Term
| What structures make up the "conducting" and "respiratory" zones of the respiratory tree? |
|
Definition
1) Conducting (anatomical dead space with smooth muscle in walls)
- Nose/pharynx/trachea/bronchi/bronchioles/TBL
- Cartilage in trachea and bronchi only
- Warms, humidifies and filters air.
2) Respiratory
- Respiratory bronchioles/alveolar ducts/alveoli
- Gas exchange |
|
|
Term
| What are the major types of Pneumocytes in the respiratory system? |
|
Definition
1) Pseudo-stratified ciliated columnar cells extend to TBL
- sweep secretions out of lungs towards mouth
- goblet cells only extend to bronchi
2) Type-1 cells (97% of alveolar surface) are flat squamous cells for gas exchange
3) Type-2 cells (3% of alveolar surface) are cuboidal and clustered, producing surfactant and serving as precursors to type 1 cells
4) Clara cells
- Non-ciliated, columnar cells that replace goblet cells in bronchioles
- Secrete surfactant component, degrade toxins and act as reserve cells. |
|
|
Term
| Explain the basic structure of the gas exchange barrier in the respiratory system? |
|
Definition
1) Capillary is closely related to Alveoli, which is wrapped in Type 1 epithelial cells (site of gas exchange)
2) Type 2 pneumocytes underneath type 1 cells produce surfactant in lemellar bodies and constituitvely secrete it into the alveolar space (reducing surface tension).
3) Alveolar macrophages take up debris. |
|
|
Term
| Which lung lobe is the most common site for inhaled foreign bodies and why? |
|
Definition
| Right Lung (3 lobes) because of right main-stem bronchus being wider and more vertical. |
|
|
Term
| What is the relation of the pulmonary artery to the bronchus at each lung hilus? |
|
Definition
RALS
1) Right anterior (right bronchus is wider, shorter and more vertical)
2) Left superior |
|
|
Term
What part of the lungs will an aspirated peanut go to while a patient is
a) upright
b) supine |
|
Definition
1) Upright
- Lower portion of right inferior lobe
2) Supine
- Superior portion of right inferior lobe (close to oblique fissure). |
|
|
Term
What structures perforate the diaphragm at each of the following thoracic levels?
1) T8
2) T10
3) T12 |
|
Definition
Innervated by phrenic (C3-C5) and pain can be referred to shoulder.
I (IVC) ate (8) ten (10) eggs (esophagus) at (aorta) twelve (12)
1) IVC
2) Esophagus, vagus (2 trunks)
3) Aorta, thoracic duct, azygous vein |
|
|
Term
| What muscles of respiration are utilized in quiet breathing and during exercise? |
|
Definition
1) Quiet
- Inspiration= Diaphragm
- Expiration= Passive
2) Exercise
- InSpiration= external intercotals, Scalene, SCN
- Expiration= internal intercostals, rectus abdominus, transversus abdominis, int/ext obliques. |
|
|
Term
What are the functions of each of the following lung products?
1) Surfactant
2) Prostaglandins
3) Histamine
4) ACE
5) Kallikrein |
|
Definition
1) Produced by type II pnuemocytes to reduce alveolar surface tension, especially in smaller alveoli increase compliance and decrease inspiratory work.
2) Smooth muscle dilation
3) Bronchoconstriction ( parasympathetic response)
4) Ang-II signaling and inactivation of bradykinin
- Ace-inhibitors produce cough because increased bradykinin
5) Activates bradykinin (cough) |
|
|
Term
Why do airways tend to collapse on expiration?
What is the role of surfactant? |
|
Definition
Collapsing pressure P= 2T/r by law of Laplace
1) Radius decreases on expiration, so pressure increases.
2) Surfactant lowers T for a given r, by disrupting intermolecular forces between liquid molecules, and therefore lowers P, preventing atelectasis of small alveoli. |
|
|
Term
What lung volume is described below?
1) Air that can still be breathed out after normal expiration
2) IRV + TV
3) IRV + TV + ERV + RV
4) Air in lung after maximal expiration (cannot be measured on spirometry)
5) Air that moves into lung with each quiet inspiration (500 ml)
6) Air in excess of tidal volume that moves into lung on maximal inspiration.
7) TV + IRV + ERV
8) Volume in lungs after normal expiration (RV + ERV) |
|
Definition
1) Expiratory reserve volume (ERV)
2) Inspiratory capacity (IC)
3) TLC (6L)
4) Residual volume (RV)
5) Tidal volume (TV)
6) Inspiratory reserve volume (IRV)
7) Vital capacity (VC)
8) Functional residual capacity (FRC) |
|
|
Term
| How can you mathematically determine physiological dead space? |
|
Definition
Vd= [Vt (PaCo2-PeCo2)]/PaCo2
Taco, Paco, Peco, Paco
Vd= anatomical dead space of conducting airway + functional dead space in alveoli (apex of healthy lung is biggest contributor)
Fraction represents "dilution" of alveolar PCO2 by dead-spac air, that does not contribute to CO2 expired in air. |
|
|
Term
| Explain what is happening to the chest wall and lungs at FRC. |
|
Definition
Inward pull of lungs (Pl) is balanced by outward push of the chest wall (Pw) at -5 and +5
Airway and alveolar pressure are 0 and intrapleural pressure is negative. |
|
|
Term
| What conditions are known to decrease lung compliance? |
|
Definition
Change in volume over change in pressure.
Generally restrictive conditions
1) Pulmonary fibrosis
2) Decreased surfactant (ARDS, RDS)
3) Pulmonary edema |
|
|
Term
| What are the 2 major forms of hemoglobin and how do they differentially bind oxygen? |
|
Definition
Unlike myoglobin, Hb exhibits positive cooperatively and negative allostery (Sigmoid O2 dissociation curve)
1) T (taut) form has low affinity
2) R (relaxed) form has high affinity (300x) |
|
|
Term
| How does the structure of fetal hemoglobin differ from adult hemoglobin? |
|
Definition
1) Adult is composed of 2 alpha and 2 beta subunits
2) Fetal has 2 alpha and 2 gamma, with lower affinity for 2,3-BPG than the adult form, thereby increasing its affinity (won't let go!) |
|
|
Term
What do each of the following do to Hemoglobin O2 saturation curve?
