Respiratory system Flashcards
List the anatomical components of the lung from largest to smallest
- Trachea
- Bronchi
- Terminal bronchioles
- Respiratory bronchioles
- Alveolar ducts
- Alveolar sacs
Where does gas exchange happen in the lung?
Alveoli
NO GAS EXCHANGE between bronchioles and terminal bronchioles AKA DEAD SPACE
What part of the respiratory system are goblet cells, cilliated columnar cells, and submucosal cells found in? What is their role?
- Upper respiratory system
- Keep lungs clean and effcient and conducts air
- Cilia clears airways of particles
- Mucus also clears particles
What are type I and II pneumocytes?
- Alveoli cells
- Type I are cells through which gas exchage/diffusion occurs
- Type II are cells that make surfactant
How does alveolar pressure decrease so air can get into lungs?
- Thorax volume increases leads to reduced alveolar pressure
- Diaphragm and intercostal muscles increase volume of thorax
When diaphram contracts, it drops down, and increases vertical volume of thoracic cage
Intercostal muscles exsist as well and exsist between the ribs - When they contract it lifts sternum and increases circumferencial volume of thoracic cage
How are gasses expelled from the lungs?
- Elastic forces act inwards
What causes the stretchiness of lungs? What happens if there is too little or too much compliance?
compliance=stretchiness
- Collagen and elastin coat the outside of alveoli cells
- LOW compliance (aka fibrotic lungs w lots of scar tissue) are diseased/unhealthy lungs and needs MORE pressure to inflate the lungs
- HIGH compliance (emphisema) and means they can feel their lungs much more but have problems with getting air out of their lungs
What problem does LaPlaces law illustrate in alveoli gas expulsion? What is the solution?
Because smaller alveoli have greater pressure than larger alveoli, it means that gas from smaller will go into larger instead of out of lungs
Surfactants (90% phospholipids and 10% protein) reduce surface tension in the smaller alveoli, so under laplaces law the pressure equalizes
What is Henry’s Law?
At a constant temperature, the number of molecules dissolving in the liquid is directly proportional to the partial pressure of the gas in equilibrium with that liquid
conc O2 = PO2 gas phase
How many molecules of O2 can hemoglobin carry at once?
4 molecules O2
HHb + O2 <=> HHb + H
What is the oxygen capacity of hemoglobbin?
1.39 ml O2 per g Hb
What is the Bohr effect?
When hemoglobbin has a lower affinity for O2 (P50= 5kPa) due to decrease in blood pH
lower affinity also caused by increase in partial pressure of CO2, temp, 2,3 DPG
“CADET, face Right!” for CO2, Acid, 2,3-DPG, Exercise and Temperature
lower affinity= more oxygen is going into tissues
What causes the O2-Hb dissociation
curve to shift left?
- Increase in pH, decrease in PCO2/temp
- P50= 2.5kPa
in a standard curve P50=3.5 kPa
How does carbon monoxide effect O2 transport?
occupies 40% of O2 binding sites
How does fetal hemoglobbin effect the O2-Hb dissociation curve?
- 2α + 2γ-chains have higher affinity for O2 ; aids O2 transfer to fetus
- shifts the curve left: P50 = 2.5 kPa
What are the three ways of CO2 transportation?
- dissolved
- As bicarbonate (HCO3-)
- Bound to hemoglobbin (carbamino Hb formation, Hb.COOH)
in plasma, h20+CO2= H2CO3 (slow) -> dissociates to HCO3- and H+
in RBC, same thing happens with carbonic anhydrase (fast) except Cl- transported in and HCO3- out
What is the Haldane Effect?
Carrying capacity for CO2 is greater for deoxygenated blood
(1) O2 release from Hb(O2) increases affinity of deoxygenated Hb subunits for H+
(2) H.Hb combines with CO2 to form carbaminohaemoglobin (Hb.COOH)
Deoxygenation of blood at the tissues – able to take-up more CO2
Oxygenation of blood in lung – assists unloading of CO2 from blood
What three things are responsible for hypoventilation?
- Decreased lung compliance (e.g. fibrotic lung)
- Increased resistance (e.g. a lot of mucus bc infection/allergy/ inflammation of bronchial tubes)
- CNS depression of ventilation rate and/or depth
What are three pathological changes that adversely affect gas exchange?
- emphysema (Decrease in alveolar surface area)
- fibrotic lung diseases (Inc in thickness of alveolar-capillary exchange barrier)
- pulmonary edema (inc in diffusion distance between alveloar space and blood)
What happens when the ventilation/perfusion of alveoli is disrupted?
V/Q= 0 when perfusion but no ventilation
V/Q= infinte when ventilation but no perfusion
V/Q=0 (Chronic bronchitis, asthma, acute pulmonary edema)
V/Q=infinite (Pulmonary embolism)
How do the pons and medulla regulate respiration?
- Pontine respiratory groups (PRG) (in Pons) integrate sensory information
- They stimulate Ventral respiratory group (VRG) (in Medulla) control expiratory/inspiratory muscles
- Dorsal respiratory group (DRG) (in Medulla) receive peripheral and central sensory input (medullary chemoreceptors monitor CO2)
What are three pulmonary mechanoreceptors and their functions?
- Slowly Adapting Receptors (SARs, ‘stretch receptors’): Prevent over inflation
- Rapidly Adapting Receptors (RARs, ‘irritant receptors’): Respond to noxious stimuli
- ‘J’ receptors: Respond to increased alveolar fluid, pulmonary congestion, inflammatory mediators – all associated with lung disease
What are the two types of chemoreceptors and what do they do?
- Central (slow response)
- Peripheral (stimulate carotid sinus nerve – increased ventilation) (fast)
- Detect PCO2, pH and PO2
Normal PCO2 = 5.3 kPa
