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Respiratory > Week 3 Respiratory > Flashcards

Week 3 Respiratory Flashcards

1
Q

What is the cardiac notch?

A

The only place where the lungs don’t separate the ribcage from the heart- at about the 3rd-5th intercostal space

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2
Q

Where is the lung base?

A

Diaphragmatic surface

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3
Q

Where are the lungs apexes?

A

Adjacent to thoracic inlet

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4
Q

What is the root composed of?

A

Grouped principal bronchus, pulmonary artery, veins, and nerves wrapped together in pleural covering, location of tracheobronchial lymph nodes, enters at the hilus

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5
Q

How many lobes does a dog have?

A

2 left; 4 right

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6
Q

How many lobes does a horse have?

A

2 left; 3 right

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7
Q

How are the lungs subdivided into lobules?

A

Bronchopulmonary segments- by connective tissue septa

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8
Q

Connective tissue septa contain what?

A

Collagen, elastin, blood vessels

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9
Q

What species have what consistency connective tissue septa (implications for spread of infection)?

A

thick in ruminants and pig
thin and incomplete in horse
almost non-existent in dog

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10
Q

How many lobes in the right lung? Larger or smaller than left lung?

A

3-4 lobes; larger

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11
Q

Who does not have a middle lobe?

A

Horse

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12
Q

What is the cranial lobe ventilated by in ruminants and pigs?

A

Tracheal bronchus

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13
Q

How do the pulmonary arteries travel?

A

oxygen depleted blood from RV–> pulmonary trunk–> left and right pulmonary arteries–> lungs (Follow bronchi down to the level of the alveoli)

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14
Q

What do the pulmonary veins follow?

A

Oxygen rich blood from the lungs–> Left atrium. Follow bronchi and also provide venous return from bronchi

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15
Q

What is the bronchial artery?

A

Arises from the aorta to supply bronchi and connective tissue (i.e. tissues not participating in gas exchange)

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16
Q

What are the two networks of lymphatic vessels in the lungs?

A

Superficial network- drains subpleural tissue into vessels at hilus of lung; deep network- drains deeper tissues via vessels running along airways (from level of bronchioles)

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17
Q

Where do the two networks of lymphatic vessels merge?

A

At the hilus; tracheobronchial lymph nodes–> cranial mediastinal nodes–> tracheal lymphatic vessels or thoracic duct

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18
Q

What are the lymphatics responsible for?

A

Removal of material phagocytosed by macrophages in airways; mounting immune response to infectious agents

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19
Q

Efferent innervation?

A

Regulates activity of bronchial glands

Smooth muscle of bronchi

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20
Q

Afferent innervation?

A

Stretch receptors- reflex modification of respiration

Mechanoreceptors– reflex coughing

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21
Q

Where are the alveoli?

A

Scattered in walls of respiratory bronchioles. Continuous in walls of alveolar ducts

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22
Q

What do alveolar ducts lead to?

A

Terminal alveolar sacs

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23
Q

What are type I alveolar epithelial cells?

A

Very flattened, cover majority of alveolar wall, sit on basement membrane, terminally differentiated (cannot divide), allow gas diffusion across cytoplasm

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24
Q

What are type II alveolar epithelial cells?

A

Cuboidal, cytoplasmic granules contain surfactant (coat alveolar and reduce surface tension), divide to replace type I and type II cells, also contain some macrophages

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25
Q

What are alveoli separated by?

A

Interalveolar septa: fibroblasts, mast cells, macrophages, rich in capillaries (endothelial cells, endothelial basement membrane)

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26
Q

What are alveolar pores?

A

Holes in septa that allow passage of air between alveoli

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27
Q

What is the blood air barrier?

A

Between the air and the blood plasma, oxygen must diffuse across:
* alveolar fluid
* alveolar epithelial cell
* basement membrane of alveolar epithelium (+/- thin interstitium)
* basement membrane of capillary endothelium
* capillary endothelial cell
barrier 0.2-2 microns thick
once in plasma, oxygen is taken up by the erythrocyte, then binds to haemoglobin

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28
Q

Where are pulmonary macrophages present (3)?