1) Increased Cl-
2) Increased pH
3) Increased CO2
4) Decreased 2,3-BPG
5) Increased temperature |
|
Definition
Remember Bohr Shift and Haldane effect.
In tissues, PCO2 rises and pH decreases (H+ increases). As a result, Hb is hydrated by H+ (from bicarbonate reaction) (Bohr shift), O2 is unloaded and the curve is "right-shifted." At the same time, when Hb gives up O2, CO2 forms carbamino compounds with Hb (Haldane) and is transferred to lungs
In lungs, PCO2 falls and pH increases (less H+), making less Hb hydrated (Bohr) and less CO2 bound to Hb (Haldane), which facilities oxygen loading and "left-shifts" the O2 dissociation curve.
1) Tissue- Balances increased H+ (replaces HCO3-) and right shifts curve (delivery)
2) Lungs- Left shift (less H+ means "hold on")
3) Tissue- (delivery)
4) Lungs- ("hold on")
5) Tissue- (delivery) |
|
|
Term
| What Hemoglobin modifications lead to tissue hypoxia from decreased O2 saturation and content? |
|
Definition
1) Methemoglobin
- Oxidized (ferric, Fe3+) form that does not bind O2 readily, but has increased affinity for CN-
- Use METHylene blue to treat METHemoglobinemia
2) Carboxyhemoglobin
- Hb bound to CO in place of O2, which decreases binding capacity with a left shift in dissociation curve (increased affinity). |
|
|
Term
| How do you treat CN- poisoning? |
|
Definition
Remember, oxidized Hb (ferric, Fe3+) will bind CN- readily (Methemoglobin).
1) Use nitrates to oxidize Hb to methemoglobin (bind up CN-)
** will allow cytochrome oxidase to function**
2) Use thiosulfate to bind this cyanide, forming thiocyanate, which is readily excreted. |
|
|
Term
| What factors can cause a right-shift in the oxygen-hemoglobin dissociation curve? |
|
Definition
C-BEAT
1) CO2
2) BGP (2,3)
3) Exercise
4) Acid/Altitude
5) Temperature |
|
|
Term
| What is the effect of CO on the oxygen-hemoglobin dissociation curve? |
|
Definition
Increases Hb saturation at any given Po2 due to positive cooperativity of CO.
Left shift and reduce delivery |
|
|
Term
|
Definition
Consequence of pulmonary hypertension, which leads to RVF (JVD, edema and hepatomegaly).
Normally a low-resistance, high compliance system. Pulmonary hypertension increases pre-load on RV and causes it to hypertrophy and eventually fail.
Patients die of decompensated cor pulmonale due to cyanosis and RVH from respiratory distress |
|
|
Term
| What is the difference between "perfusion limited" and "diffusion limited" pulmonary circulation? |
|
Definition
1) Perfusion limited is normal.
- Gas equilibrates early along the length of the capillary, and diffusion can ONLY be increased if BF is also increased.
2) Diffusion-limited is abnormal (emphysema and fibrosis)
- Gas does not equilibrate by the time blood reaches the end of the capillary.
Diffusion of gas V= [Area/Thickness] x (P1-P2)
** Emphysema decreases area
** Fibrosis increases thickness |
|
|
Term
| What is the clinical definition of pulmonary hypertension and what are the common clinical consequences? |
|
Definition
>25 mm Hg at rest or >35 mm Hg during exercise.
- results in atherosclerosis, medial hypertrophy and intimal fibrosis of pulmonary arteries |
|
|
Term
| What is the difference between the pathophysiological basis of primary and secondary pulmonary hypertension? |
|
Definition
1) Primary
- Mutation in BMPR2 gene (normal functions to suppress vascular smooth muscle proliferation)
- Poor prognosis
2) Secondary
- COPD (destruction of lung parenchyma)
- Mitral stenosis (increased R leading to increased P)
- Recurrent thromboemboli (decreased SA)
- Autoimmune (systemic sclerosis)
- L-R shunting (increased shear stress...endothelial injury)
- OSA or living at high altitude (hypoxic vasoconstriction)
**DIE from decompensated cor pulmonale due to cyanosis and RVH from respiratory distress** |
|
|
Term
| What is pulmonary vascular resistance? |
|
Definition
PVR= (Ppa-Pla)/CO (R= deltaP/Q)
- pressure differential between pulmonary artery and left atrium (wedge) divided by CO being fed through.
R= 8nL/(pi)r^4 |
|
|
Term
| What determines the oxygen content of blood? |
|
Definition
(O2 binding capacity X % saturation) + dissolved O2
- usually, 1g Hb binds 1.34 ml O2 and normal Hb amount in blood in 15g/dL
(if deoxygenated Hb is > 5g/dL, you get cyanosis)
O2content= (Hb in blood)(SAO2) + dissolved O2
DLco= CO X O2content (X 10) |
|
|
Term
| What is the alveolar gas equation and how is it used? |
|
Definition
Predict an A-a gradient!
PAO2= (Pb-PH20)(FiO2) - PaCO2/R
Normally is 150 - PaCO2/0.8
If PAO2-PaO2 > 15 mmHg (normal 10-15), you have V/Q mismatching |
|
|
Term
What are the 3 major causes of an increased A-a gradient in hypoxemia?
What are the 2 major causes with a normal A-a gradient? |
|
Definition
Hypoxemia produces decreased PaO2
Increased A-a gradient
1) V/Q mismatch
2) Shunting (right to left)
3) Fibrosis (impaired diffusion).
