Pulmonary

Question 0

COPD reading: What are some risk factors for Post-op Pulmonary Complications (PPC)?

Answer 0

Dyspnea with activity (quality of life assessment)
Inc age, dec functional status, BUN (high and low), type of surgery
History of cardiac failure, ASA 2+, COPD, renal failure, emergency surgery, smoker, alcohol use, steroid use
Positive cough test (repeated coughing after the first cough)

Question 1

COPD reading: 90% of patients develop some degree of atelectasis during anesthesia. What predisposes a patient to compression atelectasis vs. reabsorption atelectasis?

Answer 1

Compression atelectasis results from patient positioning and loss of FRC, so obesity and large proportions of poorly aerated lung predispose patients to VQ mismatching
Reabsorption atelectasis results from low tidal volumes with high FiO2. Oxygen diffuses across the alveolar membrane causing a pressure difference that leads to airway collapse

Question 2

COPD reading: Do PFTs have a role in predicting PPC?

Answer 2

No, they are only done before a lung resection or to classify the degree of lung impairment, they are also done to get a baseline lung function in myasthenia gravis patients.

Question 3

COPD reading: Although cessation of smoking 48 hours before surgery decrease carboxyhemoglobin levels and cyanide levels, sputum production increases and symptoms of cough may worsen. To avoid PPC, smokers should quit ___ weeks before surgery (this also helps with wound healing and immune function.

Answer 3

8 weeks

Question 4

COPD reading: A postbronchodilator FEV1/FVC ratio less than ___ confirms the presence of airflow limitation and is recommended for the diagnosis and assessment of severity of COPD

Answer 4

0.7

Question 5

COPD reading: Should bronchodilators be continued before/during/after surgery for patients with COPD?

Answer 5

YES!!

Question 6

COPD reading: What is a COPD exacerbation treated with?

Answer 6

Short acting inhaled Beta agonists with or without anticholinergics (ipratropium)
Systemic corticosteroids and antibiotics improve FEV1 and shorten recovery time.

Question 7

COPD reading: What is the major preoperative goal for a patient with COPD?

Answer 7

Prevention of PPC with smoking cessation, bronchodilators, early recognition/treatment of infection or COPD exacerbation, and preoperative pulmonary conditioning for some high-stage COPD patients

Question 8

COPD reading: Surgical patients with asthma have increased risk for perioperative complications, so what must be done to limit these complications?

Answer 8

Thorough pre-op evaluation including physical exam, management of any electrolyte abnormalities secondary to meds (B2 agonists), EKG to identify cardiac arrhythmias or abnormalities, continuation of asthma treatments, and treatment of other associated comorbidities (such as cor pulmonale)

Question 9

COPD reading: If an asthma patient receives steroids within 6 months of surgery, what must be done peri-operatively?

Answer 9

They should receive systemic doses of steroids during the surgical period with a rapid wean within 24 hours postoperatively

Question 10

COPD reading: What are the quick-acting and long-acting asthma medications?

Answer 10

Quick acting meds for acute exacerbations: B2 adrenergic agonists (albuterol) and corticosteroids can be used
Long-acting meds include long-acting B2 agonists (salmeterol), inhaled steroids, leukotriene modifier, inhaled anticholinergics, and IgE immunotherapy
These meds should be continued perioperatively

Question 11

COPD reading: What is restrictive pulmonary disease characterized by?

Answer 11

Reduction of lung volume, both total and vital capacity

These patients are at risk for exaggerated pulmonary dysfunction postoperatively

Question 12

COPD reading: What are pulmonary and extra-pulmonary conditions that lead to restrictive pulmonary disease?

Answer 12

Pulmonary: sarcoidosis, silicosis, TB, hypersensitivity pneumonitis, eosinophilic granulomatosis, pulmonary alveolar proteinosis, lung resection, atelectasis, ARDS, pulmonary edema
Extrapulmonary: obesity, skeletal/costovertebral deformities (scoliosis), sternal deformities (pectus excavatum), neuromuscular disorders, pneumothorax

Question 13

COPD reading: What is the gold standard for diagnosing OSA? (obstructive sleep apnea)

Answer 13

Overnight polysomnography

Question 14

COPD reading: Patients with OSA having increased risk of perioperative complications. More than ___% are undiagnosed, making the surgical preoperative assessment critical to optimized morbidity and mortality in these patients

Answer 14

80%

Question 15

COPD reading: Before elective surgery, patients with OSA or at high risk of OSA should have what done?

