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N552 Patho > Pulmonary > Flashcards

Pulmonary Flashcards

0
Q

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

A

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)

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1
Q

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

A

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

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2
Q

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

A

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.

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3
Q

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.

A

8 weeks

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4
Q

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

A

0.7

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5
Q

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

A

YES!!

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6
Q

COPD reading: What is a COPD exacerbation treated with?

A

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

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7
Q

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

A

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

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8
Q

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

A

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)

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9
Q

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

A

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

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10
Q

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

A

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

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11
Q

COPD reading: What is restrictive pulmonary disease characterized by?

A

Reduction of lung volume, both total and vital capacity

These patients are at risk for exaggerated pulmonary dysfunction postoperatively

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12
Q

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

A

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

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13
Q

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

A

Overnight polysomnography

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14
Q

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

A

80%

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15
Q

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

A

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

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16
Q

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

A

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

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17
Q

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

A

25%

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18
Q

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

A

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

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19
Q

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

A

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)

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20
Q

What do the conducting airways consist of?

A 
Upper airways (nasopharynx, oropharynx)
Larynx
Lower airways (trachea, bronchi, terminal bronchioles: non-respiratory)
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21
Q

What do the gas exchange airways consist of?

A

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

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22
Q

Type 1 vs. type 2 alveolar cells?

A

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

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23
Q

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

A

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

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24
Q

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

A

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

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25
Q

Are inspiration and expiration active or passive?

A

Inspiration active

Expiration passive

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26
Q

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

A

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

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27
Q

What are the accessory muscles of expiration?

A

Abdominal and internal intercostals

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28
Q

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

A

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

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29
Q

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

A

CO2 tension normally

O2 tension in hypoxemic conditions

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30
Q

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

A
  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
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31
Q

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

A

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

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32
Q

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

A

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

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33
Q

How can you mathematically figure out the oxygen content?

A

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

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34
Q

What is hypoxic vasoconstriction? What is it caused by?

A

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

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35
Q

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

A

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

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36
Q

What does FEV1 test? What does FVC test?

Forced expirational volume-1 sec, Functional vital capacity

A

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

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37
Q

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

A

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

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38
Q

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

A

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

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39
Q

Hypoxia vs. hypoxemia?

A

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

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40
Q

Kussmaul respirations vs. Cheyne-Stokes respirations?

A

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

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41
Q

Compression vs. absorption atelectasis

A

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

42
Q

Bronchiectasis vs. bronchiolitis

A

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

43
Q

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

A

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)

44
Q

Restrictive vs. Obstructive lung disease?

A

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

45
Q

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

A

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

46
Q

What are common signs and symptoms of obstructive pulmonary disease?

A 
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)
47
Q

What is asthma?

A

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

48
Q

What is the strongest identifiable predisposing factor for developing asthma?

A

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

49
Q

What is the pathophysiology of asthma?

A
  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
50
Q

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

A

Vasodilation, increased capillary permeability

51
Q

COPD: chronic bronchitis vs. emphysema?

A

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

52
Q

Risk factors and genetic predisposition to COPD?

A

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

53
Q

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

A

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

54
Q

What is emphysema?

A

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!

55
Q

Centriacinar emphysema vs. panacinar emphysema?

A

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

56
Q

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

A

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

57
Q

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

A

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.

58
Q

How do you restore collateral ventilation during absorption atelectasis?

A

Deep breathing

59
Q

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

A

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

60
Q

What are some s/s of restrictive airway disease?

A

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

61
Q

How are restrictive airway diseases classified?

A

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

62
Q

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

A

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

63
Q

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

A

Increase

Increase

64
Q

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

A

Increase

65
Q

What does ARDS do to the lungs?

A

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)

66
Q

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

A

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

67
Q

What is the treatment of aspiration pneumonitis?

A

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

68
Q

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

A

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

69
Q

How does neurogenic pulmonary edema occur?

A

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)

70
Q

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

A

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

71
Q

What is re-expansion pulmonary edema?

A

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

72
Q

What are possible causes to negative-pressure pulmonary edema

A 
Post-extubation laryngospasm
Obstructive Sleep apnea
Epiglottitis
Tumors
Obesity
Hiccups
73
Q

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

A 
DEC interstitial hydrostatic pressure
INC venous return
INC afterload on LV
INC SNS (hypertension, central pooling)
74
Q

Who gets sarcoidosis? What are characteristics of sarcoidosis?

A

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.

75
Q

Anesthetic consideration of sarcoidosis?

A

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

76
Q

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

A

Mediastinoscopy for diagnosis

Hypocalcemia

77
Q

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

A

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

78
Q

Hypersensitivity pneumonitis vs. pneumoconiosis?

A

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

79
Q

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

A

INTRINSIC

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

80
Q

What is the pathogenesis of chronic restrictive lung disease?

A

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

81
Q

Name some chronic extrinsic restrictive lung diseases

A 
Obesity
Scoliosis (lateral deformity), Kyphosis (anterior deformity); These both increase risk of hypoventilation and pneumonia with CNS depressants
Sternum abnormalities
Flail chest
Neuromuscular disorders
82
Q

Pectus excavatum vs. Pectus carinatum

A

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

83
Q

What is flail chest?

A

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

84
Q

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

A

Vital capacity

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

85
Q

Open vs tension pneumothorax?

A

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

86
Q

How does a pneumothorax work?

A

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

87
Q

S/S of pneumothorax?

A 
Acute dyspnea
Ipsilateral chest pain
Decreased PO2, increased PCO2
Hypotension, tachycardia
Decreased chest wall movement
Decreased/absent breath sounds
Hyperresonant percussion
88
Q

Treatment of idiopathic and tension pneumothorax?

A

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

89
Q

What is pleurodesis?

A

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

90
Q

Transudative vs. Exudative effusion?

A

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

91
Q

What is pleurisy?

A

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

92
Q

What is empyema?

A

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

93
Q

Where do pulmonary embolisms usually arise from?

A

DVT

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

94
Q

What is Virchow’s triad?

A

Three things that predispose thrombus formation

  1. Venous stasis
  2. Hypercoagulability
  3. Injury to endothelial cells that line the vessels
95
Q

How does Virchow’s triad lead to pulmonary embolism?

A 
Occlusion of part of pulmonary circulation causes... 
Hypoxic vasoconstriction
Decreased surfactant
Release of inflammatory substances
Pulmonary edema
Atelectasis
96
Q

S/S of pulmonary embolism?

A 
Tachypnea, dyspnea
Chest pain, decreased cardiac output
Increased dead space, V/Q mismatch
Decreased PO2
Pulmonary infarction, pulmonary hypertension
Hypotension, shock
97
Q

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

A

Normal: 25/10, mean 20

Pulmonary hypertension: Mean is 5-10 above normal or above 20 mmHg

98
Q

What can cause pulmonary hypertension?

A

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

99
Q

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

A

Overproduction of vasoconstrictors: thromboxane, endothelin

Underproduction of dilators: prostacyclin, nitric oxide

100
Q

What is cor pulmonale?

A

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

101
Q

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?

A

20x

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

102
Q

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

A

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!

103
Q

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

A

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

N552 Patho (13 decks)

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