Br Pathology: Lung

Front 1

Calculate the A-a gradient in a patient breathing 0.30 O2 who has a Pco2 of 80 mm Hg and Pao2 of 40 mm Hg?

Back 1

PAo2 = 0.30 (713) - 80/0.8 = 114 mm Hg. A-a gradient = 114 - 40 = 74 mm Hg, which is medically significant and indicates one or more of the above-mentioned lung disorders or a right-to-left shunt in the heart.

Front 2

Calculate the a-a gradient in a patient breathing room air who has a Pco2 of 80 mm Hg and Pao2 of 40 mm Hg? What is happening?

Back 2

PAo2 = 0.21 (713) - 80/0.8 = 50 mm Hg. A-a gradient = 50 - 40 = 10 mm Hg, which excludes the lung as the cause of the hypoxemia and indicates an extrapulmonary cause of hypoxemia.

Front 3

When does the A-a gradient increase? Remain normal even though there is an abnormality?

Back 3

(1) Hypoxemia due to pulmonary causes increases A-a gradient.
(2) Hypoxemia due to extrapulmonary causes has a normal A-a gradient.

Front 4

How is the PAo2 calculated?

Back 4

1) PAo2 = % O2 (713) - arterial Pco2/0.8
2) % O2 is the percentage of O2 the patient is breathing; 713 is the atmospheric pressure (760 mm Hg) minus the water vapor pressure (47 mm Hg); and 0.8 is the respiratory quotient.

Front 5

When is the A-a gradient clinically significant?

Back 5

1) Medically significant A-a gradient ≥ 30 mm Hg
(a) A-a gradient normally increases with age.
(b) A-a ≥ 30 mm Hg is set for highest specificity

Front 6

List some Causes of hypoxemia with an increased a-a gradient?

Back 6

a. Ventilation defect
(1) Impaired O2 delivery to the alveoli for gas exchange
(2) Example-airway collapse due to the respiratory distress syndrome
b. Perfusion defect
(1) Decreased or absent blood flow to the alveoli
(2) Example-pulmonary embolus
c. Diffusion defect
(1) O2 cannot diffuse through the alveolar-capillary interface.
(2) Examples-interstitial fibrosis, pulmonary edema
d. Right-to-left cardiac shunt
Example-tetralogy of Fallot

Front 7

List some Causes of hypoxemia with a normal a-a gradient?

Back 7

a. Depression of the respiratory center in the medulla
(1) Examples-barbiturates, brain injury
b. Upper airway obstruction
(1) Epiglottitis due to Haemophilus influenzae
(2) Croup due to parainfluenza virus
(3) Mucosal edema narrows the trachea.
c. Chest bellows (muscles of respiration) dysfunction
(1) Paralyzed diaphragm
(2) Amyotrophic lateral sclerosis with degeneration of anterior horn cells

Front 8

Is spirometry a direct measure of all lung volumes? What is the function residual capacity?

Back 8

1) does NOT directly measure FRC, RV, TLC
2) Total amount of air in the lungs at the end of a normal expiration

Front 9

What is tidal volume?

Back 9

Volume of air that enters or leaves the lungs during normal quiet respiration

Front 10

What is FVC?

Back 10

1) FVC is the total amount of air expelled after a maximal inspiration.
a. Normal FVC is 5 L

Front 11

What is FEV1 second?

Back 11

Forced expiratory volume in 1 second (FEV1 sec)
(1) Amount of air expelled from the lungs in 1 second after a maximal inspiration
(2) Normal FEV1 sec is 4 L

Front 12

What is the normal FEV1/FVC?

Back 12

Ratio of FEV1 sec/FVC is normally 4/5, or 80%

Front 13

What is expiratory reserve volume?

Back 13

1) ERV refers to the amount of air forcibly expelled at the end of a normal expiration.
2) ERV is commonly used to calculate residual volume (FRC - ERV = RV)

Front 14

What is seen on the flow volume loop curve of someone with obstructive lung disease?

Back 14

1) TLC is increased (e.g., ∼8.5 L) and RV is increased (e.g., 4 L).
2) Expiratory curve is shifted to the left of the normal curve.
3) Decreased PEF
4) Nonuniform emptying of the airways

Front 15

How is the Flow-volume loop curve in restrictive parenchymal disease seen?

Back 15

1) TLC is decreased (e.g.,∼4 L).
2) RV is decreased (e.g.,∼0.3 L).
3) Expiratory curve is shifted to the right of the normal curve.
4) Expiratory curve is narrow because of decreased lung volumes.

Front 16

What are receptors that lead to dyspnea? What causes dyspnea?

Back 16

1) Difficulty with breathing due to stimulation of J receptors causing decrease in full inspiration
2) Decreased compliance (e.g., interstitial fibrosis)
3) Increased airway resistance (e.g., chronic bronchitis)
4) Chest bellows disease (e.g., obesity, kyphoscoliosis)
5) Interstitial inflammation/fluid accumulation (e.g., left-sided heart failure)

Front 17

Where are cough receptors located? Cough with a normal chest x-ray is most likely from what?

Back 17

1) Cough receptors: located at bifurcations in airways, larynx, distal esophagus
2) Postnasal discharge is the most common cause
Note: When triggered, impulses travel via the internal laryngeal nerve, a branch of the superior laryngeal nerve which stems from the (vagus nerve) (CN X), to the medulla of the brain

Front 18

What is a nocturnal cough present with?

Back 18

1) GERD: due to acid reflux in tracheobronchial tree at night
2) Bronchial asthma: due to bronchoconstriction

Front 19

What are causes of a productive cough?

Back 19

1) Chronic bronchitis: due to smoking cigarettes
2) Typical bacterial pneumonia
3) Bronchiectasis

Front 20

Which drugs can cause a cough?

Back 20

1) ACE inhibitors: inhibit degradation of bradykinin; causes mucosal swelling and irritation in tracheobronchial tree
2) Aspirin: causes an increase in LT C-D-E4 (bronchoconstrictors)

Front 21

What are some mechanisms for hemoptysis?

Back 21

1) Parenchymal necrosis
2) Bronchial and/or pulmonary vessel damage

Front 22

Hemoptysis can be caused by what?

Back 22

1) Chronic bronchitis (most common cause)
2) Pneumonia, bronchogenic carcinoma
3) TB, bronchiectasis, aspergilloma (fungus living in a cavitary lesion)

Front 23

What is the normal respiratory rate? tachypnea? What are causes of tachypnea?

Back 23

1) Normal respiratory rate: 14-20 breaths per minute (bpm) in adults; up to 44 bpm in children
2) Tachypnea: rapid shallow breathing (>20 bpm)
3) Causes: restrictive lung disease; pleuritic chest pain; pulmonary embolus with infarction (key finding)

Front 24

Causes of a tracheal shift include what?

Back 24

1) Pressure in contralateral lung: large tension pneumothorax, large pleural effusion
2) Decreased volume in ipsilateral lung: large spontaneous pneumothorax, resorption atelectasis

Front 25

What is vocal tactile fremitus?

Back 25

Palpable thrill (vibration) transmitted through chest when patient says "E" or "1, 2, 3" or "99"

Front 26

Which conditions present with decreased tactile fremitus?

Back 26

1) emphysema or asthma, with increased AP diameter from an increase in total lung capacity
2) Also pleural effusion and atelectasis

Front 27

Which conditions present with absent tactile fremitus?

Back 27

atelectasis (collapse of airways); fluid (effusion); air (pneumothorax) in pleural space

Front 28

Which conditions present with increased tactile fremitus?

Back 28

(sound travels well through consolidations) with alveolar consolidation (e.g., lobar pneumonia)

Front 29

Dullness on percussion may indicate what?

Back 29

pleural effusion; lung consolidation; atelectasis (no air in the alveoli)

Front 30

Hyperresonance on percussion is found in what conditions?

Back 30

with pneumothorax; asthma; emphysema

Front 31

Where is the site for normal airway resistance? Where does the site for laminar flow begin?

Back 31

1) segmental bronchi (turbulent air flow)
2) begins at the terminal bronchioles-"small airway"

Front 32

In asthma and chronic bronchitis there is small airway inflammation. What is the result?

Back 32

air trapping, wheezing, increased airway resistance

Front 33

Bronchial breathe sounds are always what?

Back 33

always an abnormal sound

Front 34

How do bronchial and tracheal breaths sound?

Back 34

1) Loud, high-pitched sound with a peculiar hollow or tubular quality
2) Expiratory sounds longer than inspiratory

Front 35

What is the significance of bronchial breathe sounds? What is the mechanism with which they appear? What is seen on a bronchogram?

Back 35

1) Significance: consolidation (e.g., lobar/bronchopneumonia)
2) Mechanism: bronchi must be patent and partially collapsed
3) Associated with an "air bronchogram": air-filled bronchi silhouetted against airless consolidated parenchyma

Front 36

Where are vesicular breath sounds heard? What is the length of inspiration to expiration?

Back 36

1) Normal breath sounds: tracheal sounds that are modified (filtered) in alveoli
2) Sites: most lung fields except trachea and central bronchi
3) Inspiratory-to-expiratory ratio is 3:1

Front 37

In what conditions are vesicular sounds present in? diminished in? increased in?

Back 37

1) Present in: normal lungs; chronic bronchitis; emphysema
2) Diminished in: emphysema and asthma due to increased AP diameter
3) Absent in: pneumothorax; atelectasis; effusion

Front 38

how are bronchovesicular breath sounds characterized?

Back 38

1) Normal breath sounds heard over main bronchi
2) Abnormal if heard in lung periphery
3) Inspiratory and expiratory breath sounds are equal in length

Front 39

crackles usual occur on inspiration. What causes early to midinspiratory crackles? Are they cleared with a cough?

Back 39

1) Early and midinspiratory crackles: due to secretions in proximal large to medium-sized airways (e.g., chronic bronchitis);
2) clear with coughing

Front 40

What causes late inspiratory crackles? Are they cleared with a cough?

Back 40

1) Late inspiratory crackles: due to reopening of distal airways partially occluded by increased interstitial pressure (e.g., interstitial fluid-pus, transudate in CHF); do not clear with coughing; vary from fine to coarse

Front 41

What conditions cause crackles?

Back 41

pulmonary edema; lobar pneumonia; interstitial fibrosis (e.g., sarcoidosis)

Front 42

What is wheezing? Is it usually heard on inspiration or expiration?

Back 42

high-pitched musical sound usually heard in expiration; sometimes inspiration and expiration; expiration longer than inspiration

Front 43

Wheezing can be caused by what?

Back 43

inflammation segmental bronchi, small airways (e.g., asthma, chronic bronchitis); pulmonary edema constricting airway (called cardiac asthma); pulmonary infarction (release of TXA2 from platelets in embolus causes bronchoconstriction)

Front 44

What are rhonchi? Can they be cleared with a cough?

Back 44

low-pitched snoring sound heard during inspiration or expiration; due to secretions in large airways (bronchus, trachea); usually clear with coughing; common in chronic bronchitis

Front 45

What is inspiratory stridor? What is causes it?

Back 45

1) high-pitched inspiratory sound; sign of upper airway obstruction
2) epiglottitis (Haemophilus influenzae); croup (parainfluenza virus)

Front 46

Someone with inspiratory and expiratory strider most likely has what?

Back 46

sign of fixed upper airway obstruction (e.g., from cancer)

Front 47

Why do pleural friction rubs occur? Do they occur on inspiration or expiration? When do they disappear? What diseases cause them?

Back 47

1) two inflamed surfaces (pleural and parietal) rubbing against each other
2) Timing: end of inspiration and early part of expiration
3) Disappears: large effusion is present (separates inflamed surfaces); holding breath (continues with pericardial friction rub)
4) Causes: pleuritis due to cancer, infarction, pneumonia, serositis (SLE)

Front 48

Is grunting in a newborn common?

Back 48

always abnormal after 24 hours; common finding in RDS

Front 49

In the normal lung how are spoken syllables heard? In alveolar consolidation? With egophony?

Back 49

1) spoken syllables or numbers (e.g., 99) are indistinctly heard
2) syllables/numbers heard louder and more distinctly
3) patient saying "E" sounds like "A"

Front 50

Is the FEV1 sec/FVC increased or decreased in a restrictive lung disease? What about obstructive?

Back 50

1) normal to increased
2) decreased

Front 51

In choanal atresia what occurs?

Back 51

1) Unilateral or bilateral bony septum between the nose and the pharynx
2) Newborn turns cyanotic when breast-feeding.
3) Crying causes the child to "pink up" again.
4) child can't breath through nose

Front 52

What are nasal polyps? How do they develop?