Answer 15

Routine chemistry and CBC in conjunction with an EKG

If OSA is moderate to severe, ABG and rest radiograph should be considered to establish baseline levels

Question 16

COPD reading: Although studies have not showed any increased risk for postoperative complications in the obese population, a physical exam that incorporates _____ is critical

Answer 16

A physical exam that incorporates a pulmonary exam, assessment of OSA risk, airway management, and functional status is critical

Question 17

COPD reading: Because PPC occurs is over ___% of patients, preoperative diligence is imperative, especially in patients with chronic pulmonary disease, smokers, patients with COPD, asthma, restrictive lung disease, OSA, and obesity

Answer 17

25%

Question 18

IRV + TV =
Inspiratory capacity + ERV =
Inspiratory capacity + FRC =
ERV + RV =

Answer 18

IRV + TV = Inspiratory capacity
Inspiratory capacity + ERV = VC (vital capacity)
Inspiratory capacity + FRC = TLC (total lung capacity)
ERV + RV = FRC

Question 19

How many L are these normal values? TV, FRC, TLC, inspiratory capacity

Answer 19

TV 0.5 L
FRC 2.5 L (ERV 1.25 + RV 1.25)
TLC 5 L (another source says 6 L)
Inspiratory capacity 2.5 L (TV + IRV 2.0)

Question 20

What do the conducting airways consist of?

Answer 20

Upper airways (nasopharynx, oropharynx)
Larynx
Lower airways (trachea, bronchi, terminal bronchioles: non-respiratory)

Question 21

What do the gas exchange airways consist of?

Answer 21

Respiratory bronchioles
Alveolar ducts
Alveoli: epithelial cells, type 1 and type 2 alveolar cells

Question 22

Type 1 vs. type 2 alveolar cells?

Answer 22

Type 1: gas exchange, we have mostly this type, maximizes surface area (size of a tennis court)
Type 2: surfactant production

Question 23

What happens as we go up in generations of the airway?

Answer 23

Stiff at the beginning, as we move toward higher generations there is less cartilage
Generation 20 is where gas exchange begins, there are 26 generations

Question 24

What layers does oxygen travel through to go from alveoli to blood?

Answer 24

Alveolus - surfactant layer - alveolar epithelium - basement membrane - interstitial space - capillary endothelium

Question 25

Are inspiration and expiration active or passive?

Answer 25

Inspiration active | Expiration passive

Question 26

What are the major muscles of inspiration? Assessory muscles of inspiration?

Answer 26

Major: diaphragm, external intercostals Accessory: SCM (lift clavical and sternum) and scalenes (pull ribs up)

Question 27

What are the accessory muscles of expiration?

Answer 27

Abdominal and internal intercostals

Question 28

What is surfactant's role in the alveoli in helping us breathe?

Answer 28

Surfactant decreases surface tension LaPlace Law says tension = pressure x radius Therefore, surfactant allows us to inflate all the alveoli

Question 29

Under normal conditions, what drives ventilation? What drives ventilation in hypoxemic conditions?

Answer 29

CO2 tension normally | O2 tension in hypoxemic conditions

Question 30

What are the four steps of gas transport? (oxygen to tissue)

Answer 30

1. Ventilation of the lungs 2. Diffusion of O2 from alveoli to capillary 3. Perfusion of capillaries with oxygenated blood 4. Diffusion of O2 from capillaries into cells

Question 31

How do the pressures vary between the tissues and heart? PO2, PCO2, PH2O, PN2

Answer 31

Heart: PO2 104, PCO2 40, PH2O 47, PN2 569 Tissue: PO2 40, PCO2 46, PH2O 47, PN2 573

Question 32

What factors contribute to the oxyhemoglobin dissociation curve shifting to the left vs. right? Hint: acid/base, temp, 2,3-DPG

Answer 32

Left shift INCREASES affinity- acute alkalosis, decreased PCO2, decreased temp, low 2,3-DPG, carboxyhemoglobin, methemoglobin, abnormal hemoglobin Right shift DECREASES affinity- (think: running from a bear, you need the oxygen to be dropped off) acute acidosis, high PCO2, increased temp, high levels of 2,3-DPG, abnormal hemoglobin

Question 33

How can you mathematically figure out the oxygen content?