A

**Intravascular- associated with endothelium (pig, ruminants), ** interstitial, **alveolar- function to clear alveolar surface; removed via trachea (mucociliary clearance, coughing) or via interstitium–> lymphatic system

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29
Q

What is the most common cell in a healthy lung?

A

Macrophage

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30
Q

What is the interlobular septa made of?

A

Collagen and elastic fibres, blood vessels

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31
Q

What is pleura made of?

A

Squamous/ cuboidal epithelium overlying elastic and collagen fibres and capillaries

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32
Q

How do you find partial pressure?

A

If O2 is 20% of a gas mixture with a total pressure of 760 mm Hg: 0.20 x 760 = 152 mm Hg

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33
Q

What is water vapors possible partial pressure?

A

47 mm Hg

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34
Q

What is the average PO2 of alveolar air?

A

100 mm Hg

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35
Q

What is the average PCO2 of alveolar air?

A

40 mm Hg

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36
Q

When O2 is bound to haemoglobin, does it contribute to PO2 in blood?

A

No

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37
Q

What reaction does CO2 dissolved in blood undergo?

A

CO2+H2O H2CO3 H+ + HCO3- (lowered PCO2 in the blood)

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38
Q

What is PO2 in venous blood, alveolar air, arterial blood, and tissues?

A

40 (venous blood), 100, 100, 40 (tissues)

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39
Q

What is PCO2 in venous blood, alveolar air, arterial blood, tissues?

A

46 (venous blood), 40, 40, 46 (tissues)

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40
Q

How does gas exchange occur in alveoli and tissues?

A

Gas exchange in alveoli and tissues involves passive diffusion down partial pressure gradients

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41
Q

What is the Rate of gas diffusion through the tissues (DR)?

A 
DR = (PD x A x DC)/T
PD= partial pressure gradient across tissue barrier
A= surface area available for diffusion
DC= diffusion coefficient (related to solubility of specific gas in tissue)
T= thickness of tissue barrier
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42
Q

When is surface area increased and reduced?

A

SA is increased during exercise and reduced during disease (e.g. emphysema)

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43
Q

When is barrier thickness increased?

A

During disease- pulmonary oedema (e.g. left- sided heart failure)
Pulmonary fibrosis
Pneumonia

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44
Q

What is the rate of blood flow in the alveolar bed?

A

Gas transfer in alveolar capillary bed happens in about 1/3 of the time it takes for blood to travel past alveolus–> existence of enormous diffusion reserve ???

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45
Q

During exercise what happens to blow flow?

A

Rate of flow increases– there is your need for the diffusion reserve; if diffusion reserve is exhausted–> hypoxaemia without hypercapnia

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46
Q

What are gills?

A

Delicate evaginations of tissue protruding into surrounding water; consist of thin epidermis highly perfused by circulatory system, providing high surface area for gas exchange between water and blood; breathing involves taking water into mouth while operculum (gill cover) is shut; the mouth is then shut and operculum opened thus forcing water over gills and through operculum; unidirectional system

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47
Q

What percentage of O2 in blood is transported bound to Hb?

A

98.5%

48
Q

How many O2 molecules per Hb?

A

4 molecules O2 per molecule Hb, i.e. oxyhaemoglobin

49
Q

Where is the remainder of O2 dissolved?

A

In plasma (determines PO2)

50
Q

What is the oxygen-haemoglobin saturation curve?

A

Percentage saturation of Hb. Percentage of Hb with O2 bound. Non-linear relationship to PO2 of blood because affinity of Hb for O2 changes with the number of bound O2 molecules

51
Q

When does Hb loads with O2? When does it unload?

A

When PO2 is high. Unloads when PO2 is low.

52
Q

When is the curve shifted to the right? What is it called?

A
  • Bohr effect. Increased blood PCO2 or acidity. Binding of CO2 to Hb or H+ to Hb alters conformation of Hb–> reduces affinity for O2 (Increased H+ of blood during exercise results from both increased PCO2 and lactic acid (anaerobic glycolysis))
  • Increased blood temperature (high in tissues/lower in lungs during exercise)
  • Increased 2,3 diphosphoglycerate (DPG)- present in erythrocytes at varying levels depending on physiological status (high in people living at high altitude)
53
Q

How does the Bohr effect change with PO2 levels?