Normal A-a gradient
1) High altitude
2) Hypoventilation |
|
|
Term
| Why do you see Ischemia-related oxygen deprivation? |
|
Definition
1) Impeded arterial flow
2) Reduced venous drainage |
|
|
Term
| What is the normal V/Q mismatching distribution in the lungs? |
|
Definition
1) Apex- V/Q= 3 (wasted ventilation)
2) Base- V/Q = 0.6 (wasted perfusion)
**Both V and Q are greater at based |
|
|
Term
True or False:
100% O2 improves PO2 in cases of blood flow obstruction. |
|
Definition
True, assuming <100% physiological dead space.
Here, V/Q approaches infinity.
100% O2 would do nothing for airway obstruction (shunt), where V/Q approaches O. |
|
|
Term
| Why does V/Q approach 1 during exercise? |
|
Definition
| Vasodilation (increased CO) of apical capillaries decreases V/Q from 3 to 1 (increased perfusion from increased CO). |
|
|
Term
| Why is TB often found in the apex of the lungs? |
|
Definition
V/Q here is 3, and TB thrives in high O2
Also true for klebsiella |
|
|
Term
| What are the relative magnitudes of PA, Pa and Pv in zones 1-3 of the lungs? |
|
Definition
Zone 1 (apex)
PA>Pa>Pv
Zone 2 (middle)
Pa>PA>Pv
Zone 3 (lower)
PV>Pa>PA |
|
|
Term
| What are the 3 ways by which CO2 is transported from tissues to the lungs? |
|
Definition
1) Bicarbonate (90%)
2) Bound to Hb at N terminus of globin (not heme) (5%)
**favors T form and oxygen unloading
3) Dissolved (5%) |
|
|
Term
| How do the Bohr and Haldane effects account for Co2 transport from the tissues to the lungs? |
|
Definition
1) In lungs, oxygenation of Hb promotes H+ dissociation, shifting the bicarbonate equation equilibrium towards CO2 formation. CO2 is therefore released from RBC (Haldane)
2) In peripheral tissue, increased H+ from tissue metabolism shifts curve to right, unloading O2 (Bohr effect) |
|
|
Term
| What are the 7 major responses to high altitude? |
|
Definition
1) Acute increase in ventilation, decreased PO2 and PCO2
2) Chronic increase in ventilation
3) Increase in EPO (increased H & H in chronic hypoxia)
-appropriate EPO-sensitive polycythemia
4) Increased 2,3 BPG (binds Hb so O2 is released)
5) Cellular changes (increased mitochondria)
6) Increased renal bicarbonate excretion (give acetazolamide) to compensate for respiratory alkalosis
7) Chronic hypoxic pulmonary vasoconstriction results in RVH |
|
|
Term
What happens to each of the following during exercise?
1) CO2 production
2) O2 consumption
3) ventilation rate (Ve)
4) V/Q ratio from apex to base
5) Pulmonary blood flow
6) pH
7) paO2 and PaCo2
8) venous CO2 content |
|
Definition
1) Increased
2) Increased
3) Increased to make up for oxygen demand
4) Becomes uniform
5) Increased (increased CO)
6) Decreased (secondary lactic acidosis)
7) No change
8) Increased |
|
|
Term
| What are the major types of emboli? What is the imaging modality of choice for PE? |
|
Definition
Move like a FAT BAT
PE presents with chest pain, tachypnea and dyspnea
1) Fat (long bone fractures and liposuction)
2) Air
3) Thrombus
4) Bacteria
5) Amniotic fluid (DIC post-partum)
6) Tumor
**Helical CT** |
|
|
Term
| What is Virchow's triad of DVT? |
|
Definition
Look for Homan's sign! (dorsiflexion of foot causes tender calf). Treat and prevent with heparin
1) Stasis
2) Hypercoagulability (Factor V, AT-III deficiency, Prothrombin varient, ect)
3) Endothelial damage (exposed collagen triggers platelet clotting) |
|
|
Term
| What are the typical changes in lung volumes seen in obstructive lung diseases? What about PFTs? |
|
Definition
Asthma, COPD, bronchitis, bronchiolitis
1) Increased RV (air trapping)
2) Decreased FVC (less gets out)
FEV1 decreases even more than FVC, making FEV1:FVC <0.7.
V/Q mismatching is also seen |
|
|
Term
A patient has had a productive cough for 4 months in each of the past 3 years.
On PE you note wheezing, crackles, cyanosis (shunting) and dyspnea.
What pathological features define this condition? |
|
Definition
Classic Chronic Bronchitis (BLUE BLOATER)
- Productive cough >3 months over >2 years from small airway disease
Look for Hypertrophy of mucus-secreting glands in bronchioles leading to a Reid index >50% in COPD (gland thickness/total thickness of bronchial wall)
Recall, Diffusion= A/T X Dx (P1 -P2) |
|
|
Term
What disease is associated with the "pink puffer," barrel-chested individual?
What are the typical pathological/pathophysiological changes associated with it? |
|
Definition
Emphysema (obstructive disease).
1) Grossly, look for cavitations linked by heavy black carbon deposits.
2) On histology, you see enlargement of air spaces separated by very thin septa.
3a) Decreased elastic recoil from alveolar wall destruction.
3b) Increased elastase activity (alpha-1-anti-trypsin deficiency) leads to increased compliance due to loss of elastic fibers. |
|
|
Term
| Why do patients with emphysema exhale through "pursed lips"? |
|
Definition
| Increase airway pressure to prevent airway collapse during respiration (lack of elastic recoil) in highly compliant, inelastic lungs. |
|
|
Term
Which obstructive lung disease is described by each of the following?
1) Bronchial hyperresponsivess causing reversible bronchoconstriction, smooth muscle hypertrophy and Curshmann's spirals
2) Chronic necrotizing infection of bronchi leading to permanently dilated airways, purulent sputum and hemoptysis.
3) Enlargement of air spaces and decreased elastic recoil due to alveolar wall damage.
4) Hypertrophy of mucus-secretion glands in terminal bronchioles with an increased Reid index. |
|
Definition
1) Asthma (triggered by viral URIs, allergens and stress and presents with cough, wheezing, tachypnea, dyspnea, hypoxemia, decreased I/E ratio and mucus pluging).