Answer 33

O2 content = 1.34 x hematocrit x O2 sat (+ 0.003 x PO2; but this is an insignificant number)

Question 34

What is hypoxic vasoconstriction? What is it caused by?

Answer 34

Caused by low alveolar pO2 Blood is shunted to other, well-ventilated portions of the lung to provide better V-Q matching If hypoxia affects all segments of the lungs, pulmonary hypertension can result Acidemia also causes pulmonary artery constriction

Question 35

Compare PA (alveolar pressure), PV (venous pressure), and Pa (arterial pressure) in the 3 zones of the lung.

Answer 35

Zone 1: PA > Pa > PV Zone 2: Pa > PA > PV Zone 3: Pa > PV > PA

Question 36

What does FEV1 test? What does FVC test? | Forced expirational volume-1 sec, Functional vital capacity

Answer 36

FEV1: How fast you can let air out in 1 sec. Should be 90% FVC: all the way filled to all the way empty These are types of spirometry tests

Question 37

What changes in the aging population? IRV? TV? ERV? RV?

Answer 37

IRV decreases TV doesn't change ERV doesn't change RV increases

Question 38

How many weeks in fetal development do they get type 1 and type 2 alveolar cells?

Answer 38

Week 28 At week 24, they can store surfactant At term, they can secrete surfactant as needed

Question 39

Hypoxia vs. hypoxemia?

Answer 39

Hypoxia: low O2 content Hypoxemia: low O2 tension Hypoxemia can result in hypoxia but not necessarily the other way around

Question 40

Kussmaul respirations vs. Cheyne-Stokes respirations?

Answer 40

Kussmaul: compensation for metabolic acidosis (ketoacidosis), breathing faster to blow off CO2 Cheyne-Stokes: alternating apnea and tachypnea (brain damage)

Question 41

Compression vs. absorption atelectasis

Answer 41

Compression: compression of alveoli Absorption: obstructed airway and gas absorption

Question 42

Bronchiectasis vs. bronchiolitis

Answer 42

Bronchiectasis: chronic abnormal dilation of bronchi Bronchiolitis: inflammatory obstruction of bronchioles

Question 43

What are these different types of pleural effusion? Transudative, exudative, hemothorax, chylothorax, empyema?

Answer 43

Transudative: low protein content (HF) Exudative: high protein content (EXudative has EXtra stuff) Hemothorax: blood in pleural space Chylothorax: lymph in pleural space Empyema: pus in pleural space (NOT the same as emphysema)

Question 44

Restrictive vs. Obstructive lung disease?

Answer 44

Restrictive: difficulty getting air IN the lung, types: ARDS, intrinsic (pulmonary fibrosis) and extrinsic (SCI) Obstructive: difficulty getting air OUT of the lung, types: asthma, COPD

Question 45

How do FVC, FEC1, and FEV1/FVC change in restrictive and obstructive pulmonary disorders?

Answer 45

Restrictive: Dec FVC, normal/dec FEV1, normal FEV1/FVC ratio Obstructive: Dec FEV1 (normal FVC), dec FEV1/FVC ratio

Question 46

What are common signs and symptoms of obstructive pulmonary disease?

