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449 Cards in this Set
- Front
- Back
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What is V? |
Ventilation |
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What is Q? |
Blood flow |
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What is the difference between conducting and respiratory zones? |
The respiratory zones are the gas exchange areas (alveoli) The conducting area is "dead space" ventilation (nose to terminal bronchioles) |
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What are the upper and lower airways? |
Upper is from nares to the larynx Lower is from the trachea to the alveoli |
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What are major functions of the conducting airways? |
To transport and condition inhaled air, including warming, humidifying, and filtering inhaled particles |
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What part of the conducting pathways helps to warm inhaled air? |
Subepithelial vascular plexus (in the nose and large airways) |
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How do the conducting pathways humidify air?
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With serous secretions from the submucosal glands as well as goblet cells themselves |
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How do the conducting pathways filter inhaled particles (>10 um)? |
The nasal turbinates increase the SA of the pathway and mucociliary apparatus traps and removes particles (~5 to 10 um) This traps and removes a lot of bacteria Then the epithelium from the nasopharynx to the bronchi uses its cilia to move mucous to upper airways where it will be coughed up or swallowed |
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What is a common problem with sheep dogs, especially in particularly inbred ones, where they are prone to lung infections? |
Ciliary dyskinesis They get lung infections because their cilia are not moving particles, including bacteria, out This also affects the motility of their sperm and the cilia in their ears so they are more prone to otitis media as well |
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Do the bronchioles have ciliated epithelium too? |
Yes, and so does the trachea |
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What is atmospheric pressure? |
760 mmHg at sea level |
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What are the pressure ranges in the respiratory system? |
"Normal" is -4 to +22 mmHg (-5 to 30 cmH20) |
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What are the pressure ranges in an exercising horse? |
-36 to +40 mmHg (-49 to +54 cmH20) |
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1 mmHg = how much cmH20? |
1.4 cm H20 |
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What is inspiration the result of? |
Negative pressure gradient from the atmosphere to alveoli |
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How are non-rigid upper airway structures kept from collapsing during inspiration? |
Abductor muscles dilate/stabilize them |
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How many L/sec does a horse utilize while doing intense exercise? |
24 L/sec (geemany christmas..) |
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What are some components of the extrathoracic airways? |
-Nares -Nose (mouth) -Nasal turbinates -Pharynx -Larynx -Trachea |
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What are some species that are obligate nose breathers? |
Horses, rabbits, rodents |
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How should the epiglottis be placed in relation to the soft palate in obligate nose breathers? |
It should always be above the soft palate (otherwise it is dorsally displaced) |
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What are some common conditions that lead to extrathoracic airway collapse? |
-Left laryngeal hemiplegia in horses -Laryngeal paralysis (GOLPP) in dogs -Brachycephalic syndrome (stenotic nares and elongated soft palate and inversion of laryngeal saccules) -Collapsing trachea in toy breeds |
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What is a somewhat common problem with extrathoracic airways? |
Abductor muscle dysfunction can lead to collapse on inhalation |
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Which side is most commonly affected in horses with laryngeal hemiplegia and why? |
The left side This is because the left recurrent laryngeal nerve wraps around the aorta and has a long, tortuous path so it's susceptible to pathology So, you get a lack of abduction on the left side |
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What does GOLPP stand for? Describe GOLPP. |
Geriatric onset laryngeal paralysis polyneuropathy Generalized neurologic deterioration (larynx, pharynx, and hind limbs), affects older dogs. Observable voice change in half of affected dogs and gradual onset of stridor and exercise intolerance. Gagging and throat-clearing (~30%), 70% Labs |
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What causes the gagging, throat clearing, voice change, stridor, and exercise intolerance in dogs affected with GOLPP? |
Recurrent laryngeal nerve paralysis It was formerly called idiopathic laryngeal paralysis. |
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How can the dyspnea associated with GOLPP be corrected? |
With tie-back surgery in the larynx |
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Which part of the respiratory tract has the lowest cross-sectional area? |
Upper airways |
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Which part of the respiratory tract has the highest resistance to air flow? Why is this? |
Upper airways This is because a large volume of air moves through a small area |
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About how many bronchioles are there, and about how many alveoli? |
1 trachea, 500k bronchioles, 6-8 million alveoli! That's important because there is a great proliferation of surface area in a lung |
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The upper airways have a ______ total area, ______ velocity flow, and a _________ flow |
Small total area High velocity flow Turbulent flow |
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If you have an animal in respiratory distress, should you look in the upper or lower airways first? |
Upper airways |
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The lower airways have a _______ total area, _____ velocity flow, and a ________ flow |
Large total area Low velocity flow Laminar flow |
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What is another name for respiratory crackles? |
Rales |
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What are some abnormal respiratory sounds? |
-Stridor -Sterdor -Crackles (rales) -Wheeze (rhonchi) -Pleural friction rub |
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A "breathing through a straw" sound would be called what? |
Stridor It's a high-pitched noise, inspiratory, expiratory, or biphasic (both) |
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What causes stridor? |
Airway obstruction in larynx or pharynx |
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Is stridor something to be concerned about? |
Yes, it's a serious/emergency situation! |
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What are some things that can cause stridor? |
-Laryngeal paralysis -Foreign body -Laryngeal mass |
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Describe what stertor sounds like |
Low-pitched, snoring or snuffling-like inspiratory and/or expiratory noise |
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What causes stertor? |
Airflow obstruction rostral to the larynx (nasal passages, choanae, nasopharynx, soft palate) |
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What is a common example of something that causes stertor? |
Brachycephalic airway syndrome (or dorsal displacement of the soft palate in horses) |
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If you have a pH of 7.2, what does that tell you? |
Acidosis |
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If you have a paCO2 of 74.0 mmHg, what does that tell you, combined with a pH of 7.2? [ref. range for paCO2 is 35-45] |
Respiratory acidosis |
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If you have a paO2 of 58.2 mmHg, what does that tell you? [ref. range is 80-100] |
Hypoxia |
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If you have a low pH, hypoxia, high paCO2, and high HCO3, what does that tell you? |
Respiratory acidosis with metabolic compensation |
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Describe what the 1 for 10 rule is with acute respiratory acidosis |
The [HCO3-] will increase by 1 mmol/L for every 10 mmHg rise in pCO2 above 40 mmHg |
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Describe what the 4 for 10 rule is with chronic respiratory acidosis |
The [HCO3-] will increase by 4 mmol/L for every 10 mmHg rise in pCO2 above 40 mmHg Because the renal system is starting to kick in for additional compensation |
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What is hypoventilation? |
The state in which the ventilation is decreased enough that the CO2 is retained (increased PaCO2) |
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What are the main causes of hypoxemia? |
-Hypoventilation -Low inspired PiO2 (partial pressure of inspired O2) -Ventilation/perfusion mismatch -Right-to-left vascular shunt -Diffusion abnormality -(Intense exercise) |
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What are some possible causes of hypoventilation? |
-Intracranial disease affecting respiratory center -Cervical disease affecting phrenic nerves -Neuromuscular disease (like with GOLPP or laryngeal paralysis) -Airway obstruction -Thoracic pain -Pleural space disease -Lung disease |
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What helps change the diameter of bronchi? |
Helical muscle (and it has cartilage for rigidity) |