2) Bronchiectasis- associated with obstruction, poor ciliary motility (smoking), kartagener's syndrome (can see Aspergillosis)
3) Emphysema, exhale through ursed lips)
4) Chronic bronchitis, disease of small airways (TBL) |
|
|
Term
| What are the 2 major types of restrictive lung diseases and the major examples of each? |
|
Definition
FVC and TLC decrease, with FEV1/FVC > 0.8
1) Poor breathing mechanics (extra-pulmonary, peripheral hypoventilation)
- Poor muscular effort (myasthenia gravis)
- Poor structural apparatus (kyphoscoliosis, obesity)
2) Interstitial lung disease (pulmonary, lowered diffusing capacity)
- ARDS
- RDS
- Pneumoconiosis
- Sarcoid
- IPF
- Goodpasture's
- Wegener's
- Eosinophilic granuloma (histiocytosis X)
- Drugs (bleomycin, busalfan, amiodarone) |
|
|
Term
| Which pneumoconiosis preferentially affects the lower lung lobes and what are the classic pathological findings? |
|
Definition
Remember, Coal miner's and Silicosis are UPPER lobes.
- Asbestosis (ship-building, roofing and plumbing) with asbestos bodies (brown fusiform rods resembling dumbbells) inside macrophages.
- Look for "ivory white," calcified pleural plaques and watch out for bronchogenic carcinoma and mesothelioma! |
|
|
Term
Which pneumoconiosis is associated with "eggshell" calcification of hilar lymph nodes and TB infection?
What are the classic pathological/pathophysiological features? |
|
Definition
Silicosis found in upper lobes of individuals working in foundries, sandblasting and mines.
1) Macrophages release fibrogenic factors that produce fibrous
2) Phagolysosome disruption and macrophage impairment occurs, increasing susceptibility to TB. |
|
|
Term
| Which Pneumoconiosis is associated with Caplan's syndrome? |
|
Definition
Coal miner's which affects upper lobes (like Silicosis, but unlike Asbestosis)
Remember, Caplan's syndrome involves rheumatoid nodules in LUNGS of RA patients.
It is also associated with cor pulmonale and RVF (edema, JFD and hepatomegaly). |
|
|
Term
| What is the pathophysiological basis of Neonatal RDS? |
|
Definition
Surfactant (dipalmitoyl phosphatidylcholine) deficiency due to alveolar immaturity (type II pneumocytes don't start making surfactant) leads to increased ST, resulting in alveolar collapse on expiration (restrictive)
**Lecithin-to-sphingomyelin (L:S ratio in amniotic fluid (measure of lung maturity) is usually <1.5 in nRDS**
- Persistent low O2 tension increases risk of PDA and therapeutic O2 can cause retinopathy** |
|
|
Term
| Why should you be careful giving supplemental O2 to patients with neonatal RDS even though they are hypoxemic? |
|
Definition
Patients tend to have PDA because of low O2 tension.
If you give O2, Retinopathy of prematurity can result |
|
|
Term
| What are the primary risk factors/treatments for neonatal RDS? |
|
Definition
Remember, nRDS is deficient surfactant from alveolar immaturity.
1) Risk factors
- Prematurity
- Maternal diabetes (elevated insulin inhibits GC production)
- Cesarean delivery (low stress means low GC)
2) Treatment
- Maternal steroids before birth
- Artificial surfactant for infant
- Thyroxine (to increase GC) |
|
|
Term
| What is the pathophysiological basis for ARDS? |
|
Definition
DAD, hyaline membranes (sometimes called hyaline membrane disease), PMNs
1) Multiple causes (trauma, sepsis, shock, gastric aspiration, uremia, pancreatisis, amniotic fluid embolism) of DIFFUSE ALVEOLAR DAMAGE
2) Damage increases permeability and leads to protein-rich leakage into alveoli (hylaine membranosis occurs)
3) Initial damage due to PMN-release of toxic substances, activation of coagulation and oxygen-derived, free radical damage. |
|
|
Term
A patient comes in because he has been failing to breathe for >10s repeatedly during sleep (says his wife), despite extreme effort.
What are the concerning associations with this condition and how do you treat? |
|
Definition
This is sleep apnea, and since he is making effort against an obstructive airway, it is OSA (no effort would be Central)
1) Associated with pulmonary/systemic hypertension, obesity, arrhythmias, loud snoring and sudden death.
2) Treat with weight loss, CPAP (continuous positive airway pressure) and surgery |
|
|
Term
| Why are patients with OSA polycythemic? |
|
Definition
| Hypoxia increases EPO release and causes erythrocytosis. |
|
|
Term
Diagnose the following condition based upon the lung physical finds described below.
1) Breath sounds: Decreased over affected area
2) Resonance: Decreased
3) Fremitus: Decreased
4) Tracheal deviation: Towards side of lesion |
|
Definition
|
|
Term
Diagnose the following condition based upon the lung physical finds described below.
1) Breath sounds: Decreased over affected area
2) Resonance: Dull
3) Fremitus: Decreased
4) Tracheal deviation- None |
|
Definition
|
|
Term
Diagnose the following condition based upon the lung physical finds described below.
1) Breath sounds: Bronchial sounds over lesion
2) Resonance: Dull
3) Fremitus: Increased
4) Tracheal deviation- None |
|
Definition
Pneumonia (lobar)
Sounds like an effusion, but Fremitus indicates Pneumonia |
|
|
Term
Diagnose the following condition based upon the lung physical finds described below.
1) Breath sounds: Decreased
2) Resonance: Hyperresonant
3) Fremitus: Absent
4) Tracheal deviation: Away from lesion |
|
Definition
|
|
Term
Diagnose the following condition based upon the lung physical finds described below.