Answer 46

``` Dyspnea and wheezing Air trapping, caused by mucous plugs Decreased elastic recoil on expiration Difficulty getting air OUT Asthma and COPD (emphysema and chronic bronchitis) ```

Question 47

What is asthma?

Answer 47

Chronic inflammatory disorder of the airway Inflammation causes recurrent wheezing episodes, breathlessness, chest tightness, cough (particularly at night and early morning), hyper-responsive to stimuli

Question 48

What is the strongest identifiable predisposing factor for developing asthma?

Answer 48

Atopy- the genetic predisposition for the development of an IgE-mediated response to common aeroallergens

Question 49

What is the pathophysiology of asthma?

Answer 49

1. inhaled antigen binds to IgE on mast cell 2. mast cell releases chemical mediators (histamine, leukotrienes, prostaglandin, platelet-activating factor), acute inflammation opens tight junctions allowing antigen to penetrate and active mast cells 3. Mediators induce bronchospasm, edema, mucus secretion 4. Inflammatory cells are recruited by chemokines and upregulate adhesion molecules. Eosinophils eventually cause epithelial damage

Question 50

Asthma: Allergen causes Immune activation, mast cell degranulation, vasoactive mediators, vaso____, ____ capillary permeability, causing abnormal response of bronchospasm, mucus secretion, thickening of airway walls, bronchial hyperresponsiveness, airway obstruction, and epithelial desquamation and fibrosis

Answer 50

Vasodilation, increased capillary permeability

Question 51

COPD: chronic bronchitis vs. emphysema?

Answer 51

Chronic bronchitis: small airway disease (bronchioles) results in airflow obstruction, large airway disease (trachea, bronchi) is responsible for mucus hypersecretion Emphysema: Respiratory bronchiole, alveolar ducts, and alveoli lose elastic recoil

Question 52

Risk factors and genetic predisposition to COPD?

Answer 52

Smoking!! Air pollution, hyper-responsive airways, occupational factors Alpha1-antitrypsin deficiency is the only known genetic abnormality that leads to COPD

Question 53

Chronic bronchitis is hypersecretion of mucus and chronic productive cough that lasts for at least ___ months of the year and for at least ___ consecutive years

Answer 53

Hypersecretion of mucus and chronic productive COUGH that lasts for at least 3 months of the year and for at least 2 consecutive years Inspired irritants increase mucus production and size and number of mucous glands Mucus is thicker than normal

Question 54

What is emphysema?

Answer 54

Abnormal permanent enlargement of the gas-exchange airways accompanied by destruction of alveolar walls without obvious fibrosis The big key here is loss of elastic recoil!

Question 55

Centriacinar emphysema vs. panacinar emphysema?

Answer 55

Centriacinar: the middle of the bronchiole has very enlarged alveoli which leads to loss of surface area, loss of recoil Panacinar: the whole bronchiole has slightly enlarged uniform alveoli which again leads to loss of surface area and loss of recoil

Question 56

When nicotine activates neutrophils, how does this lead to tissue damage?

Answer 56

Neutrophils destroy the elastase that give alveoli its "springiness", also activates ROS creating free radicals This is one of the ways that smoking causes emphysema

Question 57

If we inherit alpha-1 antitrypsin deficiency, how does that lead to similar symptoms as emphysema due to long-term smoking? Use antitrypsin, trypsin, elastase, and elastin to explain

Answer 57

Elastase breaks up elastin fibers. Without as much trypsin, we increase elastase (we make this endogenously), which breaks down extra elastin so we don't have as much elastin left over which leads to loss of recoil, the main issue with emphysema.

Question 58

How do you restore collateral ventilation during absorption atelectasis?

Answer 58

Deep breathing

Question 59