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What are the conducting parts of the lower airways? |
-Trachea -Bronchi -Bronchioles |
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Describe characteristics of bronchioles |
-No cartilage -Strong helical muscles -Cuboidal epithelium -Ciliated, have club cells |
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Describe characteristics of bronchi |
-Cartilage -Helical muscle -Ciliated -Size decreases with branching |
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Describe characteristics of the trachea |
-Cartilage (C or U shaped) -Muscle -Ciliated |
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Where does gas exchange take place? |
Within alveoli |
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What is important about respiratory bronchioles? |
They are the transition from the conducting and respiratory airways |
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How does collateral ventilation occur? |
Through intra-alveolar pores They are small pores between adjacent alveoli so that air can come in through the bronchioles but if for some reason, the air to one path is obstructed, those alveoli can get air form the other alveoli as well |
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List some important features of the lower airways |
-Gas exchange occurs -Extensive gas exchange area -Low resistance to airflow -Collateral ventilation (low resistance in dog and sheep, high in horse, cow, and pig) |
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What is "flow"? (and how is it calculated)? |
Aka V, it's volume passing through a given surface area / unit time (L/sec) Flow = ∆P/R |
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What is resistance? (and how is it calculated)? |
Resistance = ∆P/flow R sub aw = (Patm - Palv)/flow |
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How is conductance calculated? |
Conductance (G) = 1/resistance |
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What does the rate of flow depend on? |
-Driving pressure (air flows from high P to low P) -Resistance to flow |
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Which is louder, the upper airway or lower airway and why? |
Upper airway because it has high resistance, rapid flow, and high turbulence so it's noisy Whereas the lower airway (distal lung) has a large cross-sectional area with low resistance, slow flow, and laminar, quiet flow |
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Upper airway or obstruction requires __________ for symptoms to appear |
little |
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Bronchiolar (lower airway) obstruction requires ___________ for symptoms to appear |
an extensive amount |
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What is residual volume? |
The amount of air that remains in the lungs after fully exhaling |
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Does resistance to breathing vary with lung volume? How or how not? |
Yes, at the minimal size, the lung faces higher resistance, is smaller, and the conducting airways beyond the main bronchi change in size When they change in inhalation, the resistance drops and the resistance becomes lowest with maximal volume |
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What effect does the parasympathetic branch of the autonomic nervous system have on airway smooth muscles? How does it do this? |
It causes airway smooth muscle contraction Through the vagus nerve, it uses Ach on muscarinic receptors to contract smooth muscles in the airways |
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What effect does the sympathetic branch of the autonomic nervous system have on airway smooth muscles? How does it do this? |
It causes airway smooth muscle relaxation Through sympathetic nerves, it uses circulating catecholamines (epinephrine and norepinephrine) on beta-2 adrenergic receptors to relax smooth muscles in the airways |
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Other than through the sympathetic branch of the autonomic nervous system, how can airway muscles be induced to relax? |
Through the inhibitory non-adrenergic non-cholinergic system (iNANC) Through the vagus nerve, nitric oxide is released to activate guanylyl cyclase and increase cGMP to relax smooth muscles of airways |
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What are 3 inflammatory mediators that contract airway smooth muscle? |
-Histamine -Serotonin -Leukotrienes |
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What is an inflammatory mediator that relaxes airway smooth muscle? |
PGE2 |
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Describe feline asthma |
-Chronic, allergic -Airway inflammation, eosinophilic -Bronchoconstriction -Dyspnea, cough |
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Describe recurrent airway obstruction in horses (RAO, heaves, or COPD) |
Exposure to organic dust results in neutrophilic inflammation, bronchoconstriction, mucus accumulation, dyspnea, and cough |
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What is compliance? (how is it calculated)? |
Yielding to changes in pressure without disruption of structure or function; the amount of stretching (∆V) that occurs per unit of force (∆P) C = ∆V / ∆P |
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What is elastance? |
Aka elastic recoil, it is the capacity to recover size and shape after deformation So, for our case it is the rebound of the lungs after having been stretched as well as the force opposing distortion or stretching |
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What are two components that contribute to the elastance of lungs? |
-Elastin and collagen fibers -Surface tension |
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What unites the lungs with the chest wall? |
Pleural membranes |
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What pulls the pleural membranes in? |
The elastic recoil of lungs |
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What pulls the pleural membranes out? |
The elastic recoil of the chest wall |
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What leads to a negative pleural pressure? |
The sealed pleural space (and the little bit of pleural fluid holding the lungs to the thoracic wall) |
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Where does pleural fluid come from? |
Pleural fluid is a serous fluid produced by the serous membrane covering normal pleurae, filtered from pleural capillaries. |
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Where does pleural fluid go? |
It is reabsorbed into lymphatics connecting with the pleural space |
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What is the purpose of the pleural fluid? |
-It lubricates the pleural surfaces -It keeps the lung and chest wall in tight apposition |
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What is inflammation of the lungs called? |
Pleuritis |
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What does trauma to the lungs often lead to? |
-Breaking of the seal, loss of negative pressure -Lung collapse |
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If you are listening to an animal with pleural effusion, what would you expect to hear? |
Louder lung sounds dorsally Ventrally, quieter; less air movement and thicker wall due to the fluid filling the space |
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What is the typical range of alveolar pressure? |
+2 to -2 |
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Describe the steps involved in inspiration |
-Inspiratory muscles contract -Thorax expands -Pleural pressure become more subatmospheric -Increase in transpulmonary pressure -Lungs expand -Alveolar pressure become subatmospheric -Air flows into alveoli (moving down the pressure gradient) |
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What happens to alveolar pressure during inspiration and expiration? |
The alveolar pressure becomes slightly negative during inspiration so air flows in It becomes slightly positive during expiration so air flows out |
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What happens to pleural pressure during inspiration and expiration? |
It becomes more negative during inspiration and less negative (but still negative) during expiration |
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What is the alveolar pressure at the end of
expiration? |
It's zero because no air is moving |
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What is functional residual capacity? |
Functional Residual Capacity (FRC) is the volume of air present in the lungs, specifically the parenchyma tissues, at the end of passive expiration. At FRC, the elastic recoil forces of the lungs and chest wall are equal but opposite and there is no exertion by the diaphragm or other respiratory muscles. |
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What is the lung volume at the end of expiration? |
Just the functional residual volume (FRC) |
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What is the lung volume at mid-inhalation? |
FRC + 1/2 of tidal volume |
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What is the lung volume at the end of inhalation? |
FRC + tidal volume |
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What is the lung volume at mid-exhalation? |
FRC + 1/2 tidal volume |
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Is inspiration or expiration active? Describe why. |
Inspiration. Muscles contract and energy is required to overcome elastic recoil of the lung and the surface tension of alveoli |
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What is the most important muscle of inspiration? |
The diaphragm |
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What are the muscles of inspiration? |
-Diaphragm -External intercostals -Sternocephalicus -Abductor muscles of upper airways (open the nares, pharynx, and larynx) |
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Why is expiration an active process all of the time in horses? |