A

Bohr effect results in readier dissociation of O2 from Hb at mid-range PO2 levels, but at PO2 of 100 mm Hg (as in the lung), saturation of Hb still remains almost complete

54
Q

What is the majority of CO2 transported as?

A

majority (60%) transported as HCO3- (30% bound to Hb; 10% dissolved CO2)

55
Q

What reaction does CO2 undergo in the plasma? What is it catalyzed by?

A

CO2+ H2O H2CO3 H+ + HCO3- ; catalyzed by carbonic anhydrase

56
Q

When is the CO2 reaction driven to the right? And to the left?

A

Peripheral circulation, it is driven to the right

In the lungs, it is driven to the left

57
Q

Why is the CO2 reaction driven to the right in the peripheral circulation?

A

HCO3- is removed by diffusion out of the erythrocyte in exchange for Cl- (chloride shift) to maintain electrical neutrality. This exchange of anions is necessary because cations (i.e. H+) do not readily cross the plasma membrane. Flow of Cl- and HCO3- is reversed in pulmonary circulation.

58
Q

What are H+ ions partially buffered by?

A

Hb (combine with carboxyl and imidazole group of proteins)

59
Q

What is the Haldane effect?

A

Works in synchrony with Bohr effect to facilitate CO2 and O2 exchange in the tissues. Reduced Hb has greater affinity for both CO2 and H+ than does HbO2

60
Q

What happens to the blood pH in diarrhoea? Why?

A

More HCO3- is lost than H+ (HCO3- excreted into duodenum to neutralize material arriving from the stomach- normally reabsorbed further down the tract but not reabsorbed in severe diarrhoea). So metabolic acidosis.

61
Q

With increased PCO2 in the blood, what kind of acidosis, why?

A

Usually Respiratory acidosis. Inadequate ventilation.

62
Q

What can decreased PCO2 result from?

A

Hyperventilation. Respiratory alkalosis (usually)

63
Q

What causes metabolic alkalosis?

A

Severe vomiting- excess loss of H+ (HCl from stomach acid)

64
Q

What measurements do you take to distinguish between resp. and metabolic acidosis/alkalosis?

A

PaO2- arterial PO2, PaCO2- arterial PCO2, pH

65
Q

When pH and HCO3 move in the same direction, what do you have?

A

Metabolic in origin

66
Q

When pH and HCO3 move in opposite directions, what do you have?

A

Respiratory in origin

67
Q

If you have a PaCO2 elevation and PaO2 decreased, what do you have?

A

Respiratory acidosis

68
Q

What if you have PaO2 low and normal PaCO2?

A

Diffusion defect like oedema. (because CO2 can diffuse rapidly and easily)

69
Q

What is pulmonary minute ventilation?

A

= tidal volume x respiratory rate

70
Q

What can limit an animal’s ability to maximize its tidal volume?

A

Airway resistance; compliance and elasticity (mechanical factors)

71
Q

Where is resistance lower, smaller or larger airways?

A

Smaller airways lower resistance because greater surface area

72
Q

Where is the narrowest part of upper respiratory tract?

A

Larynx (glottis)

73
Q

when does the glottis tend to collapse? Why?

A

During inspiration. Due to subatmospheric pressure- pressure gradient necessary to pull air in. Resisted collapse by cartilaginous support and muscular action

74
Q

How do the lower airways meet body’s needs with O2 for example?

A

Autonomic NS adjustments- bronchoconstriction (parasympathetic) and bronchodilaton (sympathetic)

75
Q

In the lower airways, where might increased resistance come from?

A

Bronchoconstriction, excessive production of mucous, oedema (fluid infiltration) of bronchial walls

76
Q

How are bronchiolar walls kept from collapsing?

A

Transmural pressure gradient (between pleural cavity and bronchiolar lumen)

77
Q

What happens in obstructive airway disease?