Restrictive lung disease: What values does it reduce, what does it have no change in? TLC, FRC, RV, Expiratory flow rate, VC, FEV1, FVC, FEV1/FVC ratio, exhaled volume

Answer 59

Reduction in: TLC, FRC, RV, VC, FEV1, FVC, total volume exhaled No change in: expiratory flow rate, FEV1/FVC ratio

Question 60

What are some s/s of restrictive airway disease?

Answer 60

Reduced compliance = stiff lungs, increased work of breathing, dyspnea Rapid, shallow breathing = increased dead space ventilation Normal gas exchange Until advanced disease, inc PCO2, dec PO2, pulmonary hypertension, cor pulmonale

Question 61

How are restrictive airway diseases classified?

Answer 61

Acute intrinsic: pulmonary edema Chronic intrinsic: diseased lung parenchyma (lung interstitium) Chronic extrinsic: chest wall, intra-abdominal and neeuromuscular diseases, (ex. SCI) Disorders of the pleura and mediastinum

Question 62

What is pulmonary edema? What are the two mechanisms in which it can occur?

Answer 62

Fluid leakage from the intravascular space to the lung interstitium and alveoli. Mechanisms: 1. Increased capillary/hydrostatic pressure (heart failure) 2. Increased capillary permeability (ARDS) CXR will show opacities

Question 63

Valve dysfunction, CAD, LV dysfunction -> __ (inc/dec) LA pressure -> ___ pulmonary capillary hydrostatic pressure -> pulmonary edema

Answer 63

Increase | Increase

Question 64

Injury to capillary endothelium -> ___ capillary permeability, disruption of surfactant production -> movement of fluid from capillary to interstitial space and alveoli -> pulmonary edema

Answer 64

Increase

Question 65

What does ARDS do to the lungs?

Answer 65

Diffuse pulmonary endothelial injury (neutrophils help with this) Water, solutes, molecules diffuse from intravascular space into alveoli ROS and cytokines released Complement system activation leads to damage to type 2 pneumocytes, disruption of alveolar-capillary membrane, micro-thrombi in pulmonary circulation (pulm htn), and fibroblast growth factors (pulmonary fibrosis)

Question 66

What does aspiration pneumonitis look like clinically? When does CXR show changes?

Answer 66

Increased permeability pulmonary edema with atelectasis, similar to ARDS, because acidic gastric secretions destroy surfactant, damaging the endothelium Clinical s/s: hypoxia, tachypnea, bronchospasm, pulmonary constriction can turn into pulmonary HTN CXR changes 6-12 hrs later, usually R lower lobe

Question 67

What is the treatment of aspiration pneumonitis?

Answer 67

Increased FiO2, PEEP, B2 agonists for bronchospasm Lavage, antibiotics, steroids might help Fiberoptic bronchoscopy if solid material was aspirated

Question 68

What does cardiogenic pulmonary edema look like clinically? What are the causes?

Answer 68

Causes: LV failure with increased pulmonary vascular hydrostatic pressures, transudate fluid leaks out leading to greater surface tension Clinical s/s: SNS activation, extreme dyspnea, tachypnea, hypertension, tachycardia, diaphoresis

Question 69

How does neurogenic pulmonary edema occur?

Answer 69

Occurs after acute brain injury Generalized vasoconstriction with shift large blood volume into pulmonary vessels leads to vessel injury and transudation of fluid into alveoli It looks similar to cardiogenic pulm edema (medulla is cardio-resp center)

Question 70

What does high altitude pulmonary edema look like? What is the treatment?

Answer 70

Increased pulmonary vascular pressures result in high permeability pulmonary edema, intense hypoxic pulmonary vasoconstriction after 2-3 days Treat with O2, descent from altitude, and inhaled nitric oxide

Question 71

What is re-expansion pulmonary edema?

Answer 71

Follows evacuation of pneumothorax or pleural effusion, more common if over 1L fluid/air, for over 24 hours, and if re-expansion occurs rapidly Don't give diuretics! Supportive treatment

Question 72

What are possible causes to negative-pressure pulmonary edema

Answer 72