They have a very stiff, non-compliant chest wall, which the recoil forces of the lung must have assistance with returning to a smaller volume |
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What are the muscles that are used with active expiration? |
Internal intercostals Rectus abdominis External and internal abdominal obliques Transversalis |
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Again, how is compliance calculated (for the lungs in particular)? |
Compliance = ∆ V / ∆P So, = ∆ Lung Vol. / (Alv. P - Pleural P) |
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When is lung compliance naturally least? |
At high and low lung volumes |
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What are some things that can decrease lung compliance? |
-Lung fibrosis -Alveolar edema -Pulmonary venous pressure increase |
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Surface tension is a force that resists __________ |
Distension |
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What is a source of tension in alveoli? Describe how this affects the lung's movements. |
They are lined with liquid, and the air-liquid interface is a source of surface tension Cohesive forces (H bonding) between adjacent water molecules is greater between water and air Liquid assumes the smaller SA possible, so the lung resists inflation and promotes deflation |
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What decreases the surface tension in the alveoli? |
Surfactant |
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What produces surfactant? |
Type II alveolar epithelial cells (pneumocytes) |
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What is surfactant? How does it work? |
A mixture of lipids and proteins that lowers surface tension by decreasing the H bonding between water molecules at the alveolar surface As the alveolus decreases in size, surfactant molecules become concentrated so there is a great reduction in surface tension |
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Why is it important that we sigh every now and then? (or otherwise breathe deeply) |
This deep inhalation stretches the lung, and this stimulates surfactant production from type II cells. This brings surfactant to the surface of alveoli. This is essential in maintaining normal lung compliance. |
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What is hysteresis? |
The value of a physical property (∆V) lags behind the effect that is causing it (∆P) It describes the nonlinear nature of the pressure-volume curve of the lung in which the lung volume at any given pressure during inhalation is less than the lung volume at any given pressure during exhalation |
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What creates hystersis in the lung? |
Surface tension More P is required than "expected" to inflate the lung and less recoil is available than "expected" to deflate the lung Inspiration must overcome the surface tension forces, which change with volume |
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When is surfactant produced (in relation to gestation), and describe the process |
It is produced late in gestation, and is stimulated by the increase in cortisol. It is deficient in premature newborns, and essential for lung stability after birth. |
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What are some things that can lead to a decrease in surfactant production? |
Pain, neuromuscular disease, chest wall abnormality, etc. Basically anything that would limit one's ability to expand the chest would decrease the surfactant production |
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What is tidal volume? |
The volume of each breath |
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What does tidal volume vary with? |
The needs for ventilation or thermoregulation Sigh, yawn: large tidal volume Panting: small tidal volume |
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What is the approximate tidal volume in resting animals based on their body weight? |
~10 ml/kg of body weight So for a 500 kg horse, it's 5,000 ml |
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What is minute ventilation? (VE) |
The volume of air breathed per minute |
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What is minute ventilation a product of? |
VE = tidal volume x breathing frequency per min. |
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What do we call the volume left in the lung at the end of passive expiration? |
Functional residual capacity (FRC) |
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What is in balance at FRC? |
The elastic recoil of the lung and the chest wall |
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What is the maximum amount of volume that a lung can hold? |
Total lung capacity |
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What is vital capacity? |
The amount of air from the total lung capacity to the residual volume; that is the total amount and the maximum amount of air that you can move |
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What is residual volume? |
The volume of air in the lungs that you cannot exhale |
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What causes obstructive lung disease? |
Airway narrowing and closure |
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Obstructive lung disease is associated with ________ difficulty |
Expiratory difficulty |
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What are some examples of obstructive lung disease? |
Asthma Bronchitis RAO (recurrent airway obstruction) Emphysema |
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Obstructive lung disease is associated with _______ residual volume and _______ vital capacity |
Increased residual volume (the volume of air left in the lungs that you cannot exhale) Decreased vital capacity (the total amount of air that you can move) |
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What is restrictive lung disease? |
A condition where the lungs cannot fully expand; "small lung" Lung compliance is decreased, and chest wall stiffness may be increased. This could be due to muscle or nerve damage. |
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What are some possible causes of restrictive lung disease? |
-Interstitial lung disease (fibrosis) -Alveolar edema or hemorrhage -Pleural disease -Neuromuscular disease -Thoracic/extrathoracic (obesity, ascites) |
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Restrictive lung disease is associated with _______ total lung capacity |
Decreased total lung capacity |
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What is deadspace? (VD) |
The volume of air in airways that does not participate in gas exchange |
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What is the anatomic deadspace? |
Conducting airways; they are not designed for gas exchange |
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What is the alveolar deadspace? |
Alveoli are supposed to have gas exchange but if they are ventilated but not perfused, then it is not an effective gas exchanging unit and that is deadspace |
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What is physiologic deadspace? |
Anatomic VD + Alveolar VD |
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What is alveolar ventilation? |
The volume of air participating in gas exchange per minute |
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How is alveolar ventilation (VA) assessed? |
Through PCO2 |
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What is deadspace ventilation (VD)? |
The volume of air breathed per minute that is not participating in gas exchange |
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What is minute ventilation the sum of? |
It is the sum of deadspace and alveolar ventilation VE = VD + VA |
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What do the relative amounts of deadspace and alveolar ventilation depend on? |
The pattern of breathing |
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Explain how the relative amounts of deadspace and alveolar ventilation depend on the pattern of breathing. |
Small tidal volume (VT) increase deadspace ventilation Large tidal volume (VT, from sigh or exercise) results in greater alveolar ventilation |
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What is VD? |
Deadspace ventilation |
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What is VA? |
Alveolar ventilation |
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VD + VA = ? |
VE (minute ventilation) |
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VT x F (frequency) = ? |
VE (minute ventilation) |
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What is VD/VT? |
Deadspace/tidal volume ratio; the fraction of "wasted" ventilation That is the fraction of air that isn't involved in gas exchange |
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What is the average deadspace/tidal volume ratio for small animals? |
33% |
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What is the average deadspace/tidal volume ratio for large animals? |
50-65% |
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What is a typical breathing rate for panting? |
300 breaths/minute |
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What does the VD/VT ratio change to during panting? |
~50% |
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What happens to the VE during panting? |
It increases |
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What factors are involved in optimizing the work of breathing? |
-Meeting alveolar ventilation demands -Minimizing energy expenditure |
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Alveolar ventilation is greatest at slower, deeper breaths. Why don't we breathe this way all of the time then? |
Because that requires additional work because you need to expand the lungs more and that takes a lot of work to overcome their elasticity |
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You move more air through with a rapid breathing frequency. Why don't we breathe this way all of the time then? |
Because that requires additional work because it is associated with added deadspace ventilation |
