: PO2 is lowest, PCO2 is highest
    - Due to lower V/Q, gas exchange is less efficient
160
Q

How are PO2 and PCO2 affected in airway obstruction?

A

V/Q = 0

Will approach their values in mixed venous blood

161
Q

How are PO2 and PCO2 affected in pulmonary embolism?

A

V/Q = infinity

Will approach their values in inspired air

162
Q

The dorsal respiratory group controls (inspiration/expiration)

A

Inspiration

Generates a rhythm for breathing

163
Q

The ventral respiratory group controls (inspiration/expiration)

A

Expiration

*Not active during normal breathing

164
Q

The pneumotaxic center (inhibits/stimulates) inspiration

165
Q

How are the following affected by high altitude?

  1. Alveolar and arterial PO2
  2. Acid/Base status
  3. [Hemoglobin]
  4. [2,3 DPG]
  5. Right Ventricle
A
  1. Alveolar PO2 is decreased, so arterial PO2 is also decreased
  2. Respiratory alkalosis (hypoxemia stimulates peripheral chemoreceptors → hyperventilation)
  3. Increased [hemoglobin] (hypoxemia stimulates EPO production)
  4. Increased [2,3 DPG], HGB-O2 curve shifts right → facilitates O2 offloading
  5. Right ventricle hypertrophy (due to increase in pulmonary vasoconstriction)
166
Q

Which respiratory parasite can mimic asthma?

A

Aleurostrongylus

167
Q

What is normal tidal volume?

A

10-15 ml/kg

168
Q

Positive end-expiratory pressure (PEEP) will increase which lung volume?

A

Functional residual capacity

169
Q

What is the major side effect of positive end expiratory pressure (PEEP)?

A

Increased thoracic pressure → decreased venous return

170
Q

What is indicated by a PaO2 <65

A
  1. Right to left shunt

2. SEVERE pulmonary disease → need for positive pressure ventilation

171
Q

The A-a gradient should always be (number)

A

<10

*Otherwise there is a V/Q mismatch

172
Q

What does an increased A-a gradient indicate?

A
  1. Shunt
  2. V/Q Mismatch
  3. Diffusion impairment
173
Q

A low PaO2, high PCO2, and normal A-a gradient would indicate what?

A

Hypoventilation with normal lungs

174
Q

The (PO2/PCO2) is the most important regulator of ventilation and most of the control is via the (peripheral/central) chemoreceptors

A
  1. PCO2

2. Central

175
Q

The (central/peripheral) chemoreceptors control most of the breathing and the (central/peripheral) chemoreceptors respond the fastest

A
  1. Central

2. Peripheral

176
Q

Which chemoreceptors can respond to hypoxia?

A

Peripheral

177
Q

What are the best drugs to achieve effective concentrations in bronchial secretions?

A
  1. Macrolides
  2. Tetracyclines
  3. Chloramphenicol
  4. Fluoroquinolones
178
Q

Abnormalities in which location will cause stertor?

A

Nose/nasopharynx

*Reverse sneezing is specific for the nasopharynx

179
Q

Abnormalities in which location will cause stridor?

A

Larynx/trachea

180
Q

Where do polyps arise in cats? dogs?

A
  1. Eustachian tube or middle ear

2. Caudal nasal turbinates (consequence of chronic rhinitis)

181
Q

Under diseased conditions, which portion of the airways give the highest resistance?

A

Smallest airways - due to smooth muscle contraction, congestion from edema or mucus

182
Q

How does acetylcysteine break up mucus?

A

Breaks down disulfide bonds in mucus glycoproteins

183
Q

Which breed is predisposed to bronchiectasis?

A

Cocker spaniels

184
Q

Neutrophilic (+/- eosinophilic) infiltration of bronchial mucosa will result in production of what?

A
  • Can occur in chronic bronchitis
    1. Proteases
    2. Elastases
    3. Oxidizing products
185
Q

What is a physical exam hallmark of chronic bronchitis?

A

Expiratory wheeze

186
Q

What must be in the history for a cat to be diagnosed with chronic bronchitis?

A

DAILY cough

187
Q

What is the primary mediator of feline mast cells?

A

Serotonin

*Important in feline asthma

188
Q

Which bacteria that may be diagnosed on a BAL is not present in healthy cats?

A

Mycoplasma

189
Q

How does mycoplasma increase bronchoconstriction/edema

A

Mycoplasma degrades endopeptidases → allows substance P to increase

190
Q

Which lung lobe is most commonly torsed?

A

Right middle

191
Q

What is Bernoulli’s equation for use in calculating tricuspid regurgitation?

A

4xV^2 where V is the regurgitant jet

192
Q

Which conditions will not respond to 100% oxygen supplementation?

A
  1. Cyanide toxicity
  2. Shunt
  3. V/Q to infinity (ventilation but no perfusion)
193
Q

How does the lung adapt to accommodate more blood during exercise?

A
  1. Increases pulmonary blood flow (blood vessel dissension)

2. Decreases physiologic dead space (blood vessel recruitment)

194
Q

How is bradykinin metabolized in the lung?

A

Degraded by ACE - 80%

195
Q

How is serotonin metabolized in the lung?

A

There is uptake and storage - almost completely removed

196
Q

How much norepinephrine is metabolized in the lung?

A

30% is removed

197
Q

What happens to prostaglandins in the lung?

A

Prostaglandins E1, E2, F2α, and leukotrienes are inactivated

198
Q

What is the mechanism behind cyanide toxicity?

A

Inhibits cytochrome C oxidase → prevents mitochondrial aerobic respiration (blocks the ETC)

199
Q

What is the effect of cyanide toxicity on venous blood?

A

The venous O2 will increase (cherry red blood) due to the non-use of iron

200
Q

How is cyanide toxicity treated?

A
  1. Hydroxycobalamine

2. Nitrates/Thiocyanate

201
Q

What substances are involved in pulmonary hypertension?

A
  1. Decreased NO
  2. Decreased prostacyclin
  3. Increased endothelin-1
  4. Increased thromboxane A2
  5. Increased serotonin
202
Q

What changes to epithelia are seen in bronchiectasis?

A

Squamous metaplasia and loss of pseudo stratified columnar epithelium

ACVIM General Exam (15 decks)

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