Back 52

1) non-neoplastic tumefactions
2) Develop as a response to chronic inflammation

Front 53

What is the most common polyp?

Back 53

1) allergic polyps
2) Most often seen in adults with a history of IgE-mediated allergies

Front 54

What are nasal polyps associated with?

Back 54

aspirin and other nonsteroidal drugs

Front 55

what is the asthma triad? Who does it primarily occur in?

Back 55

1) aspirin, nasal polyp, asthma
2) Most often occur in women with chronic pain syndromes

Front 56

Pathologically what occurs with nasal polyps associated with NSAIDs?

Back 56

1) Drugs block cyclooxygenase leaving the lipoxygenase pathway open.
(2) Leukotrienes (LT) C-D-E4 are increased, causing bronchoconstriction

Front 57

Children with nasal polyps should have what test performed?

Back 57

order a sweat test to rule out cystic fibrosis

Front 58

What is obstructive sleep apnea? What causes it?

Back 58

1) Excessive snoring with intervals of breath cessation (apnea)
2) Obesity (very common)
a. Pharyngeal muscles collapse due to the weight of tissue in the neck.
3) Tonsillar hypertrophy, nasal septum deviation

Front 59

What are clinical findings with obstructive sleep apnea?

Back 59

1) Excessive snoring with episodes of apnea
2) Daytime somnolence often simulating narcolepsy

Front 60

What are complications of obstructive sleep apnea?

Back 60

1) Pulmonary hypertension (PH) leading to right ventricular hypertrophy
a. Called cor pulmonale
2) Secondary polycythemia
a. Due to a hypoxemic stimulus for erythropoietin release

Front 61

What is the confirmatory test for obstructive sleep apnea?

Back 61

Confirmatory test that documents periods of apnea during sleep is Polysomnography

Front 62

Which sinus is most often inflamed in adults? In children?

Back 62

1) Maxillary sinus is most often involved in adults.
2) Ethmoid sinus is most often involved in children.

Front 63

What is the most common cause of sinusitis?

Back 63

viral infection

Front 64

Common pathogens causing sinusitis include? Which species commonly infects diabetics?

Back 64

(1) Rhinoviruses
(2) Streptococcus pneumoniae (most common)
(3) Anaerobes (chronic sinusitis)
(4) Systemic fungi (e.g., Mucor or Aspergillus species)
a. Diabetics commonly have sinusitis due to Mucor species

Front 65

What are clinical findings with sinusitis?

Back 65

1) Fever
2) Nasal congestion
3) Pain over sinuses
4) Postnasal drip

Front 66

How is sinusitis diagnosed?

Back 66

1) Gold standard for bacterial culture is sinus aspiration
2) Sinus radiographs
3) CT scan is the most sensitive test.
4) Recommended if surgery is an option

Front 67

How is sinusitis treated?

Back 67

1) Decongestants
Antimicrobial therapy
a. Recommendation is not to use antibiotics.
b. Most cases are viral and resolve within 2 weeks
c. If resolution does not occur, antibiotics often used include the following:
Amoxicillin (most common drug), erythromycin, trimethoprim-sulfamethoxazole (TMP/SMX)

Front 68

Who does nasopharyngeal carcinoma occur in?

Back 68

1) Most common malignant tumor of the nasopharynx
2) Male dominant
3) Increased incidence in the Chinese and African populations

Front 69

What is nasopharyngeal carcinoma associated with?

Back 69

Causal relationship with Epstein-Barr virus (EBV)

Front 70

What are pathologic findings in nasopharyngeal carcinoma?

Back 70

1) Squamous cell carcinoma or undifferentiated cancer
2) Metastasizes to cervical lymph nodes

Front 71

Does laryngeal carcinoma occur more in men or women? What are risk factors? Where do the majority occur?

Back 71

1) More common in men than in women
Risk factors
(1) Cigarette smoking (most common cause)
(2) Alcohol (synergistic effect with smoking)
(3) Squamous papillomas and papillomatosis
a. Human papillomavirus type 6 and 11 association
4) Majority are located on the true vocal cords

Front 72

What are the majority of laryngeal carcinomas? What are clinical findings?

Back 72

1) keratinizing squamous cell carcinomas
2) Persistent hoarseness is often associated with cervical lymphadenopathy.

Front 73

What is atelectasis?

Back 73

Loss of lung volume due to inadequate expansion of the airspaces (collapse)

Front 74

Pathologically what occurs to produce atelectasis?

Back 74

1) Airway obstruction by thick secretions prevents air from reaching the alveoli.
2) Obstruction occurs in bronchi, segmental bronchi, or terminal bronchioles.
3) Causes of obstruction
a. Mucus or mucopurulent plug after surgery
b. Aspiration of foreign material
c. Centrally located bronchogenic carcinoma
4) Lack of air and distal resorption of preexisting air through the pores of Kohn in the alveolar walls
5) Collapse may involve all or part of a lung.

Front 75

Clinically how does someone present with resorption atelectasis?

Back 75

1) Fever and dyspnea
2) Both usually occur within 24 to 36 hours of collapse.
3) Absent breath sounds and dullness to percussion
4) Absent vocal vibratory sensation (tactile fremitus)
5) Alveoli are collapsed.
6) Ipsilateral elevation of the diaphragm and tracheal deviation
a. Only occurs if large areas of the lung are atelectatic
7) Collapsed lung does not expand on inspiration (inspiratory lag)

Front 76

How is resorption atelectasis treated?

Back 76

1) Incentive spirometry after surgery
2) Positive-pressure breathing (CPAP) by face mask
3) Positive end-expiratory pressure (PEEP) on mechanical ventilation

Front 77

What is compression atelectasis?

Back 77

1) Air or fluid in the pleural cavity under increased pressure collapses small airways beneath the pleura.
2) Examples:
a.Tension pneumothorax where air compresses the lung
b. Pleural effusion where fluid compresses the lung

Front 78

Where is surfactant made? What is the main component? When does it begin to be made?

Back 78

1) Synthesized by type II pneumocytes
a) Stored in lamellar bodies
b) Synthesis begins in 28th week of gestation.
2) Phosphatidylcholine (lecithin) is the major component

Front 79

Which hormones increase surfactant production? Which decrease it?

Back 79

1) Synthesis is increased by cortisol and thyroxine, prolactin
2) Synthesis is decreased by insulin.

Front 80

What are 3 things that can lead to RDS in a newborn?

Back 80

(a) Prematurity
(b) Maternal diabetes
1. Fetal hyperglycemia increases insulin release.
(c) Cesarean section
2. Lack of stress-induced increase in cortisol from a vaginal delivery

Front 81

what are collapsed alveoli from RDS in a newborn lined by?

Back 81

1) lined by hyaline membranes
2) Derived from proteins leaking out of damaged pulmonary vessels

Front 82

What are clinical findings in RDS?

Back 82

(1) Respiratory difficulty begins within a few hours after birth.
(2) Grunting
(3) Tachypnea
(4) Intercostal retractions
(5) Infants develop hypoxemia and respiratory acidosis.

Front 83

how is RDS in a newborn diagnosed? how is it treated?

Back 83

1) Chest radiograph shows a "ground glass" appearance
2) CPAP therapy with endotracheal tube with O2 and surfactant

Front 84

What are complications that occur as a result of RDS?

Back 84

(1) Superoxide free radical damage from O2 therapy
a. May result in blindness and permanent damage to small airways (bronchopulmonary dysplasia)
(2) Intraventricular hemorrhage
(3) Patent ductus arteriosus
a. Due to persistent hypoxemia
(4) Necrotizing enterocolitis
a. Intestinal ischemia allows entry of gut bacteria into the intestinal wall.
(5) Hypoglycemia in newborn
a. Excess insulin decreases serum glucose, producing seizures and damage to neurons.
b. Must give newborns glucose to prevent hypoglycemia

Front 85

Whats the most common cause of pulmonary edema due to Starling pressures? What are others due to Starling pressures?

Back 85

1) Left-sided heart failure (most common), volume overload, mitral stenosis
2) Decreased oncotic pressure
a. Nephrotic syndrome, cirrhosis

Front 86

What are causes of pulmonary edema due to microvascular or alveolar injury?

Back 86

1) Infections
Examples-sepsis, pneumonia
2) Aspiration
Examples-drowning, gastric contents
3) Drugs
Example-heroin
4) High altitude
5) Acute respiratory distress syndrome

Front 87

What is ARDS?

Back 87

Noncardiogenic pulmonary edema resulting from acute alveolar-capillary damage

Front 88

Risk factors for ARDS include?

Back 88

(1) Gram-negative sepsis (>40% of cases)
(2) Gastric aspiration (>30% of cases)
(3) Severe trauma with shock (>20% of cases)
(4) Diffuse pulmonary infections
a. Severe acute respiratory syndrome (SARS), hantavirus
(5) Heroin
(6) Smoke inhalation
(7) Acute pancreatitis
(8) Cardiopulmonary bypass
(9) Disseminated intravascular coagulation
(10) Amniotic fluid embolism, fat embolism

Front 89

Pathologically what occurs in ARDS?

Back 89

a. Acute damage to alveolar capillary walls and epithelial cells
b. Alveolar macrophages and other cells release cytokines.
(1) Cytokines are chemotactic to neutrophils.
(2) Neutrophils transmigrate into the alveoli through pulmonary capillaries.
(3) Capillary damage causes leakage of a protein-rich exudate producing hyaline membranes.
(4) Neutrophils damage type I and II pneumocytes.
*Decrease in surfactant causes atelectasis with intrapulmonary shunting.
c. Late findings
(1) Repair by type II pneumocytes
(2) Progressive interstitial fibrosis (restrictive lung disease)

Front 90

How does ARDS present on physical exam?

Back 90

1) Dyspnea/tachypnea
2) Late inspiratory crackles

Front 91

What is the most common cause of ARDS?

Back 91

sepsis most common cause

Front 92

When testing for ARDS what will be seen in blood work and on chest x-ray?

Back 92

1) Severe hypoxemia not responsive to O2 therapy
2) Pulmonary artery wedge pressure < 18 mm Hg
a. Important in distinguishing ARDS from cardiogenic pulmonary edema
3) Respiratory alkalosis or normal Paco2
4) Increased a-a gradient, due to:
a. Intrapulmonary shunting
b. Related to atelectasis
c. Diffusion abnormalities
d. Related to hyaline membranes, alveolar infiltrate
5) Chest x-ray
a. Bilateral interstitial infiltrates initially
b. Progresses to widespread alveolar consolidation with air bronchograms (80%)

Front 93

How is ARDS treated and what is the prognosis?

Back 93

1) Treat underlying disease
2) Hemodynamic monitoring
3) Mechanical ventilation
4) Nitric oxide inhalation
5) Corticosteroids
6) Poor prognosis (40-50% mortality rate)

Front 94

What is the most common cause of typical community-acquired pneumonia?

Back 94

Streptococcus pneumoniae

Front 95

What are two ways typical pneumonia is acquired?

Back 95

(1) Inhalation of aerosol from an infected patient
(2) Aspiration of nasopharyngeal flora while sleeping

Front 96

How does bronchopneumonia begin? How does it progress?

Back 96

(1) Begins as an acute bronchitis and spreads locally into the lungs
(2) Usually involves the lower lobes or right middle lobe
(3) Lung has patchy areas of consolidation
(4) Microabscesses are present in the areas of consolidation

Front 97

What is lobar pneumonia?

Back 97

Complete or almost complete consolidation of a lobe of lung
a. occurs in typical pneumonia

Front 98

What are complications of typical pneumonia?

Back 98

(1) Lung abscesses, empyema (pus in the pleural cavity)
(2) Sepsis

Front 99

During the physical exam what would signs of consolidation be?

Back 99

(a) Dullness to percussion
(b) Increased vocal tactile fremitus
*Sound is transmitted well through alveolar consolidations.
(c) Late inspiratory crackles
(d) Bronchial breath sounds
(e) Bronchophony and egophony

Front 100

What are clinical findings in typical pneumonia?

Back 100

(1) Sudden onset of high fever with productive cough
(2) Chest pain
(3) Tachycardia
(4) Signs of consolidation (alveolar exudate)
(5) Chest radiograph (gold standard screen)
(a) Patchy infiltrates (bronchopneumonia) or lobar consolidation
(b) Sensitivity 50% to 85%

Front 101

What do cultures and CBCs show in someone with typical pneumonia?