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What is the bronchovascular bundle? |
The connective tissue sheath containing the bronchi, arteries, and veins with the alveolar septa attached to it. Lymph also travels in the alveolar sheath. |
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Where does edema fluid accumulate when in the lung? |
In the peribronchial sheath |
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Describe the layers of the alveolar epithelium for the thick and thin side |
Thin side:
-capillary endothelium (innermost) -basement membrane -alveolar endothelium (outermost) Thick side: -capillary endothelium (outermost) -basement membrane -interstitial space -basement membrane -alveolar epithelium (innermost) |
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Does gas exchange occur on the thick or thin side of the alveolus? |
Thin side |
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The pulmonary arteries leave the _____ side of the heart
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Right |
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What is the pressure in the pulmonary arteries? |
9-24 mmHg, average of 14 mmHg |
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What is the pressure in capillaries? |
10 mmHg |
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What is the pressure in pulmonary veins? |
9 mmHg |
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What is the pressure in the left atrium? |
8 mmHg |
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How do you calculate vascular resistance? |
R = ∆P / flow R= (P arterial - P atrial) / cardiac output |
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How do you calculate systemic vascular resistance? |
SVR = (P aorta - P right atrium) / cardiac output |
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How do you calculate pulmonary vascular resistance? |
PVR = (P pulm. artery - P left atrium) / cardiac output |
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What is the driving pressure in systemic circulation? |
Aka SVR = 87/CO=87/2.4= 36.25 |
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What is the driving pressure in pulmonary circulation? |
Aka PVR = 6/CO=6/2.4=2.4 Low resistance to blood flow |
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Pulmonary vasculature has _____ pressures and ______ driving pressures with _____ resistance to blood flow |
Low pressures Low driving pressures Low resistance to blood flow The lung must accommodate the entire cardiac output |
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More resistance is provided by ____________ than arteries and arteries provide more pressure than _________ |
Capillaries Veins |
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_______ decreases pulmonary vascular resistance |
Exercise The driving pressure goes up a little but the resistance goes down significantly |
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The cardiac output increases about how much during exercise? |
About 6-fold |
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How does exercise decrease the pulmonary vascular resistance and why is that important? |
-It recruits previously unperfused vessels -It dilates perfused vessels (passively due to the increase in pressure) -Pulmonary vessels distend at higher lung volumes This is important because the pulmonary circulation accommodates the entire cardiac output |
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__________ circulation receives the entire cardiac output |
Pulmonary |
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Why is the pulmonary circulation a low pressure system? |
Because the pressures of the pulmonary artery and left atrium are both low |
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Why does the pulmonary circulation have a low driving pressure? |
Because there is little difference between the pressures of the pulmonary artery to the left atrium |
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The pulmonary vascular resistance is less than ________ that of systemic vascular resistance |
10% |
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In exercise, pulmonary pressure _______ but the pulmonary vascular resistance (aka driving pressure) ________ |
Pulmonary pressure increases Pulmonary vascular resistance decreases dramatically |
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Blood flow tends to be greatest in which regions of quadruped lungs? |
Dorso-caudal regions It's posture and gravity independent |
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How does exercise-induced pulmonary hemorrhage occur? |
Pulmonary capillary pressure increases a lot, and is almost 2x that in the horse vs. other species Blood leaks from capillaries (they can rupture) so blood enters the airway and because ventilation is so tremendous, it can look dramatic |
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What is the pulmonary capillary pressure in the exercising horse vs. other species? |
60 mmHg in the horse 35 mmHg in other species |
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The distribution of exercise induced pulmonary hemorrhage lesions matches what? |
The distribution of blood flow |
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Alveolar _______ regulates pulmonary blood flow |
Hypoxia |
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What effect does hypoxia have on systemic circulation? |
It dilates systemic circulation (through a direct, local effect on smooth muscle) |
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What effect does alveolar hypoxia have on pulmonary arteries? |
It constricts the pulmonary arteries (though a direct, local effect on smooth muscle) |
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Alveolar hypoxia leads to artery _______ |
Constriction |
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Blood flow to hypoxic alveoli _______ |
Decreases |
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Blood flow to normoxic alveoli _________ |
Increases |
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Why is it important that blood flow to hypoxic alveoli decreases, whereas it increases to normoxic alveoli? |
Because this improves gas exchange efficiency because it matches perfusion to ventilation More blood passes by normoxic alveoli |
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Species differences in vascular reactivity correlate with the amount of what? |
Smooth muscle in their small arteries |
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Describe the downside of hypoxic vasoconstriction at high altitude (describe the mechanism of it) |
-At high altitude, the barometric pressure decreases -The partial pressure of inspired O2 decreases, which leads to alveolar hypoxia (which is diffuse, so all vessels constrict) -This leads to pulmonary hypertension -The workload of the right heart therefore increases -This leads to brisket disease, aka right heart failure |
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What sign will be commonly seen in brisket disease? |
Ventral edema |
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What are some things that can lead to pulmonary hypertension? |
-Pulmonary disease or hypoxia -Heartworm disease -Pulmonary artery obstruction (thrombose, embolism, tumor, foreign body) -Left-sided heart failure -Congenital shunts like PDA, atrial septal defect, ventricular septal defect) |
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Describe cor pulmonale |
-"Pulmonary heart disease" -It's a diffuse lung disease leading to pulmonary hypertension leading to right heart failure -The right heart work increases so the right heart fails (because it's dealing with a higher vascular resistance) |
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How is pulmonary lymph produced and where does it go? |
Through passive filtration from the capillaries to the interstitium; it's continuously produced then it drains out through the bronchovascular bundle lymphatics |
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What happens if pulmonary lymph production > drainage? |
Edema ensues |
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How can you calculate the rate of fluid filtration out of pulmonary capillaries into the interstitium? |
Fluid flux = K{(Pcap - Pif) - (PIcap - PIif)} |
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_______ pressure drives pulmonary fluid outward and _______ pressure pulls water into capillaries |
Hydrostatic pressure drives it outward Oncotic pressure pulls it into capillaries |
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Where are the two places that pulmonary edema can be found? |
-Pulmonary interstitium -Intra-alveolar |
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What are some factors that lead to pulmonary edema? |
-High capillary pressure (exercise, left-sided heart failure) -Increased capillary permeability to proteins (inflammation--increased interstitial fluid oncotic pressure) -Low plasma oncotic pressure (hypoproteinemia of disease or malnutrition) |
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Which edema is FIRST produced in the lungs? |
Pulmonary interstitial edema |
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Which edema is produced SECONDARILY in the lungs? |
Pulmonary intra-alveolar edema |
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Where does pulmonary interstitial edema occur? |
In the bronchovascular bundle |
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How can you see pulmonary interstitial edema on radiographs? |
-See fluid accumulation -See bronchial wall thickening |
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What are some things that you would see on radiographs for left-sided chronic heart failure? |
-Cardiomegaly: dorsal deviation of the trachea, increased sternal contact, loss of the caudal cardiac wrist -Diffuse interstitial pulmonary pattern due to pulmonary edema -Enlarged pulmonary veins |