1) Breath sounds: Decreased
2) Resonance: Hyperresonant
3) Fremitus: Decreased
4) Tracheal deviation: Towards side of lesion |
|
Definition
| Sounds like bronchial obstruction, but Hyper-resonance indicates Spontaneous Pneumothorax (usually from ruptured sub-pleural bleb) |
|
|
Term
| What are the 6 major complications associated with lung cancer? |
|
Definition
SPHERE
1) Superior vena cava syndrome
2) Pancoast tumor
3) Horner's syndrome
4) Endocrine (paraneoplastic)
5) Recurrent laryngeal symptoms (hoarseness)
6) Effusions (pleural or pericardial) |
|
|
Term
| Which lung cancers are found centrally vs. peripherally? |
|
Definition
1) Central
- Small cell (endocrine Kulchitsky cells- small dark blue)
- Squamous cell (Keratin pearls and intracellular bridges)
2) Peripheral
- Adenocarcinoma (bronchial and bronchioloalveolar)
- Large cell (Pleomorphic giant cells with leukocyte fragments in cytoplasm) |
|
|
Term
What type/location of lung cancer is associated with each of the following histological findings?
1) Neoplasm of endocrine Kulchitsky cells
2) Keratin plugs and intracellular bridges
3) Pleomorphic giant cells with leukocyte fragments in cytoplasm.
4) Clara cells, type II pneumocytes; multiple densities on CXR |
|
Definition
1) Central, Small cell (oat cell)
2) Central, Squamous cell (smoking)
3) Peripheral, Large cell
4) Peripheral Adenocarcinoma (bronchial, bronchioloalveolar) |
|
|
Term
| Which lung cancers are/are not associated with smoking? |
|
Definition
1) Smoking is central Squamous Cell
- Look for Caviatation
- Linked to Parathyroid-like activity (PTHrP)
2) Non-smoking is Peripheral Adenocarcinoma (bronchial and bronchioloalveolar)
- Bronchial develops at site of prior pulmonary inflammation (most common lung cancer in non-smokers and females)
- Bronchioloalveolar grows along airways and can present like pneumonia, sometimes leading to osteoarthropathy. |
|
|
Term
| What is the most common lung cancer of women and non-smokers? |
|
Definition
Bronchial Adenocarcinoma (peripheral).
You will find multiple densities on x-ray of chest. |
|
|
Term
What lung cancer is associated with each of the following?
1) High anaplastic, undifferentiated tumor that is removed surgically.
2) Cavitation and parathyroid-like activity (PTHrP)
3) Grows along airways and presents like Pneumonia
4) Agressive tumor associated with ectopic ACTH and ADH production, sometimes leading to Lambert-Eaton syndrome.
5) Secretes 5-HT causing flushing, diarrhea, wheezing and salivation
6) Pleural malignancy associated with asbestos |
|
Definition
1) Large cell carcinoma (peripheral)
- Look for pleomorphic giant cells and leukocyte fragments in cytoplasm
2) Squamous cell carcinoma (Central and smoking)
- Look for keratin pearls and intracellular bridges
3) Bronchioloalveolar adenocarcinoma (periphera)
- Can result in osteoarthropathy
4) Small cell carcinoma (central) associated with paraneoplastic syndromes (Cushings/ACTH, SIADH/ADH, Lambert-Eaton/calcium channel autoantibodies)
- INOPERABLE, MUST USE CHEMO
5) Carcinoid with carcinoid syndrome
- Fibrous deposits in RH valves leading to tricuspid insufficiency, pulmonary stenosis and RVF
6) Mesothelioma resulting in hemorrhagic pleural effusions and pleural thickening
- Loop for Psammoma bodies |
|
|
Term
| What kind of tumor produces Ptosis, Miosis and Anhidrosis? |
|
Definition
| Pancoast tumor in apex of lung that affects cervical sympathetic plexus, causing Horner's syndrome. |
|
|
Term
A patient presents with facial plethora, JVD and upper extremity edema.
The patient is also starting to have headaches and dizziness.
What could be going on? |
|
Definition
Signs of impaired blood drainage from upper half of body sounds like SVC syndrome, which is associated with Neoplasms and Thromboses.
It is also raising intracranial pressure, so aneurysms may rupture! |
|
|
Term
What organisms should you think of if you see each of the following characteristics?
1) Intra-alvelar exudate leading to consolidation of entire lung
2) Acute inflammatory infiltrates from bronchioles into adjacent alveoli in a patchy distribution involving 3 lobes.
3) Diffuse patchy inflammation localized to interstitial areas at alveolar walls of 3 lobes. |
|
Definition
1) Lobar pneumonia
- Pneumococcus or Klebsiella
2) Bronchopneumonia
- S. aureus, H. influenzae, Klebsiella, S. pyogenes
3) Interstitial (atypical)
- Mycoplasma, Chlamydia, Legionella, RSV/adenovirus |
|
|
Term
| What is the most common cause of lung abscess and what are the common organisms? |
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Definition
Aspiration of oropharyngeal contents in patients predisposed to losses of consciousness
- See air-fluid levels on CXR
- S. aureus or Anaerobes (Bacteroides, Fusobacterium, Peptostreptococcus)
**Could also be due to bhronchial obstruction |
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Term
A farmer presents with dyspnea, cough, chest tightness, and a headache.
What type of reaction is this? |
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Definition
Mixed Type III/IV hypersensitive Pneumonitis
Could be Farmer's or Silo |
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Term
| What are the 3 major types of Pleural effusions? Under what conditions are they seen? |
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Definition
1) Transudate (low protein seen in CHF, nephrotic syndrome and hepatic cirrhosis)
2) Exudate (high protein/cloudy seen in malignancy, pneumonia, collagen VD, trauma)
**DRAIN IT
3) Lymphatic (chylothorax) is milky-appearing fluid with high TGA levels. |
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Term
A patient presents with unilateral chest pain and dyspnea.
On PE, you note unilateral chest expansion, decreased tactile fremitus, hyperresonance and diminished breath sounds.