Back 101

1) Positive Gram stain
a. More useful than culture
b. Cultures are still obtained.
c. Sensitivity 80%
2) Neutrophilic leukocytosis
3) Blood cultures positive in 20% of cases.

Front 102

Atypical pneumonia is caused by what?

Back 102

(1) Usually caused by Mycoplasma pneumoniae
(2) Other pathogens
(a) Chlamydophilia pneumoniae
(b) Viruses
Respiratory syncytial virus, influenzavirus, adenovirus
(c) Chlamydia trachomatis in newborns
(d) legionella

Front 103

How is atypical pneumonia characterized?

Back 103

Patchy interstitial pneumonia
(1) Mononuclear infiltrate
(2) Alveolar spaces usually free of exudate

Front 104

What are clinical findings in someone with atypical pneumonia?

Back 104

(1) Insidious onset, low-grade fever
(2) Nonproductive cough
(3) Chest pain
(4) Flu-like symptoms
a. Pharyngitis, laryngitis, myalgias, headache
(5) No signs of consolidation

Front 105

What are risk factors in nosicomial pneumonia?

Back 105

(1) Severe underlying disease
(2) Antibiotic therapy
(3) Immunosuppression
(4) Respirators
a. Most common source of infection

Front 106

What are the pathogens in nosicomial pneumonia?

Back 106

(1) Gram-negative bacteria
a. Pseudomonas aeruginosa (respirators), Escherichia coli
(2) Gram-positive bacteria (e.g., Staphylococcus aureus)

Front 107

What are common causes of pneumonia in an immunocompromised person?

Back 107

(1) Cytomegalovirus
(2) Pneumocystis jiroveci is most common in AIDS
a. Trimethoprim-sulfamethoxazole is used for prophylaxis and treatment.
(3) Aspergillus fumigatus

Front 108

How is TB contracted? How does it evade the immune system? What type of organism is it? What is virulence factor?

Back 108

(1) Contracted by inhalation of Mycobacterium tuberculosis
(2) Organism resides in phagosomes of alveolar macrophages
a. Produces a protein that prevents fusion of lysosomes with phagosome
(3) Characteristics
(a) Strict aerobe, acid-fast (due to mycolic acid in cell wall)
(b) Cord factor is virulence factor

Front 109

How is TB screened?

Back 109

(a) Purified protein derivative (PPD) intradermal skin test
(b) Does not distinguish active from inactive disease

Front 110

How does resistance in TB occur?

Back 110

(a) Chromosome mutations involving mycolic acid
(b) Chromosome mutations involving catalase peroxidase
*Enzyme is required to activate isoniazid

Front 111

How is primary TB characterized? Where does it grow in the lungs?

Back 111

(1) Subpleural location
(a) Upper part of the lower lobes or lower part of the upper lobes
(b) Ghon focus (caseous necrosis) in periphery
(c) Ghon complex (caseous necrosis) in hilar lymph nodes
(2) Usually resolves
(a) Produces a calcified granuloma or area of scar tissue
(b) May be a nidus for secondary TB

Front 112

how is secondary TB characterized?

Back 112

(1) Due to reactivation of a previous primary TB site
(2) Involves one or both apices in upper lobes
a. Ventilation (oxygenation) is greatest in the upper lobes.
(3) Cavitary lesion due to release of cytokines from memory T cells

Front 113

What are clinical findings in TB?

Back 113

Fever, drenching night sweats, weight loss

Front 114

What are complications of TB?

Back 114

(1) Miliary spread in lungs due to invasion into the bronchus or lymphatics
(2) Miliary spread to extrapulmonary sites
(a) Due to invasion of pulmonary vein tributaries
(b) Kidney is the most common extrapulmonary site.
(c) Adrenal involvement may result in Addison's disease.
(3) Massive hemoptysis, bronchiectasis, scar carcinoma
(4) Granulomatous hepatitis, spread to vertebra (Pott's disease)

Front 115

How is TB diagnosed?

Back 115

(1) Bronchoalveolar lavage best for staining and culture
(2) Sputum cultures

Front 116

How is TB treated?

Back 116

(1) Isoniazid + rifampin + pyrazinamide + ethambutol + vit B6
(2) Noninfectious in 2 to 3 weeks
(3) Treat for additional 9 to 12 months
a. Kills metabolically inactive persisters in lesions

Front 117

What is Mycobacterium avium-intracellulare complex? Who is it most common in? How is it treated?

Back 117

1) Atypical mycobacterium
2) Most common TB in AIDS (often disseminates)
3) Occurs when CD4 TH count falls below 50 cells/mm3
5) Treatment:
Clarithromycin + rifabutin + ethambutol

Front 118

What do systemic fungal infections do in the lungs? How are they contracted?

Back 118

1) Contracted from inhalation of the pathogen
2) Produce a granulomatous inflammatory reaction with or without caseation

Front 119

Most lung abcesses are due to aspiration of oropharyngeal material. What are risk factors?

Back 119

(a) Alcoholism
(b) Loss of consciousness
(c) Recent dental work

Front 120

What are pathogens that cause lung abcesses?

Back 120

(a) Aerobic and anaerobic streptococci
(b) Staphylococcus species
(c) Prevotella
(d) Fusobacterium
(e) mixed aerobic/anaerobic infection

Front 121

Which organisms cause lung abscess as a result of bacterial pneumonia?

Back 121

Staphylococcus aureus, Klebsiella pneumoniae

Front 122

Lung abscesses as a result of aspiration are located where?

Back 122

Superior segment, right lower lobe

Front 123

What are clinical and diagnostic findings of a lung abscess?

Back 123

1) Spiking fever with productive cough (foul-smelling sputum)
2) Chest imaging shows cavitation with an air-fluid level

Front 124

Aspiration of foreign material in the standing or seated position goes where?

Back 124

material localizes in the posterobasal segment of the right lower lobe

Front 125

Aspiration of material in the supine position goes where?

Back 125

the superior segment of the right lower lobe

Front 126

Aspiration in a right sided position goes where?

Back 126

the right middle lobe or the posterior segment of the right upper lobe

Front 127

what is the most common cause of a cold? How is it transmitted? What are other organisms that cause a cold?

Back 127

1) Rhinovirus
2) Transmitted by hand to eye-nose contact
3) Other causes of colds: coronaviruses, adenoviruses, influenza C virus, coxsackievirus

Front 128

What does coxsackievirus do in the lungs?

Back 128

Acute chest syndrome: fever with pleuritis

Front 129

What is the Most common viral cause of atypical pneumonia and bronchiolitis (wheezing) in children? otitis media in older children? How can each be diagnosed? What is the passive immunity?

Back 129

1) RSV
2) Occurs in late fall and winter
3) Rapid diagnosis with antigen detection in nasopharyngeal wash
4) Passive immunization: palivizumab (monoclonal antibody) reduces hospitalization rates

Front 130

What is the Most common cause of laryngotracheobronchitis in infants? What is seen on clinical exam? What sign is present on x-ray? how is it treated?

Back 130

1) croup (parainfluenza)
2) inspiratory stridor (upper airway obstruction) due to submucosal edema in trachea;
3) brassy cough; signs of respiratory distress
4) Anterior x-ray of neck shows "steeple sign," representing mucosal edema in the trachea (site of obstruction)
5) Bronchiolitis in infants
6) Treatment: cold water humidifiers and aerosolized racemic epinephrine

Front 131

Histologically how is CMV characterized?

Back 131

Enlarged alveolar macrophages/pneumocytes, contain basophilic intranuclear inclusions surrounded by a halo (owls eye)

Front 132

Which influenza occurs more often? What are its virulence factors?

Back 132

1) Type A viruses are most often involved
2) Hemagglutinins bind virus to cell receptors in the nasal passages
3) Neuraminidase dissolves mucus and facilitates release of viral particles

Front 133

What does influenza A cause? Influenza B?

Back 133

1) Influenza A: worldwide epidemics; pneumonia may be complicated by a superimposed bacterial pneumonia (usually Staphylococcus aureus)
2) Influenza B: causes major outbreaks

Front 134

What are the major modes that influenza is able to change?

Back 134

1) Antigen drift: minor mutation; does not require new vaccine
2) Antigen shift: major mutation in hemagglutinin or neuraminidase; new vaccine required (reassortment of 8 chromosomes)

Front 135

Clinically how does influenza present? Who is vaccination mandatory in? How is it treated? What is influenza associated with?

Back 135

1) Clinical: fever, headache, cough, myalgias, chest pain
2) Vaccination: mandatory for people > 65 years old, people with chronic illnesses
3) Treatment: neuraminidase inhibitors zanamivir, oseltamivir
4) Associations: Reye syndrome with salicylate ingestion; Guillain-Barré syndrome

Front 136

Clinically how does Rubeola present? what is seen histologically?

Back 136

1) Fever, cough, conjunctivitis, and excessive nasal mucus production
2) Koplik spots in the mouth precede onset of the rash
3) Warthin-Finkeldey multinucleated giant cells are a characteristic finding

Front 137

How does SARS effect the lungs? How was it first transmitted? How is it diagnosed?

Back 137

1) Infects lower respiratory tract and then spreads systemically
2) First transmitted to humans through contact with masked palm civets (China) and then from human-to-human contact through respiratory secretions (e.g., hospitals, families)
3) Develop severe respiratory infection
4) Diagnose with viral detection by PCR assay or detection of antibodies

Front 138

What does hanta virus do in the body? how is transmitted? how is it diagnosed and treated?

Back 138

1) Transmission: inhalation of urine/feces from deer mice in Southwestern United States
2) Pulmonary syndrome: ARDS, hemorrhage, renal failure
3) Diagnosis: detect viral RNA in lung tissue
4) No effective treatment
5) High mortality rate

Front 139

The Second most common cause of atypical pneumonia is? What is it associated with? How is it treated?

Back 139

1) Chlamydophilia pneumoniae
2) Seroepidemiologic association with coronary artery disease
3) Treatment: doxycycline

Front 140

What does Chlamydia trachomatis cause in newborn? What are symptoms and how is it treated?

Back 140

1) Newborn pneumonia (passage through birth canal)
2) Afebrile, staccato cough (choppy cough), conjunctivitis, wheezing
3) Treatment: erythromycin (Nathe says azythromycin)

Front 141

Who is M. pneumoniae common in? What is presentation and complications? how is it treated and diagnosed?

Back 141

1) Common in adolescents and military recruits (closed spaces)
2) Insidious onset with low-grade fever
3) Complications: bullous myringitis, cold autoimmune hemolytic anemia due to anti-I-IgM antibodies.
4) Treatment: erythromycin; azithromycin; clarithromycin
(nath says azythromycin or levofloxacin + ceftriaxone)
5) Cold agglutinins in blood

Front 142

How is Coxiella burnetii transmitted? What is it associated with? What does it cause? How is it treated?

Back 142

1) Usually transmitted without a vector
2) Contracted by dairy farmers, veterinarians
3) Associated with the birthing process of infected sheep, cattle, and goats, and handling of milk or excrement
4) Atypical pneumonia, myocarditis, granulomatous hepatitis
5) Treatment: doxycycline
6) intracellular, gram -

Front 143

How is Streptococcus pneumoniae characterized? How does it present? What is an excellent screen test? How is it treated?

Back 143

1) Gram-positive lancet-shaped diplococcus
2) Most common cause of typical community-acquired pneumonia
3) Rapid onset, productive cough, signs of consolidation
4) Urine antigen test excellent screen
5) Treatment: penicillin G; amoxicillin

Front 144

What color sputum is found with s. aureus infection? What infection is it found with? What diseases? what does it cause? How is it treated?

Back 144

1) Yellow sputum
2) Commonly superimposed on influenza pneumonia and measles pneumonia
3) Major lung pathogen in cystic fibrosis and IV drug abusers
4) Hemorrhagic pulmonary edema, abscess formation, and tension pneumatocysts (intrapleural blebs), which may rupture and produce a tension pneumothorax.
5) Treatment: TMP-SMX

Front 145

What type organism is C diphtheriae? How is it pathogenic? What organ is affected? how is it treated?

Back 145

1) Gram-positive rod with metachromatic granules
2) Toxin inhibits protein synthesis by ADP-ribosylation of elongation factor 2 involved in protein synthesis
3) Toxin also impairs β-oxidation of fatty acids in the heart
4) Toxin-induced pseudomembranous inflammation produces shaggy gray membranes in the oropharynx and trachea; toxic myocarditis (death)
5) Treatment: erythromycin

Front 146

B anthracis is characterized as? What is it habitat? Virulence factors? How is it transmitted?