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What is the final stage of pulmonary edema, for instance in left heart failure? |
Intra-alveolar edema |
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Where is intra-alveolar edema found? |
The edema leaks into alveoli |
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How is it that intra-alveolar edema forms a stable foam? |
It mixes with surfactant That obscures gas exchange even further |
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What are some causes of non-cariogenic pulmonary edema? |
-Electrocution -Near-drowning -Upper airway obstruction -Seizures |
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What does non-cardiogenic pulmonary edema appear as on radiographs? |
Dorsocaudal interstitial to alveolar pattern |
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Bronchial circulation is a branch of ________ circulation |
Systemic |
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Why is bronchial circulation important? |
It provides nutritive blood flow to bronchi, large vessels, and pleura |
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What participates in conditioning air in the bronchioles? |
Submucosal plexus |
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Describe venous drainage for bronchial circulation |
-Bronchial veins -Pulmonary veins (anastomose)--so that you have some deoxygenated blood mixing with your oxygenated blood |
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Can bronchial circulation help heal damaged lung? |
Yes, it proliferates to help heal damaged regions of lung |
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What are the two modes of O2 transport? |
-Gas dissolved in blood -Bound to Hb |
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Only ________ O2 contributes to PaO2 and PvO2 |
DISSOLVED |
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How is CO2 transported in blood? |
-Dissolved in blood -Converted to bicarb (HCO3-) -Complexed with Hb -Combined with plasma proteins |
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Only _______ CO2 contributes to PaCO2 and PvCO2 |
DISSOLVED |
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What is the alveolar, arterial, and venous PO2? |
Alveolar: 105 mmHg Arterial: 100 mmHg Venous: 40 mmHg |
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What is the alveolar, arterial, and venous PCO2? |
Alveolar: 40 mmHg Arterial: 40 mmHg Venous: 46 mmHg |
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How does equilibrium occur for pulmonary gas partial pressures? |
By diffusion of dissolved gases This occurs rapidly as blood flows past alveolus Reached about halfway along the capillary |
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What are determinants of PAO2 and PACO2? |
-PO2 of inspired air (depends on altitude, supplemental oxygen) -Alveolar ventilation -Metabolism (rate of total body O2 consumption, O2 consumption increases with exertion and some disease states) |
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What effect will breathing air with DECREASED PO2 have on alveolar PO2 and PCO2? |
Decreased alveolar PO2 No change in alveolar PCO2 |
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What effect will breathing air with INCREASED PO2 have on alveolar PO2 and PCO2? |
Increased PO2 No change in alveolar PCO2 |
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What effect will decreased alveolar ventilation with negligible metabolism have on alveolar PO2 and PCO2? |
Decreased alveolar PO2 Increased alveolar PCO2 |
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What effect will increased alveolar ventilation with negligible metabolism have on alveolar PO2 and PCO2? |
Increased alveolar PO2 Decreased alveolar PCO2 |
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What effect will decreased metabolism with negligible alveolar ventilation have on alveolar PO2 and PCO2? |
Increased alveolar PO2 Decreased alveolar PCO2 |
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What effect will increased metabolism with negligible alveolar ventilation have on alveolar PO2 and PCO2? |
Decreased alveolar PO2 Increased alveolar PCO2 |
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What effect will a proportional increase in alveolar ventilation and increase in metabolism have on alveolar PO2 and PCO2? |
No change to either |
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What factors do the concentration of a gas within liquid depend on? |
-Partial pressure of the gas -Solubility of the gas in the liquid |
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Does O2 have a low or high solubility in liquid? What about CO2? |
O2 has low solubility (but has a high driving pressure of 105-40 mmHg) CO2 has high solubility (but has a low driving pressure of 46-40 mmHg) |
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Oxygen is ______ soluble in plasma |
Poorly |
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At PO2=100 mmHg, how many mL of O2 are dissolved in each 100 ml of plasma? |
0.3 ml of O2 |
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Oxygen binds to what in Hb? |
Iron in Hb |
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What color is deoxygenated Hb? |
Blue-ish Oxygenated Hb is bright red |
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Deoxygenated Hb has how many O2 bound? |
<4 |
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What is oxygen saturation? |
The % of Hb binding sites that are occupied by O2 |
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What is oxygen saturation determined by? |
PO2 |
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Is saturation dependent on the amount of Hb? |
Nope! |
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How can oxygen saturation be clinically measured? |
By measuring arterial blood gas with a pulse oximeter |
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What does pulse oximetry measure? |
It measures O2 saturation of Hb in peripheral blood |
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How does pulse oximetry work? |
A diode emits red and infrared lights, which are absorbed by Hb then transmitted through tissues to photo detector OxyHb and deoxyHb have different absorption patterns, which are detected It uses systolic and diastolic pulsing to specifically detect arterial O2 saturation |
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What is normal PaO2, and what is the normal % oxygen saturation of Hb there? |
PaO2=100 Hb=98% saturated |
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What is normal PvO2, and what is the normal % oxygen saturation of Hb there? |
PvO2=40 Hb=75% saturated |
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Should Hb be fully saturated in normal arterial blood? |
Yes |
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What effect does providing supplemental oxygen have (increasing PiO2) on O2 saturation? |
Very little; it adds no more O2 to Hb and adds little O2 to blood |
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What is oxygen carrying capacity? |
The maximal amount of O2 that can be carried by Hb |
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What is oxygen carrying capacity dependent on? |
Hb concentration |
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What is a condition where the oxygen carrying capacity would be increased? Decreased? |
Increased: polycythemia Decreased: anemia |
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How many ml of O2 can 1 g Hb carry? |
1.36 ml carried by 1 g Hb |
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How can oxygen carrying capacity be calculated? |
OCC = Hb g/dL x 1.36 ml O2/g Hb |
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How much Hb do we expect in a normal situation (in g/dL)? |
15 g/dL (that's 15 g/100 ml of blood) |
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Anemia _______ O2 carrying capacity |
Decreases |
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What are some factors that can lead to polycythemia? |
-Splenic contraction (horses) -Accommodation to high altitude -Chronic hypoxemia due to disease -Erythropoietin |
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What is oxygen content? |
The total amount of oxygen in the blood |
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How can oxygen content be calculated? |
Oxygen content = (O2 carrying capacity x % Hb saturation) + ml O2 in solution |
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What is a normal value for oxygen content in the blood? |
20.3 ml O2/dL blood |
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How much O2 is typically dissolved in 100 ml plasma/mmHg |
.003 ml O2 |
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How is oxygen unloaded in tissues? |
-O2 in solution diffuses down concentration gradient into tissues (from PaO2 of 100 mmHg to PO2 in tissue) -Plasma PO2 decreases -O2 leaves Hb and enters plasma -Hb becomes less saturated |
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Hb is exposed to _____ PO2 in tissues |
low |
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Which tissues have an even lower PO2 than typically expected? What can this value reach? |
Metabolically active tissues (exercising tissue) ~15 mmHg |
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When Hb is exposed to exceptionally low PO2 in tissues, what happens to the amount of O2 that is released from Hb? |
More O2 is released from Hb |
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What is 2,3-diphosphoglycerate? |
It's a molecule that's produced in RBCs during glycolysis that reversibly binds Hb |
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What effect does 2,3-diphosphoglycerate have on Hb's affinity for O2? |
DPG binds reversibly to Hb, which allosterically decreases Hb's affinity for O2 |
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When does the production of DPG increase by RBCs? |
When animals are lacking O2 (high altitude, disease) |
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What is the importance of DPG binding to Hb?