``` Post-extubation laryngospasm Obstructive Sleep apnea Epiglottitis Tumors Obesity Hiccups ```

Question 73

With negative-pressure pulmonary edema, ___ interstitial hydrostatic pressure, ___ venous return, ___ afterload on LV, ___ SNS outflow and hypoxemia, failure to maintain sats over 95, tachypnea, cough

Answer 73

``` DEC interstitial hydrostatic pressure INC venous return INC afterload on LV INC SNS (hypertension, central pooling) ```

Question 74

Who gets sarcoidosis? What are characteristics of sarcoidosis?

Answer 74

Most often found in young, black females Systematic granulomatous disorder, often found in thoracic lymph nodes and lungs. Cor pulmonale and pulmonary hypertension are likely. Decreased alveolar diffusion capacity. Liver, spleen, optic, and facial nerve often affected. Myocardial rarely.

Question 75

Anesthetic consideration of sarcoidosis?

Answer 75

Laryngeal sarcoid in 1-5% of patients can interfere with ETT passage Patient may need a dose of steroids peri-operatively, often on chronic corticosteroids Minor surgery- 2x normal dose; moderate surgery- 25mg hydrocortisone pre-op, 75 mg intra-op, 50mg IV post-op; major- 50mg pre-op, 100mg intra-op, 100mg post-op

Question 76

What diagnostic procedure is done for sarcoidosis? What electrolyte may be off-balance?

Answer 76

Mediastinoscopy for diagnosis | Hypocalcemia

Question 77

Chronic intrinsic vs. extrinsic restrictive lung disease? What are some of the characteristics for each?

Answer 77

Intrinsic: pulmonary fibrosis, loss of pulmonary vasculature (pulmonary hypertension, cor pulmonale likely), pneumothoracies are common with advanced disease, dyspnea (rapid, shallow breathing) Extrinsic: Thoracic cage abnormalities, interferes with lung expansion (outside the lung); characteristics- increased WOB (dec lung volume with increased airway resistance), thoracic deformity (RV dysfunction common), impaired cough

Question 78

Hypersensitivity pneumonitis vs. pneumoconiosis?

Answer 78

Both are chronic intrinsic restrictive lung disease Hypersensitivity pneumonitis: diffuse interstitial granulomatous reactions in lungs after inhaled dust containing fungi, spores, or animal material; inhaling stuff that HAS proteins that was alive, causes B/T cells to respond Pneumoconiosis: silicosis, coal worker (black lung), asbestosis; result to non-protein containing material, no B/T cells respond

Question 79

Are these intrinsic or extrinsic restrictive pulmonary disease? Eosinophilic granuloma, pulmonary alveolar proteinosis, lymphangiomyomatosis

Answer 79

INTRINSIC | Lymphangiomyomatosis: proliferation of smooth muscle in the abdominal and thoracic lymphatics, veins, and bronchioles

Question 80

What is the pathogenesis of chronic restrictive lung disease?

Answer 80

Lung injury -> activated macrophage -> recruits neutrophils and cytokines -> injury to type 1 pneumocytes -> hypertrophy/hyperplasia of type 2 pneumocytes -> fibroblasts are formed

Question 81

Name some chronic extrinsic restrictive lung diseases

Answer 81

``` Obesity Scoliosis (lateral deformity), Kyphosis (anterior deformity); These both increase risk of hypoventilation and pneumonia with CNS depressants Sternum abnormalities Flail chest Neuromuscular disorders ```

Question 82

Pectus excavatum vs. Pectus carinatum

Answer 82

Deformities of the sternum Pectus excavatum: inward concavity of sternum Pectus carinatum: outward protuberance of the sternum

Question 83

What is flail chest?

Answer 83

Secondary to rib fracture or sternotomy dehiscence Paradoxical inward movement of the unstable part of the thoracic cage during inspiration Lung increases volume during exhale and decreases during inhale Dec PO2, increased PCO2 due to alveolar hypoventilation, PPV helps

Question 84

For someone with a neuromuscular disorder, what is useful to measure extent of impact of disease on ventilation?

Answer 84

Vital capacity | With some neuromuscular disorders, patients are very sensitive to CNS depressants

Question 85

Open vs tension pneumothorax?

Answer 85

Open: knife to chest for example, creates a hole so the lungs can't be inflated Tension: Air can come in and not out, risk of lung collapsing, it is considered a medical emergency, symptoms are more sudden and severe

Question 86

How does a pneumothorax work?

Answer 86

Outside air enters pleural space bc of disruption in chest wall and parietal pleura Lung air enters the pleural space bc of disruption of visceral pleura Mediastinum may be pushed toward the opposite lung

Question 87

S/S of pneumothorax?