Back 146

1) Gram-positive rod
2) Habitat: soil
3) Capsule inhibits phagocytosis
4) Exotoxins: edema factor (activates adenylate cyclase); lethal factor (inhibits a signal transduction protein involved in cell division); protective antigen (assists entry of above toxins into cells)
5) Transmission: direct contact with animal skins or products (most commonly sheep and cattle) and entry of the organisms through abrasions or cuts; inhalation (use in germ warfare)

Front 147

What are the 2 types of anthrax? How is it prevented? How is it treated?

Back 147

1) Cutaneous anthrax (90-95% of cases): occurs through direct contact with infected or contaminated animal products; resembles insect bite but eventually swells to form a black scab, or eschar, with a central area of necrosis ("malignant pustule"); if untreated, death occurs in 20% of patients
2) Pulmonary anthrax: "first sign of the disease is death"; inhalation of spores present in contaminated hides or germ warfare; necrotizing pneumonia, meningitis, pronounced splenomegaly, and dissemination throughout the rest of the body
3) Prevention: vaccine available for high-risk patients; e.g., veterinarians, soldiers entering developing countries
4) Treatment: ciprofloxacin

Front 148

What is Actinomyces israeli? What does it produce? how is it treated?

Back 148

1) Gram-positive filamentous bacteria; strict anaerobe; normal flora in tonsils and adenoids
2) Produces draining sinuses in the jaw, chest cavity, and abdomen; pus contains sulfur granules (yellow specks) that contain the bacteria
3) Treatment: ampicillin or penicillin G
Note: for comparison Nocardia is weakly-staining Gram-positive, catalase-positive, rod-shaped bacteria. It forms partially acid-fast beaded branching filaments

Front 149

What is Nocardia asteroides? What does it do in lung? Where does it spread to? How is it treated?

Back 149

1) Gram-positive filamentous bacteria; strict aerobe; partially acid-fast
2) Produces granulomatous microabscesses in the lungs
3) Frequently disseminates to the CNS and kidneys
4) Treatment: TMP-SMX

Front 150

What is B pertussis? pathologically what does it do? What does it produce?

Back 150

1) Gram-negative rod
2) Pili attach to cilia in upper respiratory tract; toxin stimulates adenylate cyclase, which catalyzes the addition of ADP-ribose to the inhibitory subunit of the G protein complex; toxin also produces absolute lymphocytosis (normal-appearing lymphocytes) often in leukemoid reaction range
3) Produces whooping cough, transmitted by droplet infection

Front 151

What are the 3 phases of B pertussis?

Back 151

1) Catarrhal phase: lasts 1-2 weeks; mild coughing, rhinorrhea, conjunctivitis
2) Paroxysmal coughing phase: lasts 2-5 weeks; characteristic 4-5 coughs in succession on expiration followed by an inspiratory whoop; absolute lymphocytosis (20,000-50,000 cells/mm3)
3) Convalescence phase: lasts 1-2 weeks; slow decline in coughing and lymphocytosis

Front 152

What are complications of B pertussis? how is it diagnosed and treated?

Back 152

1) Complications: hemorrhage into skin, conjunctiva, bronchus, brain from coughing; otitis media; meningoencephalitis (10%); rectal prolapse from coughing; pneumonia (most common cause of death in children < 3 years old; children < 1 year old have no protection from mother's immunoglobulins)
2) Diagnosis: nasopharyngeal swabs using special cough plate; direct immuno-fluorescence of swab material
3) Treatment: erythromycin

Front 153

What is H influenzae? What is it the most common cause of? What does it cause? What sign is seen? How is it treated?

Back 153

1) Gram-negative rod
2) Common cause of sinusitis, otitis media, conjunctivitis ("pinkeye")
3) Inspiratory stridor may be due to acute epiglottitis
4) Swelling of epiglottis produces "thumbprint sign" on lateral x-ray of the neck
5) Most common bacterial cause of acute exacerbation of COPD
6) Treatment: cefotaxime; ceftriaxone

Front 154

What is M catarrhalis? What does it commonly cause and in who? How is it treated?

Back 154

1) Gram-negative diplococcus
2) Common cause of typical pneumonia, especially in the elderly
3) Second most common pathogen causing acute exacerbation of COPD
4) Common cause of chronic bronchitis, sinusitis, otitis media
5) Treatment: amoxicillin-clavulanate

Front 155

What is P aeruginosa? What type of mucus is seen? What is it the most common cause of? Where is it found and how is it treated?

Back 155

1) Green sputum (pyocyanin)
2) Water-loving bacteria most often transmitted by respirators
3) Most common cause of nosocomial pneumonia and death due to pneumonia in cystic fibrosis
4) Pneumonia often associated with infarction due to vessel invasion
5) Treatment: piperacillin + tobromicin (gentamicin) + antipseudomonal quinolone or macrolide
6) Gram-negative, aerobic, rod-shaped bacterium with unipolar motility, alginate capsule, lactose fermentor and oxidase +

Front 156

Klebsiella pneumoniae is what? Who is it common in? What does it cause? how is it treated?

Back 156

1) Gram-negative fat rod surrounded by a mucoid capsule
2) Most common gram-negative organism causing lobar pneumonia and typical pneumonia in elderly patients in nursing homes
3) Common cause of pneumonia in alcoholics; however, S. pneumoniae is still the most common pneumonia
4) Atypical pneumonia associated with blood-tinged, thick, mucoid sputum
5) Lobar consolidation and abscess formation are common
6) Treatment: ceftriaxone

Front 157

Legionella pneumophila is what? Seen with what stains? How are antigens detected? Where are the bacteria found? What are risk factors?

Back 157

1) Gram-negative rod (requires IF stain or Dieterle silver stain to identify in tissue)
2) Antigens can also be detected in urine
3) Water-loving bacterium (water coolers; mists in produce section of grocery stores; outdoor restaurants in summer; rain forests in zoos)
4) Risk factors: alcoholic, smoker, immunosuppression

Front 158

What is Legionella pneumophila associated with? What can it damage and lead to? How is it treated?

Back 158

1) Pneumonia associated with high fever, dry cough, flu-like symptoms
2) May produce tubulointerstitial disease with destruction of the JG apparatus leading to hyporeninemic hypoaldosteronism (type IV renal tubular acidosis-hyponatremia, hyperkalemia, metabolic acidosis)
3) Urine antigen test excellent screen
4) Treatment: fluoroquinolone; azithromycin

Front 159

Yersinia pestis is what? how is it transmitted? How does it resistant the immune system?

Back 159

1) Gram-negative rod
2) Cause of plague
3) Transmitted by bite of rat flea; primary reservoir for bacteria are ground squirrels in the Southwest
4) Also transmitted person-to-person by droplet infection
5) Macrophages cannot kill bacteria due to protection by V and W antigens

Front 160

What are the 3 types of yersinia pestis infection? How is it treated?

Back 160

1) Three types of disease: bubonic (most common), pneumonic (transmitted by aerosol), septicemic
2) Bubonic type: bite by rat flea that has recently bitten an infected ground squirrel; infected lymph nodes enlarge (usually in the groin), mat together, and drain to the surface (buboes)
3) Treatment:
Pneumonic type: gentamicin + doxycycline
Bubonic type: gentamicin or streptomycin

Front 161

How is Cryptococcus neoformans characterized? What is it found in? What does it cause and how is it treated?

Back 161

1) Budding yeast with narrow-based buds; surrounded by a thick capsule.
2) Found in pigeon excreta (around buildings, outside office windows, under bridges)
3) Primary lung disease (40%): granulomatous inflammation with caseation
4) Treatment: fluconazole
Note: causes "soap bubble appearance in brain"

Front 162

How is Aspergillus fumigatus characterized? What does it do in lung?

Back 162

1) Fruiting body and narrow-angled (<45 degrees), branching septate hyphae
2) Aspergilloma: fungus ball (visible on x-ray) that develops in a preexisting cavity in the lung (e.g., old TB site); cause of massive hemoptysis

Front 163

What happens in Allergic bronchopulmonary aspergillosis?

Back 163

1) type I and type III hypersensitivity reactions; IgE levels increased; eosinophilia. Intense inflammation of airways and mucus plugs in terminal bronchioles. Repeated attacks may lead to bronchiectasis and interstitial lung disease; treatment with corticosteroids
2) Vessel invader with hemorrhagic infarctions and a necrotizing bronchopneumonia
3) Treatment: voriconazole

Front 164

how are Mucor species characterized? Who do they infect? What do they infect? how is it treated?

Back 164

1) Wide-angled hyphae (>45 degrees) without septa and appear empty
2) Clinical settings: diabetes, immunosuppressed patients
3) Vessel invader and produces hemorrhagic infarcts in the lung
4) Invades the frontal lobes in patients with diabetic ketoacidosis (rhinocerebral mucormycosis)
5) Treatment: amphotericin B

Front 165

Coccidioides immitis is seen how? how is it contracted? What are symptoms? How is it treated?

Back 165

1) Spherules with endospores in tissues
2) Contracted by inhaling arthrospores in dust while living or passing through arid desert areas in the Southwest (valley fever); increased after earthquakes (increased dust)
3) Flu-like symptoms and erythema nodosum (painful nodules on lower legs; inflammation of subcutaneous fat)
4) Granulomatous inflammation with caseous necrosis
5) Treatment: usually self-limited; if severe: itraconazole or fluconazole

Front 166

What is the most common systemic fungal infection? Where is it endemic? How is it transmitted? What results?

Back 166

1) Histoplasma capsulatum (identified by macrophages filled with yeast)
2) Endemic in Ohio and central Mississippi river valleys
3) Inhalation of microconidia in dust contaminated with excreta from bats (increased incidence in cave explorers, spelunkers), starlings, or chickens (common in chicken farmers)
4) Granulomatous inflammation with caseous necrosis

Front 167

Histologically what is seen with H capsulatum? What does it mimic? Besides the lung what is affected? How is it treated?

Back 167

1) Yeast forms are present in macrophages
2) Simulates TB lung disease; produces coin lesions, consolidations, miliary spread, and cavitation
3) Marked dystrophic calcification of granulomas; most common cause of multiple calcifications in the spleen
4) Treatment: usually self-limited; if severe, itraconazole or amphotericin B

Front 168

How is Blastomyces dermatitidis characterized? where are they located? Who does it occur in? what do lesions mimic? What occurs in lung? How is it treated?

Back 168

1) Yeasts have broad-based buds and nuclei
2) Occurs in Great Lakes region, central, and southeastern United States
3) Male dominant disease
4) Produces skin and lung disease; skin lesions simulate squamous cell carcinoma
5) Granulomatous inflammation with caseous necrosis
6) Treatment: itraconazole or amphotericin B

Front 169

what does Pneumocystis jiroveci attack? When can someone be infected? What are symptoms? how is it prevented?

Back 169

1) Cysts and trophozoites present; cysts attach to type I pneumocytes
2) Primarily an opportunistic infection; occurs when CD4 count < 200 cells/mm3.
3) Most common initial AIDS-defining infection
4) Patients develop fever, dyspnea, and severe hypoxemia
5) Treatment: TMP-SMX given prophylactically when CD4 counts < 200 cells/mm3

Front 170

How is Pneumocystis jiroveci stained? What is seen? What is seen on chest x-ray?

Back 170

1) Diffuse intra-alveolar foamy exudates with cup-shaped cysts best visualized with silver or Giemsa stains
2) Chest x-ray shows diffuse alveolar and interstitial infiltrates

Front 171

Histologically how does C neoformans present?

Back 171

The yeast form produces a clear capsule around a central faint nucleus.

Front 172

Lung biopsy stained with Gomori methenamine-silver shows fruiting body with narrow-angled, branching septate hyphae. What is it?

Back 172

Aspergillus fumigatus

Front 173

315

Back 173

7π/4

Hint 173

(√2/2),(-√2/2)

Front 174

Where do the majority of pulmonary embolisms originate?

Back 174

Majority (95%) originate in the femoral vein

Front 175

Potential consequences of pulmonary artery occlusion are what?

Back 175

(1) Increase in pulmonary artery pressure
(2) Decrease blood flow to pulmonary parenchyma
a. May cause hemorrhagic infarction

Front 176

What does a hemorrhagic infarct look like? Where are the majority located?

Back 176

1) Red-blue, raised, wedge-shaped area that extends to the pleural surface
2) Pleural surface has a fibrinous exudate (produces a pleural friction rub).
3) Hemorrhagic pleural effusion may also occur.
4) Majority are located in the lower lobes.
a. Perfusion is greater than ventilation in the lower lobes.