What could be going on and how do you narrow your ddx? |
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Definition
Sounds like Pneumothorax
Look at tracheal deviation to determine if it is spontaneous (side of lesion due to ruptured sub-pleural bled) or tension (away from lesion due to trauma or infection) |
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Term
| How are H1 blockers use to treat respiratory pathology? |
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Definition
Reversible histamine inhibitors can be 1st or 2nd generation
1st generation ("-en/-ine" or "-en/-ate"
- Diphenhyramine, dimenhydrinate, clorpheniramine
- used for allergy, motion sickness and as a sleep aid
- SE are sedation, antimuscarinic, anti-alpha-adrenergic
2nd generation ("Adine" ending)
- Loratadine, fexofenadine, deloratadine, cetirizine
- Used for Allergy with fewer sedating side effects because of LOWER CNS PENETRATION. |
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Term
| Why is Albuterol a better choice for treating asthma than Isoproterenol? |
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Definition
Isoproterenol is non-specific beta-agonist that produces tachycardia.
Albuterol (4-6h) is beta-2 specific and only produces bronchial smooth muscle relaxation. |
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Term
What beta agonists should be used for acute asthma exacerbations?
What about as a long-acting agent in prophylaxis? |
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Definition
1) Albuterol (4-6 h)
2) Salmeterol/Formeterol are long-acting agents
**Watch out for tremor and arrhythmia!** |
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Term
How would each of the following treat Asthma?
1) Theophylline
2) Ipratropium
3) Cromolyn
4) Beclomethasone
5) Zileuton
6) Zafirlukast/Montelukast |
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Definition
1) Methylxanthine that produces bronchodilation by inhibiting PDE and reducing cGMP/cAMP hydrolysis (narrow therapeutic index)
2) M3-antagonist (competitive) that prevents bronchoconstriction (used is COPD also)
3) Prevents release of mediators from mast cells (only for prophylaxis)
4) Steroid that inhibits transcriptional production of Nf-kB, TNF-a and other inflammatory factors (1st line in chronic asthma)
5) Inhibits LCT-mediated bronchoconstriction by inhibiting 5' LOX
6) Block LCT-receptors (good for aspirin-induced asthma) |
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Term
| What agents are particularly good to treat aspirin-induced asthma? |
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Definition
COX-inhibition by aspirin produces preferential increase in LCT
Zafirlukast and Montelukast block leukotriene receptors, preventing bronchoconstriction. |
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Term
| What is the 1st line therapy for chronic asthma? |
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Definition
Steroids
HDAC-medaited inhibition of inflammatory transcription (Nf-KB, AP1, TNF-a) |
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Term
| Why might you prescribe Guaifenesin and N-acetylcystein? |
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Definition
Expectorants
1) Guaifenesin is an Expectorant that removes sputum, but does not suppress cough reflex (brady-kinin mediated)
2) N-acetylcysteine is a Mucolytic that loosens plugs in CF patients (also used in acetaminophen overdose) |
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Term
| When might you prescribe Bosentan? |
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Definition
Treat pulmonary HTN
Competitively antagonizes ET-1 receptors and decreases PVR. |
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Term
| Why might you prescribe Dextromethorphan? |
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Definition
Antitussive, synthetic codeine analog (antagonizes NMDA receptor).
Mild abuse potential but can be countered by Naloxone if OD occurs. |
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Term
| Why might you prescribe Pseudoephedrine or Phenylephrine and how do they work? |
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Definition
1) Sympathomimetic alpha-agnoist nonprescription nasal decongestants
2) Reduces hyperemia, edema and nasal congestion; open obstructed Eustachian tubes
3) Can cause HTN and CNS stimulation (Pseudoephedrine) |
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Term
| How is Metacholine used clinically? |
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Definition
Asthma challenge (staging)
**Muscarinic receptor agonist** |
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Term
What lecithin-to-sphingomyelin ratio in the amniotic fluid indicates fetal lung maturity?
1. 1:2
2. 1:3
3. 3:1
4. 1.5:1
5. 1:1 |
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Definition
| 3- Anything >2.0 indicates fetal lung maturity. |
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Term
| What component is lacking i neonatal RDS? |
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Definition
Surfactant- Lecithin (Dipalmitoyl phosphatidylcholine)
- Normal adults Lecithin:Sphingomyelin ratio should be > 2 |
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Term
| What anatomical region of a normal, healthy lung is the biggest contributor to physiological dead space? |
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Definition
| Apex- volume of inspired air that cannot take place in gas exchange. |
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Term
| What happens to pulmonary circulation as PAO2 drops? |
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Definition
| As arteriole oxygen drops, there is hypoxic vasoconstriction that shifts blood away from poorly ventilated areas of lung to well ventilated areas. |
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Term
| What factors determine gas diffusion at the capillary:alveolar interface? |
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Definition
V= A/T x Dk(P1 -P2)
A= surface area (Decreased in emphysema)
T= thickness (increased in pulmonary fibrosis)
Dk (P1-P2)= partial pressure difference
Diffusion defects can be caused by fibrosis and emphysema |
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Term
| Why does PO2 fall in chronic lung disease? |
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Definition
| Physiological shunt reduces Oxygen extraction at capillaries |
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Term
| What are hee primary causes of tissue hypoxia? |
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Definition
1) Decreased CO (CHF)
2) Hypoxemia (can be normal Aa gradient or elevated)
3) Anemia
4) Cyanide poison (give nitrates and thiosulfate)
5) CO poisoning |
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Term
| Why might a hospitalized patient receiving DVT prophylaxis have mucosal bleeding episodes? |
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Definition
| Heparin Induced TP- Switch to something like Argatrabin |
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Term
| What are "Curshmann's spirals"? |
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Definition
Shed epithelium in sputum from mucous plugs in asthma (obstructive lung disease)
In asthma, you also see smooth muscle hypertrophy and reversible bronchoconstriction (B2 agonist) |
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Term
| What are the classic clinical features of the 4 major obstructive lung diseases? |
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Definition
Look for FEV1/FVC <0.7 with V/Q mismatch
1) Chronic Bronchitis
- Small airway disease with productive cough >3 months in >2 consecutive years
- Wheezing, crackles, cyanosis (early) and dyspnea (late)
2) Emphysema
- Barrel chest as "pink puffer" (complexion and dyspnea) with exhalation through pursed lips to prevent collapse
- Decreased lung elasticity and increased compliance.