A

Occurs as a result of increased resistance. Bronchiolar pressure may drop below intrapleural pressure early in expiration–> premature collapse and reduced air exchange with atmosphere (pharmacological bronchodilation necessary)

78
Q

With a less compliant lung, more or less work required?

A

More work required (greater transmural pressure gradient) to inflate it. Compliance is reduced by disease (fibrosis) or increased alveolar fluid surface tension

79
Q

What causes the recoil tendency of lung?

A

Elastic connective tissue and surface tension of fluid lining alveoli

80
Q

How does surfactant reduce surface tension?

A

surface-active substance for which water molecules have less attraction. Increases pulmonary compliance. Phospholipoprotein.

81
Q

How does surfactant keep lungs dry?

A

Without surfactant surface tension of alveolar fluids tend to pull fluid out of capillaries

82
Q

What does Laplace’s Law say about alveoli?

A

Smaller alveolus should have greater tendency to collapse than larger alveolus with same surface tension. Surfactant reduces surface tension of smaller alveoli more than that of larger alveoli because the surfactant molecules are closer together in smaller alveoli.

83
Q

What is another thing other than surfactant that helps alveoli stay open?

A

Interalveolar connective tissue helps prevent tendency to collapse- elastic tissue of surrounding alveoli resists being stretched by collapsing alveolus

84
Q

What is the inspiratory capacity?

A

Max volume of air that can be inspired after a normal quiet expiration

85
Q

What is the functional residual capacity?

A

FRC- volume of air in lungs at end of normal passive expiration

86
Q

What is the vital capacity?

A

max volume that can be expired following maximal inspiration

87
Q

What is forced expiratory volume?

A

max volume of air that can be expired during first second after maximal expiration

88
Q

What is obstructive airway disease?

A

Diseases resulting from increased resistance- premature collapse of lower airways during forced expiration- trapping air at end of maximal expiration (reduced FEV due to increased airway resistance- increased RV- reduced VC)

89
Q

What is restrictive lung disease?

A

Diseases causing loss of lung compliance–> reduced TLC

90
Q

What occurs with mesothelial cell irritation?

A

Hypertrophy, hyperplasia, and/or metaplasia to cuboidal or columnar cell, activated mesothelial cells are capable of phagocytosis, participate in pleural inflamm. through production of cytokines, activated mesothelial cells can also produce collagen and other extracellular matrix proteins, can also produce plasminogen activator–> fibrinolysis, OR procoagulants that can promote pleural fibrin deposition therefore fibrous adhesions

91
Q

With pleural injury what happens to mesothelial cells?

A

They can either slough or undergo mitotic division and regenerate rapidly which causes a release of inflamm. mediators–> increased vascular permeability–> reduced fibrinolysis–> possible fibrous adhesions

92
Q

What is bad about pleural adhesions?

A

Restrict movement of the lungs and chest wall- but only minor interference with gas exchange as this diminishes over time as adhesions stretch with continous resp. movements

93
Q

What defences other than mesothelial cells does the pleural cavity have?

A

Aggregates of lymphocytes and macrophages (Kampmeier’s foci) beneath the parietal pleura and mediastinum and may be visible grossly as tiny white foci

94
Q

What is pleurodynia?

A

Pleural pain

95
Q

What happens in pneumothorax?

A

Positive intrapleral pressure causes compression atelectasis (collapse) of the lungs–> dyspnoea and tachypnoea

96
Q

Is pneumothroax normally bilateral or unilater in dogs and cats? Cattle and horses?

A

Bilateral in dogs and cats, cattle and horses may be unilateral as complete mediastinum

97
Q

How does air get into the mediastinum?

A

Tears in the trachea, bronchi, alveoli, or oesophagus

98
Q

What species is pneumomediastinum most common?

A

Cattle with interstitial emphysema of the lungs- subcutaneous emphysema

99
Q

What happens with pleural effusion?

A

Accumulation of excess fluid within the pleural cavity caused by haemorrhage, venous or lymphatic obstruction, decreased plasma oncotic pressure, increased plasma hydrostatic pressure, inflammation or intra-cavity neoplasia. The excess fluid raises the intra-thoracic pressure and causes compression atelectasis of the lung parenchyma, especially ventrally (gravity pooling)

100
Q

What is hydrothorax?