Front 177

What are clinical findings with a saddle embolus?

Back 177

(1) Sudden increase in pulmonary artery pressure
(2) Produces acute right ventricular strain and sudden death

Front 178

What are clinical findings with a pulmonary infarct?

Back 178

(1) Sudden onset of dyspnea and tachypnea
(2) Fever
(3) Pleuritic chest pain (pain on inspiration)
(4) Pleural friction rub
(5) Pleural effusion
(6) Expiratory wheezing
a. Due to release of thromboxane A2 from platelets

Front 179

What are laboratory findings with a pulmonary infarction?

Back 179

1) Respiratory alkalosis (arterial Pco2 < 33 mm Hg)
2) Pao2 < 80 mm Hg (90% of cases)
3) Increase in a-a gradient (100% of cases)
4) Increase in d-dimers

Front 180

What is the most common sign and symptom of a pulmonary infarct?

Back 180

dyspnea and tachypnea most common symptom and sign; respiratory alkalosis; hypoxemia

Front 181

A chest x-ray of someone with a pulmonary infarct would show what?

Back 181

(1) Pleural effusion
(2) "Cut-off" sign of one or more pulmonary arteries
a. Hypovascularity behind the blocked vessel
(3) Hampton's hump
a. Wedge-shaped area of consolidation

Front 182

What are various tests used to diagnose a PE?

Back 182

(1) Ventilation scan is normal, but the perfusion scan is abnormal
(2) Pulmonary angiogram is gold standard confirmatory test.
a. Expensive and not clinically available in smaller hospitals
(3) Spiral (helical) CT is excellent if preexisting lung disease is present.

Front 183

What is Usually performed in conjunction with ventilation/perfusion (V/Q) scan or spiral CT is someone with a PE?

Back 183

d-dimer

Front 184

What is the prognosis for a PE?

Back 184

∼80% overall survival
∼60% resolve without treatment
∼90% resolve with treatment

Front 185

how is pulmonary hypertension defined?

Back 185

1) Mean pulmonary artery pressure > 25 mm Hg at rest
2) Mean pulmonary artery pressure > 30 mm Hg with exercise

Front 186

With a pulmonary infarction is a ventilation scan normal? What perfusion scan? d-dimers?

Back 186

normal ventilation scan, abnormal perfusion scan; ↑ d-dimers

Front 187

Who is primary pulmonary hypertension more common in? What is the genetic predisposition?

Back 187

(1) Primary type is more common in women.
(2) Genetic predisposition
a. Mutations in genes associated with transforming growth factor-β
(3) Vascular hyperreactivity with proliferation of smooth muscle

Front 188

What is malfunctioning in secondary pulmonary hypertension?

Back 188

(1) Endothelial cell dysfunction
(a) Loss of vasodilators (e.g., nitric oxide)
(b) Increase in vasoconstrictors (e.g., endothelin)
(2) Hypoxemia and respiratory acidosis stimulate vasoconstriction of pulmonary arteries.
a. Causes smooth muscle hyperplasia and hypertrophy

Front 189

What are causes of secondary pulmonary hypertension?

Back 189

1) Chronic hypoxemia
a. Examples-chronic lung disease; living at high altitude
2) Chronic respiratory acidosis
a. Chronic bronchitis (CB); obstructive sleep apnea
3) Loss of pulmonary vasculature
a. Increases workload for remaining vessels; emphysema, recurrent pulmonary emboli
4) Left-to-right cardiac shunts
a. Volume overloading pulmonary vasculature
5) Mitral stenosis
a. Backup of blood into pulmonary veins; pulmonary venous hypertension

Front 190

What are pathologic findings in general in pulmonary hypertension?

Back 190

1) Atherosclerosis of main elastic pulmonary arteries (PAs)
2) Due to increased pressure on the endothelium leading to injury
3) Proliferation of myointimal cells and smooth muscle cells

Front 191

Clinically how does pulmonary hypertension present?

Back 191

1) Exertional dyspnea most common presenting sign
2) Chest pain
3) Chest radiograph shows tapering of the pulmonary arteries
4) Accentuated P2 (sign of PH)
5) Left parasternal heave (sign of right ventricular hypertrophy [RVH])
6) PH imposes an increased afterload on the right ventricle.
7) Right-sided heart failure due to cor pulmonale

Front 192

How is pulmonary hypertension diagnosed?

Back 192

1) Catheterization to measure pressures
2) Can also use transthoracic Doppler echocardiogram
Chest x-ray
(1) Enlargement of main pulmonary arteries
a. Rapid tapering of distal vessels
(2) Right ventricular enlargement

Front 193

How is pulmonary hypertension treated?

Back 193

1) Diuretics
2) Oxygen
3) Vasodilators
a. Calcium channel blockers, prostanoids, endothelin receptor antagonists
4) Lung transplant

Front 194

What is cor pulmonale?

Back 194

Combination of PH and right RVH leading to right-sided heart failure

Front 195

With good pastures syndrome does renal or pulmonary damage occur first?

Back 195

Pulmonary hemorrhage with hemoptysis often precedes renal failure

Front 196

how are restrictive lung diseases characterized?

Back 196

These disorders are characterized by reduced total lung capacity in the presence of a normal or reduced expiratory flow rate

Front 197

What are chest wall disorders that cause restrictive lung diseases?

Back 197

kyphoscoliosis, pleural disease (e.g., mesothelioma), obesity

Front 198

What are examples of acute or chronic interstitial lung diseases?

Back 198

Acute interstitial disease (e.g., ARDS)
Chronic interstitial disease
(1) Fibrosing disorders (e.g., pneumoconiosis)
(2) Granulomatous disease (e.g., sarcoidosis)

Front 199

What is the earliest manifestation of interstitial fibrosis?

Back 199

1) Earliest manifestation is an alveolitis.
a. Leukocytes release cytokines, which stimulate fibrosis

Front 200

How are the lungs effected by interstitial fibrosis?

Back 200

a. Decreases lung compliance
(1) Decreased expansion of the lung parenchyma during inspiration
(2) Damage to type I/II alveolar cells and endothelial cells
b. Functional loss of alveolar and capillary units
1) Increases lung elasticity
2) Recoil of the lung on expiration is increased.

Front 201

On physical exam what is seen in someone with a restrictive lung disease?

Back 201

1) Dry cough and exertional dyspnea
2) Late inspiratory crackles in lower lung fields
3) Potential for cor pulmonale

Front 202

A pulmonary function test would show what in someone with restrictive lung disease?

Back 202

(1) All volumes and capacities are equally decreased.
(2) Decreased FEV1 sec
(3) Decreased FVC
a. Often the same value as FEV1 sec due to increased lung elasticity
(4) Increased ratio of FEV1 sec/FVC
Example-3/3 = 100% (normal is 80%)
(5) Respiratory alkalosis (arterial Pco2 < 33 mm Hg)
(6) Decreased Pao2

Front 203

Chest x-ray in a restrictive lung disease patient would show?

Back 203

Diffuse bilateral reticulonodular infiltrates

Front 204

How does
Pneumoconioses occur?

Back 204

1) Inhalation of mineral dust into the lungs leading to interstitial fibrosis
2) Mineral dust includes coal dust, silica, asbestos, and beryllium.
3) Accounts for ∼25% of cases of chronic interstitial lung disease

Front 205

With pneumoconioses particles 1- to 5-μm that aspirated will lodge where? <0.5 μm lodge where?

Back 205

1) Reach the bifurcation of the respiratory bronchioles and alveolar ducts
2) Reach the alveoli and are phagocytosed by alveolar macrophages

Front 206

What is the least and most fibrinogenic molecules?

Back 206

1) Coal dust is the least fibrogenic particle.
2) Silica, asbestos, and beryllium are very fibrogenic.

Front 207

Sources of Coal worker's pneumoconiosis include? What is the pigment that accumulates?

Back 207

1) Coal mines, large urban centers, tobacco smoke
2) (anthracotic pigment)

Front 208

What are symptoms of Pulmonary anthracosis? What is seen on examination of the lungs?

Back 208

1) Usually asymptomatic
2) Anthracotic pigment in interstitial tissue and hilar nodes
Note: this occurs in coal workers pneumconiosis
a. Alveolar macrophages with anthracotic pigment are called "dust cells."

Front 209

What occurs in simple Coal worker's pneumoconiosis?

Back 209

(1) Fibrotic opacities are smaller than 1 cm in upper lobes and upper portions of lower lobes.
(2) Coal deposits adjacent to respiratory bronchioles produce centriacinar (centrilobular) emphysema

Front 210

What changes occur in the lungs of someone with complicated Coal worker's pneumoconiosis? Is there increased risk for cancer? What syndrome may occur?

Back 210

(1) Fibrotic opacities larger than 1 to 2 cm with or without necrotic centers
(2) Crippling lung disease ("black lung" disease)
(3) No increased incidence of TB or primary lung cancer
(4) Cor pulmonale may occur.
(5) Caplan syndrome may occur.
a. CWP plus large cavitating rheumatoid nodules in the lungs

Front 211

What is the Most common occupational disease in the world? What are sources?

Back 211

1) silicosis
2) Quartz (crystalline silicone dioxide) is most often implicated.
a. Sources: foundries (casting metal), sandblasting, working in mines

Front 212

Pathologically what does quartz do in the lungs?

Back 212

1) Quartz is highly fibrogenic and deposits in the upper lungs.
2) Quartz activates and is cytolytic to alveolar macrophages.
a. Macrophages release cytokines that stimulate fibrogenesis.

Front 213

On chest x-ray what is seen in both acute and chronic quartz exposure?

Back 213

1) Acute exposure: Ground glass appearance in all lung fields
2) Chronic exposure:
a. Nodular opacities in the lungs
*Concentric layers of collagen with or without central cavitation
b. "Egg-shell" calcification in hilar nodes
*Rim of dystrophic calcification in the nodes

Front 214

What are complications of quartz exposure?

Back 214

(1) Cor pulmonale, Caplan syndrome
(2) Increased risk for developing lung cancer and TB

Front 215

What are geometric forms of asbestos disease? Where do the asbestos fibers deposit?

Back 215

(1) Serpentine
a) Curly and flexible fibers (e.g., chrysotile)
b) Produces interstitial fibrosis and lung cancer
(2) Amphibole
a) Straight and rigid (e.g., crocidolite)
b) Produces interstitial fibrosis, lung cancer, mesothelioma
(3) Deposition sites
a) Asbestos fibers deposit in the respiratory unit.
b) Respiratory bronchioles, alveolar ducts, alveoli

Front 216

Sources of asbestos include what?

Back 216

(1) Insulation around pipes in old naval ships
(2) Roofing material, ceiling tiles, floor tiles used >20 years ago
(3) Demolition of old buildings

Front 217

How do asbestos fibers appear in the lungs?

Back 217

(1) Fibers are coated by iron and protein (called ferruginous bodies)
2) Macrophages phagocytose and coat the fibers with ferritin (synthesized by macrophages)
3) Golden, beaded appearance in sputum or in distal, small airways

Front 218

What is the most common asbestos induced lung lesion? What are they a precursor of? What type of fibrosis occurs?

Back 218

(1) Benign pleural plaques
(a) Calcified plaques on the pleura and dome of the diaphragm
(b) They are not a precursor lesion for a mesothelioma.
(2) Diffuse interstitial fibrosis with or without pleural effusions

Front 219

What is the most common cancer from asbestos-related? After how many years exposure?

Back 219

1) Primary bronchogenic carcinoma (most common)
(a) Risk further increases if the patient smokes cigarettes.
(b) Occurs ∼20 years after first exposure.

Front 220

With asbestos exposure what type of cancer develops in the pleura? Describe it?

Back 220

(4) Malignant mesothelioma of pleura
(a) No etiologic relationship with smoking
(b) Arises from the serosal cells lining the pleura
(c) Encases and locally invades the subpleural lung tissue
(d) Occurs ∼25 to 40 years after first exposure

Front 221

Is there an increased risk for TB with asbestos? What are complications of asbestos?

Back 221

1) No increased risk for TB
2) Complications:
Cor pulmonale, Caplan syndrome

Front 222

where can someone get Berylliosis? Pathologically what occurs? What is there increased risk of?

Back 222

1) Exposure in the nuclear and aerospace industry
2) Diffuse interstitial fibrosis with noncaseating granulomas
3) Increased risk for cor pulmonale and primary lung cancer

Front 223

What is the most common noninfectious granulomatous disease of the lungs? Who does it occur more in?