3) Asthma
- Cough, wweezing, tachypnea, dyspnea and hypoxemia, with pulsus paradoxus and mucous plugging
- triggered by viral URI, allergens and stress
- Test with methacholine challenge with bronchodilator reversal
4) Bronchiectasis
- Associated with bronchial obstruction and dysfunction in cilia motility (Kartagener's)
- Associated with Aspergillosis |
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Term
| Which drugs are associated with interstitial lung disease |
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Definition
Restrictive disease
Bleomycin (cancer), Busalfan (cancer), Amiodarone (cardiac rhythm) |
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Term
| What is the pathological basis of idiopathic pulmonary fibrosis and what kind of pathology does it produce? |
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Definition
1) Repeated damage and wound healing with increased collagen
2) Produces restrictive lung disease (Decreased TLC and FVC with FEV1/FVC >0.8 |
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Term
| What do you expect in a patient with bilateral hilar lymphadenopathy and non-caseating granulomas? |
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Definition
Sarcoidosis (restrictive lung disease)
- Increased ACE activity
- Increased Calcium |
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Term
| What is it called when a patient with RA develops cor pumonale, RVF and pleuritic nodules? |
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Definition
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Term
| What is the main difference between OSA and central SA? |
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Definition
| Central involves no respiratory effort, and OSA has effort. |
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Term
Lung cancer is the leading cause of cancer death.
What are the classic signs at presentation? |
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Definition
1) Cough and Hemoptosis
2) Bronchial obstruction
3) Wheezing
4) Pneumonic "coin" lesion on X-ray or non-calcified nodule on CT |
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Term
| What are the most common sites of metastasis TO and FROM the lung? |
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Definition
1) Comes to lung from Colon, Breast, Prostate and Bladder
2) Goes from lung to Brain, Adrenal, Bone, Liver |
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Term
| How do Theophylline and B2 agonists function in asthma treatment? |
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Definition
1) Theophyline is a methylxanthine that inhibits PDE, which normally hydrolyzes cAMP to AMP.
- cAMP is then free to induce bronchodilation
2) B2 agonists stimulate AC to produce cAMP |
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Term
What is the major actions of adenosine and ACh on bronchial smooth muscle?
How are these chemicals exploited is asthma treatment? |
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Definition
Constriction!
- ACh inhibited by Ipratroprium (M3 antagonist)
- Adenosine inhibited by Theophyline (neuro and cardio issues) |
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Term
| What is minute ventilation and how does it relate to alveolar ventilation? |
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Definition
1) Minute ventilation= Vt X breaths/min
2) Alveolar ventilation= (Vt-Dead space) X breaths/min
- It is the minute ventilation that actually "participates" |
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Term
| Which measures of lung capacity cannot be measured by spirometry? |
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Definition
Those with RV
1) FRC
2) TLC |
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Term
| What are the "transmural" pressure and how does it relate to the compliance of the lung-chest wall system? |
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Definition
1) Transmural pressure is alveolar pressure - Intrapleural pressure (outside lungs)
2) Compliance of the lung-chest wall system is less then either individually (there is elastic recoil) |
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Term
| What happens to FRC during emphysema and fibrosis, respectively? |
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Definition
At FRC, the force causing the chest to expand is equal the force causing the lungs to collapse (elastic recoil).
FRC is high in obstructive disease and low in restrictive disease
1) In emphysema, there is airspace enlargement and compliance increases.
- FRC increases, because the tendency of the lungs to collapse decreases (less elastic recoil). Therefore, patient is "barrel chested" at new higher volume
2) In fibrosis, compliance decreases and intra-pleural pressure increases, making it more likely that the lungs will collapse.
- FRC decreases, so that the tendency of the chest wall to expand is not less than the tendency of the lungs to collapse |
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Term
True or False:
The smallest airways offer the highest resistance to airflow |
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Definition
False! you would think so, since R= 8nl/pir^4
However, the biggest contributor is the medium-sized bronchi, because the small airways are in parallel |
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Term
| How does the autonomic nervous system regulate airway resistance? |
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Definition
R= 8nl/4pir^4
1) Parasympathetic constrict airways and decrease resistance
2) Sympathetic stimulation and sympathetic agonists (Isoproterenol) dilate airways via B2 receptors, increasing radius |
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Term
True or False:
Higher lung volumes are associated with lower resistance |
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Definition
True!
This is why asthmatics "learn" to breathe at higher lung volumes to offset the high airway resistance associated with the disease. |
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Term
Describe what is happening to alveolar pressure and intra-pleural pressure at each of the following points.
1) Rest
2) Inspiration
3) Expiration |
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Definition
1) Rest
- Alveolar pressure is zero
- Intrapleural pressure is negative (measured by balloon catheter in esophagus
2) Inspiration
- As inspiratory muscles contract and cause volume in the thorax to increase, Palv drops below Patm
- Intrapleural pressure becomes even more negative as the lungs fill with air and elastic recoil forces increase
3) Expiration
- Palv > Patm and air flows out of lungs
- Intrapleural pressure increases to zero as the lungs deflate
- During forced expiration, intrapleural pressure becomes positive, causing lungs to collapse and limiting expiration |
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Term
| What is the difference between a "pink puffer" and a "blue bloater"? |
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Definition
Together, they make COPD
1) Pink Puffers have predominantly emphysema
- They have mild hyoxemia, but they maintain alveolar ventilation and have normocapnia
2) Blue bloaters have predominantly chronic bronchitis
- They have severe hypoxemia with cynaosis and because they do not maintain alveolar ventilation, they have hypercapnia. |
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Term
| Describe 2 clinical scenarios where O2 diffusion is "Diffusion-limited". |
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Definition
Gas does NOT equilibrate by the time blood reaches the end of the pulmonary capillary (there is "wasted" exchange potential)
D= A/D
Can be normal (exercise), restrictive or obstructive
1) Fibrosis: thickened alveolar membrane increases diffusion distance
2) Emphysema: decreased surface area of exchange |
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Term
| What is the difference between hypoxia and hypoxemia? |
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Definition
| Hypoxemia is decreased PaO2, while Hypoxia is decreased O2 delivery to tissues (they are related, but not the same) |
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Term
What is the respiratory quotient (R)?