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It allosterically decreases Hb's affinity for O2 by binding with Hb itself This shifts the oxyHb curve to the right, thereby helping to unload O2 from Hb at the tissues This helps animals who are hypoxic to deliver more O2 to their tissues |
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What does increased affinity for O2 with Hb have on O2 unloading at tissues and on the oxyHb dissociation curve? |
-Less O2 unloading at tissues -Left shift in the oxyHb dissociation curve |
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What does decreased affinity for O2 with Hb have on O2 unloading at tissues and on the oxyHb dissociation curve? |
-More O2 unloading at tissues -Right shift in oxyHb dissociation curve |
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What are some factors that decrease Hb's affinity for O2? |
Highly metabolically active tissues -decreased pH -increased PCO2 -increased temperature -increased 2,3-DPG |
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What are some factors that increase Hb's affinity for O2? |
-increasd pH -decreased PCO2 -decreased temperature -decreased 2,3-DPG -CO -fetal Hb |
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Why is it helpful that increased pH, decreased PCO2, and decreased temperature increase Hb's affinity for O2? |
Because that helps load oxygen onto Hb at alveoli |
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What effect does CO have on Hb's affinity for O2? |
It increases the affinity (so makes it harder for Hb to release bound O2 at tissues) |
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How is most CO2 moved around? |
As bicarbonate |
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How much more soluble is CO2 than O2? |
24x !! |
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Why can considerable amounts of CO2 be transported in solution? |
Because it's highly soluble in plasma |
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How is CO2 in solution detected as? |
PCO2 |
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Is CO2 converted to bicarb in the plasma or RBCs? |
Both |
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What is important in the formation of bicarb in the RBC? |
Carbonic anhydrase |
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Which is a better buffer, oxyHb or deoxyHb? |
DeoxyHb |
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Is Hb useful as a buffer? |
Yes, very much so! It is an important buffer for H+, and buffering of protons keeps reactions moving to the right so that CO2 can be added to the blood |
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What is generated in the production of bicarb and carbamino compounds? |
H+ |
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Where does CO bind to Hb? |
On the same sites as O2 does |
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What does CO form when it binds to Hb? |
Carboxyhemoglobin |
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What does CO2 form when it binds to Hb? |
Carbaminohemoglobin |
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How does the affinity of CO for Hb compare with that of O2? |
CO has 200x greater affinity for Hb than does O2 |
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What effect does CO have on Hb's affinity for O2? What is the result of this? |
It greatly increases Hb's affinity for O2 So, Hb won't release O2 at tissues and severe hypoxemia will ensue despite a normal PO2 |
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Is CO binding to Hb reversible? |
Yes |
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How much PCO is sufficient to saturate Hb? |
0.5 mmHg |
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What are the 5 causes of hypoxia? (decreased PaO2) |
-Low inspired PiO2 -Alveolar hypoventilation -V/Q mismatch -Right-to-left shunts -Diffusion impairment |
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Why is the alveolar-arterial O2 gradient about 5 mmHg and not zero? |
Because the lung is never a perfect gas exchanger |
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What are some hypoxemia causing conditions that increase the alveolar-arterial O2 gradient? |
-V/Q mismatch -Shunt -Diffusion impairment |
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What are some hypoxemia causing conditions that do not affect the alveolar-arterial O2 gradient? |
-Alveolar hypoventilation -Low PiO2 |
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O2 consumption is proportional to production of what? |
CO2 |
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How is respiratory quotient calculated? |
RQ = CO2 produced / O2 consumed |
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What is the RQ for glucose? |
1.0 |
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What is the RQ for fatty acids? |
0.7 |
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What is FiO2? |
Fraction of oxygen inspired (about 21%) |
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By what mechanism do both O2 and CO2 move back and forth between the air and alveolar blood? |
Diffusion |
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What sort of a pressure gradient does CO2 face for diffusion? |
Low pressure gradient |
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What sort of a pressure gradient does O2 face for diffusion? |
High pressure gradient |
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What factors are the diffusion rate directly proportional to? |
-Pressure gradient -Surface area available for diffusion -The diffusion coefficient (D)--depends on the solubility and molecular weight |
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What factor is the diffusion rate inversely proportional to? |
Membrane thickness |
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What is the total thickness of the alveolus? |
.2 - 1.0 microns |
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What effect would pleural edema have on the diffusion rate, and why is that? |
It would decrease it because it would increase the thickness of the barrier for gas exchange |
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What is the diffusion rate equation? |
={D x area x (partial pressure difference)} / membrane thickness D=diffusion coefficient |
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Why do limitations to diffusion affect O2 more than CO2? |
Because O2 is so much less diffusible than CO2 |
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Are diffusion abnormalities common? |
Nope, they're rare |
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What creates the diffusion reserve capacity |
Alveolar and blood PO2 and PCO2 equilibrium is reached before blood passes the halfway point of the alveolar capillary |
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What are some impediments to diffusion? |
-Loss of surface area (such as with edematous conditions) -Thickened barrier (inflammatory diseases, pulmonary fibrosis, pulmonary interstitial edema) -Pressure gradients |
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An increased PAO2 - PaO2 gradient causes what? |
Diffusion hypoxemia |
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What is diffusion hypoxemia responsive to? |
An increase in FiO2 (increase in the fraction of inspired O2) That increases the pressure gradient |
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The average alveolus gets ____ units of
ventilation to each ____ units of perfusion |
4 units of ventilation 5 units of perfusion V/Q = 4/5 = 0.8 |
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What results if some alveoli get too little ventilation in relation to perfusion? |
Low V/Q |
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What results if some alveoli get too little perfusion in relation to ventilation? |
High V/Q |
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What is the normal V/Q ratio? |
4/5 = 0.8 |
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What is the physiologic response to a low V/Q mismatch? |
Hypoxic pulmonary vasoconstriction |
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What is the normal PO2 and PCO2 at an alveolus? (say, PiO2=150 mmHg and PiCO2=0 mmHg) |
PO2=100 mmHg PCO2=40 mmHg |
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What is the expected PO2 and PCO2 at an alveolus with a low V/Q mismatch? (say, PiO2=150 mmHg and PiCO2=0 mmHg) |
PO2=40 mmHg PCO2=45 mmHg (blood doesn't pick up any O2 so without that, it leads to alveolar partial pressures becoming equivalent to that of venous blood passing) |
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What is the expected PO2 and PCO2 at an alveolus with a high V/Q mismatch? (say, PiO2=150 mmHg and PiCO2=0 mmHg) |
PO2=150 mmHg PCO2=0 mmHg (oxygen consumption from the alveolus isn't getting consumed) |
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What reflects the sum of individual alveolar V/Q ratios? |
Arterial blood partial pressures |
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Describe the state of a high V/Q ratio |
-Reduced perfusion relative to ventilation -Result is globally decreased PaO2 -The extreme case is alveolar deadspace ventilation |
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What are some causes of high V/Q? |
-Pulmonary hypertension -Pulmonary vascular embolism (heart worm) -Hypovolemia |
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Which is more common, high V/Q or low V/Q mismatch? |
Low V/Q mismatch (reduced ventilation) |
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What is the extreme case of low V/Q ratio? |
Right-to-left shunt (no ventilation) |
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Does hypoxic pulmonary vasoconstriction counter a high or low V/Q mismatch? |
Low V/Q (reduces perfusion to match the reduced ventilation) |
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What are common causes of low V/Q mismatch? |
-Airway obstruction (pulmonary inflammation--exudate, edema; bronchoconstriction--feline asthma, RAO; foreign body, mass) -Lung consolidation -Atelectasis (collapse of individual alveoli) |
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What does V/Q mismatch respond to? |
Increased FiO2 (fraction of inspired oxygen) |
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|
What is the most common cause of hypoxemia? |