Back 223

1) sarcoidosis
2) Accounts for ∼25% of cases of chronic interstitial lung disease
3) Common in blacks and nonsmokers
4) More common in women than men

Front 224

Pathologically what is occurring in sarcoidosis? How is the diagnosis made?

Back 224

1) Disorder in immune regulation
2) CD4 TH cells interact with an unknown antigen.
3) Releases cytokines causing formation of noncaseating granulomas
4) Diagnosis of exclusion
5) Must rule out other granulomatous diseases

Front 225

What occurs in the lung of someone with sarcoidosis? What is seen histologically? What is the most common lung symptom?

Back 225

(1) Granulomas located in the interstitium and mediastinal and hilar nodes
(2) Granulomas contain multinucleated giant cells
(3) Contain laminated calcium concretions (Schaumann bodies) and stellate inclusions (called asteroid bodies)
(4) Dyspnea is the most common symptom.

Front 226

What happens to the skin in sarcoidosis?

Back 226

1) Nodular lesions containing granulomas of biopsy
2) Violaceous rash occurs on the nose and cheeks (called lupus pernio).
3) Erythema nodosum:
a. Painful nodules on lower extremities
b. Inflammation of subcutaneous fat

Front 227

How are the eyes effected in sarcoidosis?

Back 227

1) produces uveitis
2) Blurry vision, glaucoma, and corneal opacities

Front 228

What is the most common noninfectious granulomatous disease of the liver?

Back 228

1) sarcoidosis
2) causes Granulomatous hepatitis

Front 229

How does sarcoidosis affect the mouth? What endocrine problem occurs? How are the bones affected?

Back 229

1) Enlarged salivary and lacrimal glands
2) Diabetes insipidus (hypothalamic and posterior pituitary disease)
3) Granulomas in the bone marrow and spleen

Front 230

What are laboratory findings in someone with sarcoidosis?

Back 230

1) Increased angiotensin-converting enzyme (ACE; 60%)
a. Nonspecific finding
2) Hypercalcemia (5% of cases)
a. Increased synthesis of 1-α-hydroxylase in granulomas (hypervitaminosis D)
3) Polyclonal gammopathy
4) Cutaneous anergy to common skin antigens (e.g., Candida)
a. Due to consumption of CD4 TH cells in granulomas and loss of cells in alveolar secretions

Front 231

What is seen on a chest x-ray of someone with sarcoidosis? what is the sign called?

Back 231

1) Enlarged hilar and mediastinal lymph nodes (called "potato nodes")
2) Reticulonodular densities throughout the lung parenchyma

Front 232

how is sarcoidosis treated?

Back 232

1) Majority (75-90%) have spontaneous remission in 2 years and do not require treatment.
2) Corticosteroids if treatment is required
3) Tumor necrosis factor inhibitors
4) Hydroxychloroquine useful if skin involvement is present

Front 233

What is the prognosis of sarcoidosis?

Back 233

Approximately 10% to 15% develop severe interstitial fibrosis, leading to cor pulmonale and death.

Front 234

who does idiopathic pulmonary fibrosis occur in?

Back 234

1) Accounts for ∼15% of cases of chronic interstitial lung disease
2) More common in males than in females
3) Usually occurs in individuals 40 to 70 years old

Front 235

pathologically what is occurring in idiopathic pulmonary fibrosis? What appearance does the lung take on?

Back 235

1) Repeated cycles of alveolitis are triggered by an unknown agent.
2) Release of cytokines produces interstitial fibrosis.
3) Alveolar fibrosis leads to proximal dilation of the small airways.
4) Lung has a honeycomb appearance.

Front 236

Clinically how does idiopathic pulmonary fibrosis present? What is the treatment? Prognosis?

Back 236

1) Fever
2) Dyspnea with exertion
3) Chronic, nonproductive cough
4) Late inspiratory crackles
5) Treatment:
None very useful
6) Poor prognosis

Front 237

An unexplained pleural effusion in a young woman is what until proven otherwise? What does the pleural fluid contain?

Back 237

1) SLE
2) Pleural fluid contains an inflammatory infiltrate (exudate), and lupus erythematosus cells (neutrophils with phagocytosed DNA) are sometimes present

Front 238

What is one of the key criteria for diagnosing SLE?

Back 238

he presence of serositis, pleuritis with a pleural effusion being an example of this type of inflammation.

Front 239

What are collagen vascular diseases that affect the lungs?

Back 239

1) Systemic sclerosis
a. Most common cause of death is lung disease.
2) Systemic lupus erythematosus (SLE)
a. Interstitial lung disease occurs in 50% of patients.
b. Pleuritis with pleural effusions
3) Rheumatoid arthritis (RA)

Front 240

How does RA affect the lungs?

Back 240

a. Rheumatoid nodules in lungs plus a pneumoconiosis is called Caplan syndrome.
b. Pulmonary findings in RA
(1) Interstitial fibrosis with or without intrapulmonary rheumatoid nodules
(2) Nodules often cavitating
(3) Pleuritis with pleural effusions

Front 241

What is Extrinsic allergic alveolitis associated with? What are examples? What else is called?

Back 241

1) exposure to a known inhaled antigen
2) examples:
a. farmers lung = thermophyllic actinomyces
b. mushroom workers disease = thermophyllic actinomyces
c. tobacco workers disease = asperillgius
2) Does not involve IgE antibodies (type I hypersensitivity) or have eosinophilia
3) known as HYPERSENSITIVITY PNEUMONITIS
4) TH1 mediated hypersensitivity

Front 242

What is the allergen in farmers lung? What happens on first exposure? Second exposure?

Back 242

1) Exposure to Saccharopolyspora rectivirgula (thermophilic actinomycetes) in moldy hay
2) First exposure
Patient develops precipitating IgG antibodies (present in serum)
3) Second exposure
a. Antibodies combine with inhaled allergens to form immune complexes. (type III)
b. Immunocomplexes produce an inflammatory reaction in lung tissue.

Front 243

chronic farmers lung causes what? How is farmers lung treated?

Back 243

1) Additional component of granulomatous inflammation (type IV hypersensitivity)
2) Treatment
a) Avoidance of antigen with facial mask
b) Corticosteroids

Front 244

farmers lung is what type of hypersensitivity?

Back 244

type III and IV

Front 245

What occurs in Silo fillers disease? What is cause? How is it treated?

Back 245

1) Inhalation of gases (oxides of nitrogen) from plant material
2) Causes an immediate hypersensitivity reaction associated with dyspnea
3) Treatment: Corticosteroids

Front 246

Who does byssinosis occur in? What is the allergen?

Back 246

(1) Occurs in workers in textile factories
(2) Contact with cotton, linen, hemp products
(3) Exposure to bacterial endotoxin from gram-negative bacteria growing on the cotton

Front 247

What are clinical findings of Byssinosis? When do symptoms improve? When do they return? how is it treated?

Back 247

(1) Develop dyspnea on exposure to cotton, linen, or hemp products
(2) Workers feel better over the weekend (no exposure to antigens)
(3) Depression occurs when returning to work on Monday ("Monday morning blues")
(4) treat by removing allergen

Front 248

Hypersensitivity pneumonitis lack an IgE response. What are the diseases?

Back 248

1) Farmer's lung
2) Silo filler's disease
3) Byssinosis

Front 249

Which drugs are associated with interstitial fibrosis?

Back 249

1) Amiodarone
2) Bleomycin and busulfan
3) Cyclophosphamide
4) Methotrexate and methysergide
5) Nitrosourea and nitrofurantoin

Front 250

when does radiation induced pneumonitis occur? What are clinical findings? What is seen on chest x-ray?

Back 250

1) Acute pneumonitis may occur 1 to 6 months after therapy.
2) Clinical findings:
Fever
Dyspnea
Pleural effusions
3) Chest x-ray shows infiltrates
4) Some patients develop chronic radiation pneumonitis.

Front 251

Histologically how do sarcoid granulomas appear?

Back 251

ink-staining epithelioid cells and foreign body type of multinucleated giant cells.

Front 252

What are obstructive lung diseases?

Back 252

1) emphysema
2) Chronic bronchitis
3) asthma
4) bronchiectasis

Front 253

What is emphysema?

Back 253

Permanent enlargement of all or part of the respiratory unit
a. Respiratory bronchioles, alveolar ducts, alveoli

Front 254

what are causes of emphysema?

Back 254

(1) Cigarette smoking is the most common cause.
(2) α1-Antitrypsin (AAT) deficiency

Front 255

What are the Types of emphysema associated with smoking or loss of AAT?

Back 255

(1) Centriacinar (centrilobular) emphysema
(2) Panacinar emphysema

Front 256

What happens to compliance and elastance in AAT deficient emphysema? What is the pathologic process?

Back 256

1) Increased compliance and decreased elasticity
2) Imbalance between elastase and anti-elastases (e.g., AAT)
3) Imbalance between oxidants (free radicals) and antioxidants (e.g., glutathione)
4) Elastase and oxidants derive from neutrophils and macrophages.
5) Net effect of the preceding is destruction of elastic tissue.

Front 257

How does cigarette smoke lead to emphysema?

Back 257

1) Cigarette smoke is chemotactic to neutrophils and macrophages.
2) They accumulate in the respiratory unit and release free radicals and elastases.
3) Free radicals in cigarette smoke inactivate AAT and antioxidants.
4) Produces a functional AAT deficiency

Front 258

What is the normal function of elastic tissue in the lungs? what happens when it is lost?

Back 258

(1) Fibers attach to the outside wall of the small airways
(2) Fibers apply radial traction to keep the airway lumens open.
3) Destruction of elastic tissue causes loss of radial traction.
a. Small airways collapse, particularly on expiration

Front 259

Where are the Sites of elastic tissue destruction in emphysema?

Back 259

(1) Distal terminal bronchiole at its junction with the respiratory bronchiole (RB)
(2) All or part of the respiratory unit

Front 260

Where are the Sites of obstruction and air trapping in emphysema?

Back 260

(1) During expiration, the distal terminal bronchioles collapse preventing egress of air out of the respiratory unit.
(2) Trapped air distends parts of the respiratory unit that have lost their elastic tissue support.

Front 261

What is the Most common type of emphysema in smokers? What occurs pathologically?

Back 261

1) Centriacinar (centrilobular) emphysema
2) Primarily involves the apical segments of the upper lobes
3) Distal terminal bronchioles and the RBs are the sites of elastic tissue destruction.
4) Air trapped behind the collapsed distal terminal bronchioles distends the RBs.
5) The trapped air increases RV and TLC.

Front 262

When does panacinar emphysema occur? What are the genetics behind it?

Back 262

(1) Associated with AAT deficiency
a. Genetic or acquired causes (cigarette smoke inactivates AAT)
(2) Genetic type of AAT deficiency
a. Autosomal dominant
b. MM phenotype is normal.
c. Normal amounts of AAT are synthesized in the liver.
d. Homozygous ZZ type has decreased synthesis of AAT by the liver.
(3) Emphysema develops at an early age in the genetic type.
(4) affects primarily the lower lobes

Front 263

What is the function of A1AT?

Back 263

Alpha 1-antitrypsin (A1AT) is produced in the liver, and one of its functions is to protect the lungs from the neutrophil elastase enzyme, which can disrupt connective tissue

Front 264

Which parts of the lung are primarily affected by panacinar emphysema?

Back 264

(1) Primarily affects the lower lobes
(2) Distal terminal bronchioles and all parts of the respiratory units are the sites of elastic tissue destruction
(3) Air trapped behind the collapsed terminal bronchioles distends the entire respiratory unit.

Front 265

When performing a serum protein electrophoesis what is missing in panacinar emphysema?

Back 265

Absent α1-globulin peak in a serum protein electrophoresis

Front 266

Clinical findings in centriacinar and panacinar emphysema include what?

Back 266

1) Progressive dyspnea and hyperventilation
a. Dyspnea is severe and occurs early in the disease.
b. Sometimes patients are called "pink puffers" and blow off CO2
c. Centriacinar type frequently coexists with chronic bronchitis.
2) Breath sounds are diminished due to hyperinflation.
3) Cor pulmonale is uncommon.

Front 267

Chest x-ray shows what in people with emphysema?

Back 267

1) Hyperlucent lung fields
2) Increased anteroposterior diameter
3) Vertically oriented heart
4) Depressed diaphragms due to hyperinflated lungs

Front 268

A pulmonary function in someone with emphysema would show what?