Why is it relevant to respiratory physiology? |
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Definition
The ratio of CO2 produced in the tissues to the O2 consumed.
R is normally 0.8, where more O2 is consumed than CO2 is produced.
R is used in the alveolar gas equation to determine the A-a gradient, where:
PAO2= PiO2 - (PaCo2/R)
So if R where to increase, PAO2 would increase, and the Aa gradient would also increase, producing V/Q mismatching |
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Term
| How is CO2 produced and transported in the venous blood for excretion? |
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Definition
Produced in tissues and diffuses into RCBs
1) Dissolved (small amount)- free in solution
2) Carbaminohemoglobin (small amount)
3) HCO3- (from hydration of CO2 in RBC)- 90%
- CO2 + H2O (CA) -------- H + HCO3
- HCO3 diffuses out (exchange for Cl-) of RBC and is carried in venous blood to lungs (H+ is buffered by deoxyHbg in RBCs) |
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Term
| How V/W matching differ in zones 1, 2 and 3 of the lung? |
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Definition
V decreases from apex to base MORE than Q increases
1) Zone 1 (Palv > Part> Pv)
- V/Q high
- Gas exchange is more efficient
2) Zone 2 (Part>Palv>Pv)
- V/Q normal
3) Zone 3 (Part> Pv > Palv)
- V/Q low
- Gas exchange is less efficient |
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Term
| What happens to fetal pulmonary circulation at birth? |
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Definition
PVR is very high in the womb, but drops dramatically when the infant takes its first breath, in order to match pulmonary blood flow to cardiac output.
In adults, pulmonary system is low resistance, low pressure system (vs. systemic) |
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Term
What is the difference between a right-to-left and left-to-right shunt?
Which is more common? |
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Definition
1) Right to left is admixture of deoxy blood to oxygenated blood, called a "step down" (TOF. Left-to-right is a "step up" (PDA)
2) Left-to-right is more common, because pressure is greater on left side |
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Term
| Why do you see an increases A-a gradient during shunting? How does this situation differ from that of a PE? |
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Definition
Think AIRWAY OBSTRUCTION.
1) In a shunt, blood is taken from a non-ventilated alveoli to others that are ventilated
- blood is not oxygenated, and mixing it with oxygenated blood results in a "step down," which will increase A-a gradient.
2) In PE, there is no perfusion (Q), so V/Q is infinite and there is physiological dead space.
- PaO2 and PaCO2 will approach that of inspired air! |
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Term
Which of the following descriptions about neural control of breathing is FALSE?
1) The dorsal respiratory group is responsible for inspiration and receives input form CN X & IX
2) The output of the ventral respiratory is active during passive breathing
3) The output of the dorsal motor group travels along the phrenic nerve.
4) The apneustic center is located in the lower pons
5) The pneumotaxic center in the upper pons inhibits inspiration |
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Definition
2- The ventral respiratory group in the medullary respiratory center of the reticular formation control expiration (internal intercostals, obliques, ect) and is only recruited during excercise.
The dorsal group= inspiration
- Input from CN X (peripheral chemoreceptors and mechanreceptors of lung and CN IX (peripheral chemoreceptors)
- Output to diaphragm via phrenic
The Ventral group= expiration
- only active during excercise
Lower pons causes inspiration, producing a deep and prolonged gasp (apnuestic), while the upper pons inhibits inspiration (pneumotaxic center) |
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Term
| What is the difference between central and peripheral chemoreceptors in terms of their function and location? |
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Definition
1) Central in the medulla
- Sensitive to pH of CSF: acidemia causes hyperventilation
- Signal is CO2 that diffuses from arterial blood to CSF, where it forms H+ and HCO3-
2) Peripheral (carotid and aortic bodies)
- Carotid body/common carotid bifurcation
- Aortic body/above and below aortic arch
- Decrease in PaO2 (<60) stimulates hyperventilation
- Increase in PaCO2 stimulates hyperventilation (less important than central response to CO2)
- Increases in H+ stimulate hyperventilation (independent of CO2) |
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Term
Explain how each of the following function in control of breathing.
1. Lung stretch receptors
2. Irritant receptors
3. J (juxtacapillary) receptors
4. Joint and muscle receptors |
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Definition
1) Found in airway smooth muscle and activated in response to lung distention (inspiration), DECREASING breathing frequency (Hering-Breuer reflex)
2) Between airway epithelial cells: stimulated by noxious substances
3) Located in alveolar walls, close to capillaries, causing rapid, shallow breathing in response to capillary bulging.
4) Activated during limb movement, in early stimulation of breathing during exercise. |
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Term
What happens to each of the following during exercise?
1) Arterial PO2 and PCO2
2) Arterial pH
3) Venous PCO2
4) V/Q ratio |
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Definition
1) NO CHANGE
2) only decreases in strenuous exercise (lactic acidosis)
3) Increases (increased production carried to lungs)
4) More evening distributed between zones 1-3
- Decrease physiological dead space |
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Term
| What are the physiological responses to high altitudes? |
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Definition
Hypoxemia because of reduced barometric pressure.
1) Peripheral chemoreceptors are stimulated (if PO2<60), and breathing rate increases
2) Renal EPO production stimulated, to increase Hbg concentration
3) 2,3-DPG increases (right shift)
4) Pulmonary vasoconstriction (can lead to RVH because of increased resistance) |
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