V/Q mismatch |
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Describe right-to-left shunt |
-Perfusion without ventilation -Cardiac or pulmonary in origin; bronchial or coronary circulation) -Pulmonary shunts can occur with alveolar edema or pneumonia consolidation -Cardiac shunts can occur with ventricular septal defect |
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Do right-to-left shunts have a counteractive mechanism? |
Yes, hypoxic pulmonary vasoconstriction |
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Do right-to-left shunts respond to increased FiO2? Why or why not? |
Nope. The shunted blood contacts no air so you can only increase the dissolved O2 |
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What are some causes of hypoventilation hypoxemia? |
-Central depression -Narcotics -Neuromuscular disease -Chest wall disease -Pain -Upper airway obstruction |
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Is hypoventilation hypoxemia responsive to increased FiO2? |
Yes |
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Describe the expectation for the PAO2-PaO2 gradient and the PaCO2 concentration for hypoventilation hypoxemia. |
-PAO2 - PaO2 gradient normal -PaCO2 increased |
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When does hypoxemia due to low PiO2 occur? |
When FiO2 < 0.21 or barometric pressure < 760 mmHg |
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Describe the expectation for the PAO2-PaO2 gradient and PaCO2 concentration for hypoxemia due to low PiO2 |
PAO2-PaO2 gradient normal PaCO2 decreased (secondary to hyperventilation) |
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Is hypoxemia due to low PiO2 responsive to increased FiO2 or increased PiO2? |
Yes, both |
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What is the expected PiO2 at sea level? At 9,000 ft. altitude? |
Sea level: PiO2 = 760 mmHg x .21 = 159 mmHg Altitude: PiO2 = 540 mmHg x .21 = 113 mmHg |
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Why do you expect to see decreased PaCO2 in hypoxemia due to low PiO2? |
Because the animal will be hyperventilating in an attempt to get more oxygen into their system |
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Describe hypoxemia of intense exercise |
-Body metabolizes more O2 than the lungs can deliver -Increased tissue demand for O2 leads to Hb desaturation so PvO2 is reduced -CO is increased but blood passes by the alveoli too rapidly for maximal diffusion -So, blood leaves the lungs with a reduction in PaO2 -Results in hypoxemia and hypoxia |
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What are the PaO2 and PaCO2 in a racing horse? |
PaO2 < 60 mmHg PaCO2 > 60 mmHg |
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Does intense exercise hypoxemia respond to increased FiO2? |
Yes |
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|
Where are the breathing centers in the body? |
Medulla and pons; have inspiratory and expiratory nuclei |
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|
Does expiration require firing of neurons? |
No, it's passive (other than in the horse) |
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|
What can reduce respiratory nuclei? |
Barbiturates and morphine |
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|
What is the only way to change ventilation in the inspiration-expiration rhythm? |
Modifying tidal volume (VT) and frequency |
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|
How is minute volume calculated? |
VE = VT x F |
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|
Inspiratory/expiratory rhythm is modified by what? |
Receptors -Proprioceptors (in lung, airway, resp. muscles) -Lung and upper airway receptors -Central and peripheral chemoreceptors (sense partial pressure of CO2, O2, and protons) |
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What is the primary regulator of ventilation? |
[H+] (derived from PaCO2) |
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|
Brain ECF _____ regulates breathing Describe how |
pH Have a central chemoreceptor in the medulla, bathed by interstitial fluid BBB separates the systemic vasculature from the interstitial fluid in the brain Bicarb and protons aren't diffusible, but CO2 is and once it crosses, it combines with water to form carbonic acid, which splits to produce H+ |
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What effect does a decreased ECF pH have on ventilation? |
Increases it |
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|
Where is the central chemoreceptor located? |
In the medulla, near the respiratory center |
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|
What does the central chemoreceptor sense? |
H+ concentration in the brain ECF |
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What is the [H+] in the brain ECF dependent on? |
PaCO2 |
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Where are the peripheral chemoreceptors located? |
-Carotid bodies -Aortic bodies |
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|
What do the peripheral chemoreceptors detect? |
Decreased PaO2 (they are the only receptors that sense this; not O2 content) Also sense elevated [H+] (metabolic acidosis) |
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|
The _______ chemoreceptor can detect metabolic acidosis |
Periphery It detects increased [H+] peripherally |
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|
Where do peripheral chemoreceptors' sensory nerves synapse? |
In the medulla |
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|
What effect does severe chronic lung disease have on respiratory drive? Describe how. |
It blunts it -Prolonged CO2 retention leads to bicarb crossing the BBB to neutralize H+ -The [H+] drive is lost -The drive is now from a decreased PaO2 |
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Why can it be detrimental to give patients that have severe chronic lung disease supplemental oxygen? |
Because it removes their only remaining drive for ventilation -Central stimulus from excessive [H+] is buffered so eventually lost, then remaining ventilatory drive remains from peripheral chemoreceptors from low oxygen concentration -Administering oxygen supplementally removes this drive |
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|
What extreme situations depress respiratory neurons? |
-Very high levels of PaCO2 -Very low levels of PaO2 |
|
|
Where are pulmonary stretch receptors located? |
In smooth muscle of larger airways |
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|
What activates pulmonary stretch receptors? What is the result of activation of them? |
-Large tidal volume respirations -That inhibits respiratory control center nuclei in the medulla to limit inspiration -It's important in exercise |
|
|
What are pulmonary irritant receptors? |
-Sensory neurons in the airway epithelium -They are triggered by noxious gas, dust, mucus, histamine, capsaicin, mechanical deformation -Stimulate cough, bronchoconstriction, mucus, and rapid shallow breathing |
|
|
What are pulmonary C fibers? |
-Unmyelinated capillary fibers that respond to chemicals in circulation -Triggered by inflammation to cause rapid shallow breathing, bronchoconstriction, and mucus production |
|
|
Where are pulmonary proprioceptors located? |
Within intercostal muscles |
|
|
What is the importance of pulmonary proprioceptors? |
-Their muscle spindles sense stretch -Located within intercostal muscles, they control the strength of muscle contraction and monitor respiratory effort |
|
|
What is the Valsalva maneuver? |
Forced expiratory effort against a closed glottis; raises pressure in the thorax and abdomen |
|
|
Describe the mechanism of a cough |
-Inhale deeply -Close glottis -Contract expiratory muscles to raise the intrathoracic pressure -Open the glottis -Intrathoracic bronchi compress -Pressurized air rushes out through narrowed bronchi at a high velocity |
|
|
What are the main functions of the kidney? |
-"Clean" the blood -Keep blood pressure normal -Support healthy bones |
|
|
How do the kidneys regulate blood pressure? |
Through regulation of the renin-angiotensin system |
|
|
How do the kidneys maintain bone health? |
By excreting Ca and P and actively producing vitamin D3 |
|
|
How much cardiac output does the kidney receive per minute? |
25% |
|
|
Describe the features of a cortical nephron |
-short loop of Henle -renal corpuscle in outer cortex -low filtration rate -no vasa recta |
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|
Describe the features of a juxtamedullary nephron |
-long loop of Henle--dives deep into the medulla -renal corpuscle is larger and closer to the medulla -high filtration rate -vasa recta present |
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|
Which section of the nephron is always impermeable to water? |
Ascending loop of Henle |
|
|
What are the 3 basic nephron functions? |
-Glomerular filtration -Tubular secretion -Tubular reabsorption |
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|
What is tubular secretion? |
Secretion of solutes from the peritubular capillaries into the tubules |
|
|
What is tubular reabsorption? |
The movement of materials from the filtrate in the tubules into the peritubular capillaries |
|
|
What are 4 factors influencing filtration? |
-Filtration barrier -Size of the particle -Charge on the particle -Starling forces |
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|
What is the filtration barrier freely permeable to? |
Water, solutes (Na, urea, glucose, etc.) and small proteins but not cells |
|
|
Which part of the filtration barrier is an important barrier to plasma proteins? |
Basement membrane |
|
|
Why does the filtration barrier have a negative charge? |
Because it's lined by negatively charged glycoproteins |
|
|
List the components of the filtration barrier |
Endothelium (fenestrated) Basement membrane Podocytes |
|
|
_____ molecules less than _____ Angstroms are freely filtered |
Neutral, less than 20 Angstroms |
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|
What are two reasons why albumin isn't freely filtered? |
Due to its size and negative charge |
|
|
Which are filtered more freely, neutral molecules or cationic ones? |
Cationic |
|
|
What is the clinical relevance of particle size and charge? |
Loss of negative charges on the membrane barrier secondary to immunologic damage and inflammation As a result, proteinuria ensues (especially albumin) |