Back 268

1) Increased TLC due to an increase in RV
2) Decreased FEV1 sec (e.g., 1 L versus 4 L)
3) Decreased FVC (e.g., 3 L versus 5 L)
4) Decreased FEV1 sec/FVC ratio (e.g., 1/3 = 33%)

Front 269

An arterial blood gas from someone with emphysema would show what?

Back 269

1) Decreased Pao2 develops late in the disease.
2) Destruction of the capillary bed matches destruction of the respiratory unit.
3) Normal to decreased arterial Pco2 (respiratory alkalosis)

Front 270

how is emphysema treated?

Back 270

1) Cessation of smoking most important
2) Pulmonary rehabilitation program
3) Oxygen, using 1 to 2 L/minute, through nasal prongs
4) Maintain O2 saturation of 90%
5) Bronchodilators
a. Catecholamine inhalers/nebulizers
b. Steroid inhalers controversial
c. Anticholinergics

Front 271

What are Other types of emphysema unrelated to smoking or AAT deficiency?

Back 271

1) Paraseptal emphysema
2) Irregular emphysema

Front 272

What occurs in paraseptal emphysema? What is there an increased risk of?

Back 272

(1) Localized disease in a subpleural location
a. Primarily targets the alveolar ducts and alveoli
(2) Does not produce obstructive airway disease
(3) Increased incidence of spontaneous pneumothorax
a. Due to rupture of subpleural blebs

Front 273

What is irregular emphysema?

Back 273

(1) Localized disease is associated with scar tissue.
(2) Does not produce obstructive airway disease

Front 274

Where is turbulent airflow made into laminar flow in the lungs?

Back 274

converted to laminar airflow in the terminal (nonrespiratory) bronchioles because of branching

Front 275

What is small airway disease associated with?

Back 275

expiratory wheezes due to narrowing of the terminal bronchioles by mucus plugs, inflammation, and fibrosis

Front 276

What do mucus plugs in the proximal terminal bronchiole cause?

Back 276

prevent the exodus of a large amount of CO2 arising from the distally located airways producing respiratory acidosis

Front 277

Criteria for chronic bronchitis include what? What are causes?

Back 277

1) Productive cough for at least 3 months for 2 consecutive years
2) Causes:
a. Smoking cigarettes (most common)
b. Cystic fibrosis

Front 278

Pathologically what occurs in chronic bronchitis? Where is the obstruction in comparison to emphysema?

Back 278

1) Hypersecretion of mucus in bronchi
2) Obstruction to airflow in the terminal bronchioles
3) Airflow obstruction is proximal to the obstruction in emphysema.
Irreversible fibrosis of terminal bronchioles

Front 279

How do the bronchi change with chronic bronchitis?

Back 279

(1) Hypersecretion of submucosal mucus-secreting glands in trachea and bronchi
a. Primarily responsible for sputum overproduction
(2) Acute inflammation (neutrophils) often superimposed on chronic inflammation
(3) Loss of ciliated epithelium and presence of squamous metaplasia

Front 280

How do the terminal bronchioles change in chronic bronchitis?

Back 280

(1) Mucus plugs in lumens (block the exodus of CO2)
(2) Goblet cell metaplasia
(3) Hypertrophy of mucus-secreting glands
(4) Chronic inflammation and fibrosis narrowing the lumen

Front 281

What are clinical findings in chronic bronchitis? Is cor pulmonale present? How is heart oriented on x-ray?

Back 281

1) Productive cough
2) Dyspnea occurs late in the disease.
3) Cyanosis of skin and mucous membranes
4) Decreased O2 saturation from hypoxemia
a. Patients are called "blue bloaters."
5) Tend to be stocky or obese
6) horizontally oriented heart
7) Expiratory wheezing and sibilant rhonchi
8) Cor pulmonale is commonly present.

Front 282

A chest x-ray would show what in chronic bronchitis?

Back 282

1) Large, horizontally oriented heart
2) Increased bronchial markings

Front 283

Pulmonary function tests and arterial blood gases is someone with chronic bronchitis would show what?

Back 283

1) Less increase in TLC and RV than emphysema
2) Chronic respiratory acidosis
a. Arterial Pco2 > 45 mm Hg
b. Bicarbonate > 30 mEq/L
3) Moderate to severe hypoxemia early in the disease

Front 284

Why is ozone bad?

Back 284

It forms highly reactive free radicals in the airways that cause inflammation and irritation, often precipitating asthma.

Front 285

What is asthma? Where does it occur in lungs? Who does it primarily occur in? What types are there?

Back 285

1) Episodic and reversible airway disease (most cases)
2) Primarily targets the bronchi and terminal bronchioles
3) Most common chronic respiratory disease in children
a. More common in children than adults
b. Majority (50-80%) develop symptoms before 5 years of age
4) Extrinsic and intrinsic types

Front 286

Describe the pathologic mechanism of Extrinsic asthma? Which interleukins are involved?

Back 286

(1) Type I hypersensitivity
a. Typically develops in children with an atopic family history to allergies
(2) Initial sensitization to an inhaled allergen
(a) Stimulate induction of subset 2 helper T cells (CD4 TH2) that release interleukin (IL) 4 and IL-5
(b) IL-4 stimulates isotype switching to IgE production.
(c) IL-5 stimulates production and activation of eosinophils
(3) Inhaled antigens cross-link IgE antibodies on mast cells on mucosal surfaces.
(a) Release of histamine and other preformed mediators
(b) Stimulate bronchoconstriction, mucus production, influx of leukocytes

Front 287

What is the late phase reaction of extrinsic asthma? When does it occur?

Back 287

1) Eotaxin is produced.
a. Chemotactic for eosinophils and activates eosinophils
b. Eosinophils release major basic protein and cationic protein.
c. Damage epithelial cells and produce airway constriction
2) occurs 4-8 hours after exposure

Front 288

Besides the interleukins what other mediators are involved in extrinsic asthma?

Back 288

(1) LTC-D-E4 causes prolonged bronchoconstriction.
(2) Acetylcholine causes airway muscle contraction

Front 289

How are the terminal bronchioles altered in extrinsic asthma? What histologic markers are seen?

Back 289

(1) Formation of spiral-shaped mucus plugs
(a) Contain shed epithelial cells called Curschmann spirals
(b) Pathologic effect of major basic protein and cationic protein
(2) Crystalline granules in eosinophils coalesce to form Charcot-Leyden crystals.
(3) Patchy loss of epithelial cells, goblet cell metaplasia
(4) Thick basement membrane
(5) Smooth muscle cell hypertrophy and hyperplasia

Front 290

how does extrinsic asthma present clinically?

Back 290

(1) Episodic expiratory wheezing (inspiratory as well when severe)
(2) Nocturnal cough
(3) Increased anteroposterior diameter
Due to air trapping and increase in residual volume

Front 291

What is seen on ABG in someone with extrinsic asthma? What can it progress to?

Back 291

(1) Initially develop respiratory alkalosis
(a) Patients work hard at expelling air through inflamed airways.
(b) May progress into respiratory acidosis if bronchospasm is not relieved
2) Normal pH or respiratory acidosis is an indication for intubation and mechanical ventilation.
3) Eosinophilia, positive skin tests for allergens

Front 292

how is mild to moderate extrinsic asthma treated? and severe?

Back 292

1) Treatment of mild disease
a. Metered-dose inhaler with a β2-agonist (e.g., albuterol)
2) Treatment of more advanced disease
a. Metered low-dose inhaler with corticosteroids
b. Use of leukotriene inhibitors (zarfulekast and montelukast)

Front 293

What are causes of intrinsic asthma?

Back 293

1) Nonimmune
2) Virus-induced respiratory infection
Examples-rhinovirus, parainfluenza virus, respiratory syncytial virus
3) Air pollutants
O3: free radical; O2 combining with oxides of nitrogen and sulfur
4) Aspirin or nonsteroidal drug sensitivity
(4) Stress, exercise, cigarette smoke

Front 294

What is bronchiectasis?

Back 294

1) Permanent dilation of the bronchi and bronchioles
a. Due to destruction of cartilage and elastic tissue by chronic necrotizing infections

Front 295

What are causes of
Bronchiectasis? Most common in US and most common in world?

Back 295

(1) Cystic fibrosis (CF)
a. Most common cause in the United States
(2) Infections
(a) TB is the most common cause worldwide.
(b) Adenovirus, Staphylococcus aureus, Haemophilus influenzae
(3) Bronchial obstruction
Example-proximally located bronchogenic carcinoma occludes the lumen.
(4) Primary ciliary dyskinesia
(a) Absent dynein arm in cilia
(b) Dynein arm contains ATPase (adenosine triphosphatase) for movement of the cilia.
(5) Allergic bronchopulmonary aspergillosis

Front 296

Which lobes are most commonly affected by bronchiectasis? What happens to the lobes?

Back 296

1) Most commonly occurs in the lower lobes
2) Dilated bronchi and bronchioles are filled with pus
a. Dilated airways extend to the lung periphery.
b. Dilations are tubelike and/or saccular.

Front 297

Clinically what is found in someone with bronchiectasis?

Back 297

1) Cough productive of copious sputum (bronchorrhea)
2) Hemoptysis that is sometimes massive
3) Digital clubbing
4) Cor pulmonale

Front 298

What will a chest x-ray show in someone with bronchiectasis?

Back 298

Crowded bronchial markings extend to the lung periphery.

Front 299

What type of genetic mutation occurs in cystic fibrosis? Who is primarily affected? What is the median age of diagnosis and survival time?

Back 299

(1) Autosomal recessive disease CFTR gene on chromosome 7
(2) Primarily affects whites (>98%)
a. Uncommon in Asians and blacks
(3) Median age of diagnosis ∼5 months
(4) Median survival age: 30 years

Front 300

What is the Most common fatal hereditary disorder of whites in United States?

Back 300

CF

Front 301

Which chromosome is affected in CF? What is the mutation?

Back 301

(1) Three nucleotide deletion on chromosome 7
a. Nucleotides normally code for phenylalanine

Front 302

What is defective in CF? What happens to this protein during processing?

Back 302

1) Production of a defective CF transmembrane conductance regulator (CFTR) for chloride ions
2) CFTR Cl- is degraded in the Golgi apparatus.
a. Due to defective protein folding

Front 303

What is the effect of not having a functional CFTR? What organs are particularly affected?

Back 303

1) Loss of CFTR Cl- causes decreased Na+ and Cl- reabsorption in sweat glands.
a. Basis of the sweat test
2) Effect of loss of CFTR Cl- in other secretions
a. Increased Na+ and water reabsorption from luminal secretions
b. Decreased Cl- secretion out of epithelial cells into luminal secretions
c. Net effect is dehydration of body secretions due to lack of NaCl
d. Secretions are dehydrated in bronchioles, pancreatic ducts, bile ducts, meconium, and seminal fluid.

Front 304

How is the respiratory and cooling system of the body affected by CF? What organisms commonly infect CF patients?

Back 304

(1) Nasal polyps (25% of cases)
(2) Heat exhaustion
a. Loss of sodium-containing fluid from skin
(3) Respiratory infections/failure
(a) Pseudomonas aeruginosa is the most common respiratory pathogen.
(b)Other common pathogens-S. aureus, H. influenzae
(4) Cor pulmonale commonly occurs.
(5) Pneumothorax (20%)
a. Rupture of blebs that develop from infection

Front 305

How is the digestive system affected by CF? What condition develops secondary to digestive problems?

Back 305

1) Malabsorption (80%)
(a) Pancreatic exocrine deficiency
(b) Atrophy of glands from dehydrated secretions blocking the lumens
(c) Chronic pancreatitis
(2) Type 1 diabetes mellitus (20%)
a. Due to chronic pancreatitis
(3) Gallstones (>50%)
(a) Usually in older CF patients
(b) Stasis of thickened bile
(c) Common bile duct obstruction (15-20%)
(4) Secondary biliary cirrhosis
a. Due to obstruction of bile ductules by thick secretions

Front 306

Is male or female fertility more affected by CF?

Back 306

1) Infertility in males (95%)
a. Atresia of vas deferens
2) Infertility in females (20%)

Front 307

What are signs of CF in infants?

Back 307

1) Meconium ileus (20%)
a. Small bowel obstruction in newborn
2) Rectal prolapse
a. Straining at stool

Front 308

How are newborns screed for CF?

Back 308

Increased serum immunoreactive trypsin levels

Front 309

What are sweat values in adults and children that have CF?