Answer 87

``` Acute dyspnea Ipsilateral chest pain Decreased PO2, increased PCO2 Hypotension, tachycardia Decreased chest wall movement Decreased/absent breath sounds Hyperresonant percussion ```

Question 88

Treatment of idiopathic and tension pneumothorax?

Answer 88

Idiopathic: evacuation of air via catheter aspiration or chest tube Tension: small bore plastic catheter into second anterior intercostal space Increased FiO2 improved rate of air resorption by pleura x4

Question 89

What is pleurodesis?

Answer 89

A pleural fibrosis in which the visceral pleura and parietal pleura are glued together

Question 90

Transudative vs. Exudative effusion?

Answer 90

Pleural effusions Transudative: blood without protein and cells, happens with high pressure or CHF Exudative: transudate with protein, this means there is inflammation

Question 91

What is pleurisy?

Answer 91

Pleural effusion that involves infection in the pleural space, pus, painful breathing, rubbing

Question 92

What is empyema?

Answer 92

Pus in pleural space, result of infection near or in the pleural space, it is an "infected pleural effusion"

Question 93

Where do pulmonary embolisms usually arise from?

Answer 93

DVT | Lungs are a filter for microemboli, but these are big clots coming from the deep veins in the thigh

Question 94

What is Virchow's triad?

Answer 94

Three things that predispose thrombus formation 1. Venous stasis 2. Hypercoagulability 3. Injury to endothelial cells that line the vessels

Question 95

How does Virchow's triad lead to pulmonary embolism?

Answer 95

``` Occlusion of part of pulmonary circulation causes... Hypoxic vasoconstriction Decreased surfactant Release of inflammatory substances Pulmonary edema Atelectasis ```

Question 96

S/S of pulmonary embolism?

Answer 96

``` Tachypnea, dyspnea Chest pain, decreased cardiac output Increased dead space, V/Q mismatch Decreased PO2 Pulmonary infarction, pulmonary hypertension Hypotension, shock ```

Question 97

What is normal pulmonary pressure? What is the pressure with pulmonary hypertension?

Answer 97

Normal: 25/10, mean 20 | Pulmonary hypertension: Mean is 5-10 above normal or above 20 mmHg

Question 98

What can cause pulmonary hypertension?

Answer 98

Respiratory disease or hypoxemia (COPD, high altitude) Thrombotic or embolic disease (blocks part of the vascular bed, increasing pressure) Disease of the pulmonary vasculature Can be pulmonary arterial or venous hypertension

Question 99

How can endothelial dysfunction cause pulmonary hypertension? (thromboxane, endothelin, prostacyclin, nitric oxide)

Answer 99

Overproduction of vasoconstrictors: thromboxane, endothelin | Underproduction of dilators: prostacyclin, nitric oxide

Question 100

What is cor pulmonale?

Answer 100

Hypertrophy and dilation of right ventricle due to pulmonary reasons like pulmonary hypertension

Question 101

Smokers have ____x the chance of getting lung cancers compared to non-smokers. What are some other cancers that smokers are more likely to get?

Answer 101

20x | Cancers of the larynx, oral cavity, esophagus, and urinary bladder (kidney filters the carcinogens)

Question 102

Compare the types of lung cancers: Squamous cell carcinoma, small cell carcinoma, adenocarcinoma, large cell carcinoma. Which are most and least correlated with smoking?

Answer 102

Squamous cell (epidermoid): slow, near hilus, obstructive with cough and hemoptysis Small cell (oat cell): Rapid, most correlated with smoking, high mortality, ectopic hormone production Adenocarcinoma: moderate, least correlated with smoking, usually on periphery Large cell: rapid!

Question 103

How is cystic fibrosis passed down? What are the characteristics?

Answer 103

Recessive Chloride transporter in the sweat glands does not allow Cl or Na in the sweat duct, so you have salty/Cl sweat In the lungs, too much Na and H2O reabsorbed and no Cl out, leading to dehydrated mucus, the mucus traps the germs and this leads to lots of lung infections and mucus plugging, also dilation of tracheobronchial tree