|
|
Does Bowman's capsule oncotic pressure favor filtration or oppose it? |
Favors it But in real life, it's almost zero |
|
|
What are the Starling forces that oppose filtration? |
The plasma oncotic pressure (which is determined by albumin) and Bowman's capsule hydrostatic pressure |
|
|
What are the the Starling forces that favor filtration? |
Glomerular capillary hydrostatic pressure and Bowman's capsule oncotic pressure (although it's basically zero) |
|
|
What is net filtration pressure? |
The difference between the forces favoring filtration and forces opposing it |
|
|
How do the Starling forces between the glomerulus and Bowman's capsule compare with those in the peritubular capillary? |
They are opposite; in the peritubular capillary you have to reabsorb everything |
|
|
What can the glomerular capillary hydrostatic pressure be affected by? |
-changes in afferent arteriolar resistance -changes in efferent arteriolar resistance -changes in renal arterial pressure |
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Why does fluid filtration decrease along the length of the glomerular capillary |
The oncotic pressure of the glomerular capillary opposes filtration and increases as fluid is filtered into Bowman's space, which concentrates the solutes |
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What effect will decreasing Kf have on GFR? |
It will decrease it |
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What effect does acute renal failure have on glomerular capillary hydrostatic pressure? |
It decreases it, which then decreases GFR |
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What can lead to a change in the oncotic pressure of the glomerular capillary? |
Liver disease or protein loss
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How is autoregulation of renal blood flow (and therefore, GFR) achieved by the kidney despite fluctuations in systemic blood pressure? |
By changes in vascular resistance of the afferent arteriole |
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What are the two autoregulation mechanisms? |
1. Myogenic mechanism 2. Tubuloglomerular feedback |
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List two important alterations that can be used for autoregulation |
1. Autoregulation is absent below 90 mmHg arterial pressure 2. Despite auto regulation, GFR and RBF can be changed by hormones |
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What is used clinically to estimate GFR? |
Endogenous creatinine (but a small amount is secreted into the urine at the proximal tubule so it overestimates filtration by 10-20%) |
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When there is nephron injury, what would we expect to see regarding serum creatinine? |
An increase because more is accumulated (since less is secreted) |
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What is filtration fraction? |
The volume of filtrate that is formed from a given volume of plasma entering the glomeruli FF=GFR/RPF |
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How is filtered load calculated? |
= Plasma conc. of the substance x GFR |
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How do you calculate amount reabsorbed of something? |
Amount reabsorbed = amount filtered - amount excreted |
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How do you calculate amount excreted of something? |
Amount excreted = urine flow rate x urinary conc. of the substance |
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How do you calculate tubular secretion of something? |
Amount secreted = amount excreted - amount filtered |
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What happens to >99% of glomerular filtrate? |
It is reabsorbed by the nephron (despite about 53 L of water being filtered every day in a 10 kg Beagle, only 500 ml is excreted daily) |
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How much water is filtered daily in a 10 kg Beagle? |
53 L |
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What is the filtered load of a substance? |
Plasma conc. of it x GFR |
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What is the excretion rate of a substance? |
Conc. of the substance in the urine x urine flow rate |
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What is the clearance rate of a substance? |
Excretion rate of a substance / plasma conc. of it |
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What are the two pathways of transport for reabsorption? |
Transcellular and paracellular pathways |
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Describe the transcellular pathway |
-Apical surface -Uptake into cell -Extensive brush border -Discharge into peritubular fluid -Relies on transporters |
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Describe the paracellular pathway |
-Zonula occludens -Driven by electrochemical and osmotic gradients -Permeability varies along the nephron |
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What drives the paracellular pathway? |
Electrochemical and osmotic gradients |
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Why is clearance important for measuring GFR? |
Because we can use the clearance of an endogenous substance like creatinine to estimate GFR |
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Which "transport" pathway of reabsorption does not rely on a transporter? |
Paracellular pathway (is driven by electrochemical and osmotic gradient) |
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How much of the filtered load is reabsorbed in the proximal tubule? |
60-70% |
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How does the proximal tubule sense fluid composition to be able to send signals to tubular cells to vary their transport processes? |
It has single, nonmotile cilia that protrude beyond the brush border that functions as a mechanosensor and a chemosensor |
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Where must filtered glucose be reabsorbed completely? |
In the proximal tubule |
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When would you start to see glucose being secreted in the urine? |
When the transporter is saturated That is why we see glucose in the urine in diabetes mellitis |
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Water reabsorption follows _____ reabsorption |
Na |
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Are water and Na reabsorption controlled by hormonal control? |
Nope It's just bulk transport of both of them |
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Which transporter is found throughout the whole nephron? |
Sodium-potassium ATPase
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What does sodium-potassium ATPase do? |
It pushes out Na from the peritubular capillary and brings in a K |
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Which side of the tubular membrane is the sodium-potassium ATPase located on? |
Basolateral side |
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Where are glucose and amino acids reabsorbed? |
The proximal tubule (after that, there is no way for them to be reabsorbed) |
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Where is filtered bicarbonate mainly reabsorbed? Describe what facilitates this process. |
In the proximal tubule Uses an Na-H exchanger; is an antiporter and takes a proton from the cytoplasm, puts it into the tubular lumen, and takes an Na from the lumen. The proton combines with filtered bicarb in the lumen and, with carbonic anhydrase, forms CO2 and water. CO2 then diffuses into the cell, where carbonic anhydrase then converts it back into the proton and bicarb. |
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If you inhibit Na/K-ATPase, what happens to Na reabsorption throughout the nephron? |
It will decrease greatly |
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The reabsorption of many organic substances (like glucose) is accomplished with what? |
Transport proteins |
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How are small proteins reabsorbed from the proximal tubule? |
Via endocytosis They then fuse with the lysosome where the vesicle gets degraded into amino acids and is taken up into the basolateral side |
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The proximal tubule absorbs ____% of water, ______% of Na, _____% Ca, _____% of phosphate, and ______% of glucose |
60-70% of water 60-70% of Na 65% of Ca 80% of phosphate 100% of glucose |
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Which two segments of the nephron are always permeable to water? |
Proximal tubule and descending loop of Henle |
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Which two segments of the nephron are always impermeable to water? |
Ascending loop of Henle and early distal tubule |
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When are the late distal tubule and collecting duct permeable to water? |
Only in the presence of ADH |
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What can urine osmolality range between? |
50-1200 mOsm/l |
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Does total solute excretion vary with urine flow rate or osmolality? |
Nope.
They change inversely to one another, which leaves total solute secretion to remain constant |
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How does ADH work? |
It acts by receptors on the basolateral side of the outer and inner medullary collecting ducts, and that causes the insertion of aquaporin channels in the apical side of the collecting duct |
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How can changes in body fluid osmolality be measured? |
By measuring changes in plasma osmolality |
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What is the major determinant of plasma osmolality? |
Sodium ion |
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Changes in Na+ balance result in changes in what? |
ECF volume
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Changes in water balance result in changes in what? |
Plasma Na+ concentration |
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What is the rate-limiting step of the RAS system? |
Renin |
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What is the biggest threat to alteration of pH? |
Acid from metabolism Life in general is an acidic process The end products of metabolism are CO2 and water, and CO2 will eventually form a proton |