A

Non-inflammatory transudate or modified transudate in the pleural cavity– most commonly caused by severe hypoalbuminaemia (e.g. chronic starvation, protein- losing enteropathy, protein losing nephropathy, chronic hepatic insufficiency) but also may develop in overhydrated animals

101
Q

What are some causes of modified transudation into the pleural cavity?

A

Right sided congestive heart failure (all species), left sided congestive heart failure (esp. cats), lymphatic or venous obstruction within the cavity due to neoplasia, extension of ascites via diaphragmatic lymphatics, chylous effusions, FIPV (coronavirus), lung lobe torsion, diaphragmatic hernias with incarceration of abdominal viscera, chronica inflamm. of an intra-thoracic organ without involvement of the pleura itself

102
Q

Why does chylothorax result?

A

Physical or funciton obstruction of intra-thoracic lymphatics–> leakage of chylomicron-rich lymph into cavity

103
Q

What is pleuritis?

A

Inflamm of the pleura with accumulation of exudate in the cavity (due to increased vascular permeability and chemotaxis of leukocytes, there is a high nucleated cell count and protein concentration)

104
Q

What is pyothorax?

A

Thoracic empyema (another term)- accumulation of pus (neutrophil-rich exudate) in the pleural cavity (due to increased vascular permeability and chemotaxis of leukocytes, there is a high nucleated cell count and protein concentration)

105
Q

With neoplasic pleural effusions, what effusions are normally found with thoracentesis?

A

Modified transudate or non-septic exudate

106
Q

What are most tumours in the lungs?

A

metastases from other sites e.g. lymphoma, haemangiosarcoma, oral malignant melanoma, etc.

107
Q

What are primary lung tumours normally from?

A

Epithelial origin and malignant- most common is bronchioloalveolar carcinoma- derived from bronchiolar Clara cells or alveolar type II pneumocytes

108
Q

What is thoracic scintigraphy used for?

A

To assess function. Perfusion, ventilation. (limited availability, poor anatomic resolution, animal must be isolated after the procedure due to radioactive substance).

109
Q

When would you use thoracic CT?

A

Scanning a patient for metastases, normal thoracic radiograph but further characterisation is needed to evaluate, eval of patient with pleural effusion- fluid can be distinguished from masses, and collapsed or consolidated lung lobes, eval of suspected pulmonary thromboembolism, evaluation of recurrent pneumothroax.
Eval of nasal passage, CT is preferred over radiography- complicated anatomy.

110
Q

When is thoracic ultrasound useful?

A

Assess surface of the lung, peripheral pulmonary lesions (masses or consolidations), cranial mediastinum (think of the picture of the cyst), cases of pleural effusion, thoracic wall masses, suspect diaphragmatic herniation, and to guid fine needle aspiration or biopsy. Very useful in a horse as horse too large for CT. Ultrasound can assess soft tissues and fluid, but not able to penetrate air-filled lung (sound is reflected back)

111
Q

What is bronchoalveolar lavage and trans-tracheal wash?

A

Small sample of fluid introduced into airways using a catheter and then rapidly aspirated. Cytological investigation to look for inflammation, infection, or neoplasia. BAL tends to sample the smaller airways.

112
Q

What does it mean to take orthogonal views?

A

Allows a lesion to be localised in three dimensions and may allow a lesion to be seen on one view where it was obscured on the orthogonal view.

113
Q

An increase in PCO2 in alveolus causes what?

A

Relaxation of bronchiolar smooth muscle–> localized increase in airflow

114
Q

A decrease in PCO2 in alveolus causes what?

A

Bronchiolar constriction–> localized decrease in airflow

115
Q

An decrease in PO2 in alveolus, causes what?

A

Vasoconstriction of arterioles= hypoxic pulmonary vasoconstriction–> localized reduction in blood flow. Moving blood to other alveoli that have PO2 so that you can maximize O2 pick up from alveoli to blood.

116
Q

An increase in PO2 in alveolus, causes what?

A

Vasodilation–> localized increase in blood flow

Respiratory (11 decks)

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