Back 309

(1) Sweat chloride > 60 mmol/L in children
(2) Sweat chloride > 80 mmol/L in adult

Front 310

How is CF treated? What type of vitamins need to be given?

Back 310

(1) Antibiotics for documented respiratory infections
(2) Bronchodilators
(3) Pancreatic enzyme replacement
(4) Corticosteroids in children (alternate day)
(5) Vitamin supplements
a. Fat-soluble vitamins important
(6) Recombinant human deoxyribonuclease aerosol
b. Improves mucociliary clearance of viscid sputum

Front 311

How is Centriacinar (centrilobular) emphysema is characterized histologically? What is destroyed?

Back 311

1) by trapping of air in the respiratory bronchioles. The elastic fibers of the distal TB are destroyed, causing obstruction to airflow. This causes the trapped air to distend the RBs, whose elastic tissue support is destroyed.

Front 312

How is Panacinar emphysema characterized?

Back 312

by trapping of air in the entire respiratory unit behind the collapsed TB.

Front 313

In emphysema how are the following labs affected:
1) Pao2?
2) Paco2?
3) pH?
4) Cyanosis?
5) Habitus?
6) Cor pulmonale?
7) Onset of hypoxemia?
8) Onset of dyspnea?

Back 313

1) Decreased
2) Normal to decreased
3) Normal to increased
4) Absent
5) Thin
6) Rare
7) Late
8) Early

Front 314

In chronic bronchitis how are the following labs affected:
1) Pao2?
2) Paco2?
3) pH?
4) Cyanosis?
5) Habitus?
6) Cor pulmonale?
7) Onset of hypoxemia?
8) Onset of dyspnea?

Back 314

1) Decreased
2) Increased
3) Decreased
4) Present
5) Stocky
6) Common
7) Early
8) Late

Front 315

What is the most common fatal cancer in both men and women? How is the incidence changing and what is the peak incidence?

Back 315

1) lung cancer
2) Incidence of lung cancer is declining in men but increasing in women.
3) Peak incidence is at 55 to 65 years of age.

Front 316

What are causes of lung cancer?

Back 316

1. Cigarette smoking most common cause
* Risk increases with quantity and duration of smoking
2. Radon gas (uranium mining)
3. Asbestos
4. Certain metals
a. Chromium, cadmium, beryllium, arsenic
5. Secondhand smoke
6. Ionizing radiation
7. Air pollution
8. History of tuberculosis

Front 317

how are lung cancers classified?

Back 317

Classified as small cell (13%) or non-small cell (87%) cancers

Front 318

List the Primary lung cancers by specific type in decreasing incidence?

Back 318

1) Adenocarcinoma
2) Squamous cell carcinoma
3) Small cell lung carcinoma
4) Large cell carcinoma
5) Bronchial carcinoid

Front 319

What do Squamous and small cell lung carcinomas have in common?

Back 319

1) Greatest smoking association
2) Tend to be centrally located (i.e., main stem bronchus)

Front 320

Where do adenocarcinomas occur? What is there link to smoking?

Back 320

1. Weakest smoking association
2. Tend to be more peripherally located
a. Filters in cigarettes remove large carcinogens leaving small ones to move peripherally.

Front 321

Where are common sites of primary lung cancer metastisis?

Back 321

1. Hilar lymph nodes most common site
2. Adrenal gland (50%)
3. Liver (30%)
4. Brain (20%)
5. Bone (osteolytic)

Front 322

What is the term applied to a peripheral lung nodule < 5 cm? What are causes in decreasing order of frequency?

Back 322

1) A solitary pulmonary nodule or coin lesion
2) granulomas (e.g., TB, histoplasmosis), malignancy (usually primary cancer), and a bronchial (chondroid) hamartoma

Front 323

How often are solitary nodules in the lung malignant in someone less than 35? over 50?

Back 323

Patients < 35 years old have a 1% risk of a solitary coin lesion representing a malignancy, but patients ≥ 50 years old have a 50% to 60% risk of malignancy, usually a primary cancer

Front 324

What is the most common lung cancer? Why? What is the most common symptom?

Back 324

1) extrapulmonary metastisis
a. Primary breast cancer most common cause
b. Colon cancer, renal cell carcinoma
2) Dyspnea is the most common symptom.

Front 325

What are general clinical findings in primary lung cancer?

Back 325

1) Cough is most common symptom (75%)
2) Weight loss (40%)
3) Chest pain (30%)
4) Hemoptysis (25-30%)
5) Dyspnea

Front 326

How does a pancoast tumor present? What type of cancer is it and where is it located?

Back 326

1. Usually a primary squamous cancer located at the extreme apex of lung
2. Destruction of superior cervical sympathetic ganglion produces Horner syndrome:
(1) Ipsilateral lid lag
(2) Miosis (pinpoint pupil)
(3) Ipsilateral anhydrosis (lack of sweating)

Front 327

What are paraneoplastic syndrome findings that occur in primary lung cancer?

Back 327

1)Digital clubbing
2) Muscle weakness (Eaton-Lambert syndrome)
a. Antibody directed against calcium channel in muscle
b. Usually associated with small cell carcinoma
2) Ectopic hormone secretion
a. ADH and ACT = small cell
b. PTH related protein = squamous cell

Front 328

If a central mass is seen on chest x-ray what is differential? If peripheral?

Back 328

1. Central masses
a) Squamous cell carcinoma
b) Small cell carcinoma
2. Peripheral masses
a) Adenocarcinoma
c) Scar carcinoma

Front 329

Aside from chest x-ray what are other tests used to diagnose lung cancer?

Back 329

1) Sputum cytologic examination
2) Fine needle aspiration
3) Bronchoscopy with lavage
4) New techniques for early detection
a. Low-dose spiral (helical) CT scan
b. Molecular markers in sputum

Front 330

What are treatments for lung cancer?

Back 330

1. Surgery
2. Radiation
3. Chemotherapy
4. Targeted biologic therapies
* Bevacizumab--blocks VEGF-A and erlotinib--blocks EGFR

Front 331

What is erlotinib used for? What does it do?

Back 331

1) treat non-small cell lung cancer, pancreatic cancer and several other types of cancer
2) blocks tyrosine kinase EGFR

Front 332

What is bevacizumab used for? What does it do?

Back 332

1) metastatic colon cancer and non-small cell lung cancer
2) prevents angiogenesis by blocking VEGF-A

Front 333

Do non-small cell or small cell lung cancers have a better prognosis?

Back 333

1. Non-small cell cancers fare better than small cell carcinoma.
2. Overall combined 5-year survival rate is ∼15%.

Front 334

Who is adenocarcinoma more common in? What are the different types and characterisitics of each?

Back 334

1) More common in women
2) Some types are associated with cigarette smoking
3) Scar carcinomas: develop in scars (e.g., old tuberculous granuloma); no relationship to smoking
4) Bronchioloalveolar carcinoma: derives from Clara cells (nonciliated epithelium); malignant cells spread along alveolar walls (look like pegs); radiologically mimic lobar pneumonia; no relationship to smoking

Front 335

Who is squamous cell carcinoma more common in? What is it associated with? What will the tumor tend to do? What can it secrete?

Back 335

1) More common in men
2) Strong association with cigarette smoking
3) Tend to cavitate
4) May ectopically secrete PTH-related protein (peptide)

Front 336

Who is small cell carcinoma more common in? What is it associated with? What cells does it arise from? Does it grow rapid or slow? What may it secrete?

Back 336

1) More common in men
2) Strong association with cigarette smoking
3) Arise from neuroendocrine cells (Kulchitsky cells)
4) Rapidly growing cancer that metastasizes early
5) May ectopically secrete ADH or ACTH

Front 337

where does large cell carcinoma occur? What are it characteristics?

Back 337

1) peripheral
2) Undifferentiated cancer that metastasizes early; no relationship to smoking
3) highly anaplastic

Front 338

where is bronchial carcinoma located? What cells does it arise from? What is the mean age? Does it metastisize? How does it present?

Back 338

1) central
2) Low-grade cancer of neuroendocrine origin; no association with smoking;
3) present at a mean age of 55 years old; most common primary lung tumor in children;
4) ∼ 20% locally metastasize
5) present with hemoptysis (most common), cough, carcinoid syndrome (<1%)

Front 339

What is carcinoid syndrome? What does it occur with?

Back 339

1) The syndrome includes flushing and diarrhea, and, less frequently, heart failure and bronchoconstriction.
2) It is caused by endogenous secretion of mainly serotonin and kallikrein.
3) associated with bronchial carcinoma

Front 340

When a tumor metastisizes to the lung where in the lung does it go?

Back 340

1) More common than primary cancer
2) Sites of metastasis: parenchyma (most common), pleura/pleural space, endobronchial mucosa, lymphatics (causes dyspnea)

Front 341

Where do bronchial hamaratomas occur? What type of proliferation is present? What is seen on chest x-ray?

Back 341

1) Peripheral (90%) Central (10%)
2) Non-neoplastic proliferation of cartilage and adipose tissue
3) Appears as solitary "coin" lesion on chest radiograph; popcorn calcifications

Front 342

A sputum analysis shows orange-staining, keratinized cells with irregular, hyperchromatic nuclei. What cancer is present?

Back 342

squamous cell carcinoma

Front 343

What is the difference between an anterior mediastinal mass in older and younger patients?

Back 343

1) Usually metastatic primary lung cancer in older patients
2) Usually primary disease in younger patients
3) Anterior mediastinum is the most common site (>50%)

Front 344

What are the most common mediastinal masses in decreasing order?

Back 344

(1) Neurogenic tumors
(2) Thymomas
(3) Pericardial cyst
(4) Malignant lymphomas
(5) Teratoma

Front 345

where are neurogenic tumors located in the mediastinum? What type of tumor is it if it occurs in children? In adults?

Back 345

(a) Located in the posterior mediastinum
(b) Usually malignant in children
* Neuroblastoma
(c) Usually benign in adults
* Ganglioneuroma

Front 346

Where is a pericardial cyst located? Where do malignant lymphomas present? What is it if in a woman?

Back 346

1) Located in the middle mediastinum
2)a. Located in the anterior mediastinum
b. Usually nodular sclerosing Hodgkin's lymphoma in a woman

Front 347

Where are teratomas located? Are they benign or malignant?

Back 347

(a) Located in the anterior mediastinum
(b) Majority are benign cystic teratomas.
(c) Small percentage are malignant teratomas

Front 348

Where do thymomas occur? Are they benign or malignant? is lymphoid or epithelium neoplastic?

Back 348

(1) Located in the anterior mediastinum
(2) Benign (70%), malignant (30%)
(3) Epithelium, not lymphoid tissue, is the neoplastic component.

Front 349

Which diseases are associated with thymomas?

Back 349

1) Majority express systemic symptoms of myasthenia gravis
a. Less than 15% of myasthenia patients have a thymoma.
2) Majority (65-75%) have follicular B cell hyperplasia in the thymus.
a. Site for synthesis of antiacetylcholine receptor antibodies
3) Hypogammaglobulinemia
4) Pure RBC aplasia
5) Increased incidence of autoimmune disease (e.g. Graves' disease)

Front 350

How does pleural fluid move? What is movement dependent on?

Back 350

1) Fluid moves from parietal pleura to pleural space to lungs.
2) Movement depends upon the balance of Starling pressures
a. Parietal capillary hydrostatic pressure > visceral capillary hydrostatic pressure.
b. Parietal capillary oncotic pressure equals visceral capillary hydrostatic pressure

Front 351

What are causes of plueral effusions?

Back 351

1. Increased hydrostatic pressure in visceral pleura
a. Example-congestive heart failure
2. Decreased oncotic pressure
a. Example-nephrotic syndrome
3. Obstruction of lymphatic drainage from the visceral pleura
a. Example-lung cancer
4. Increased vessel permeability of visceral pleural capillaries
a. Examples-pulmonary infarction, pneumonia
5. Metastasis to the pleura
a. Example-metastatic breast cancer

Front 352

What are the types of pleural effusions?

Back 352

1) Transudates
2) Exudates
3) Chylous
4) Pseudochylous

Front 353

What does transudate causing pleural effusion mean? What are causes?

Back 353

1. Ultrafiltrate of plasma involving disturbances in Starling pressures
2.a) Increased hydrostatic pressure in congestive heart failure most common overall cause of effusion
b) Decreased oncotic pressure in nephrotic syndrome

Front 354

What does exudate causing pleural effusion mean? What are causes?

Back 354

1. Protein-rich and cell-rich fluid
a. Due to an increased vessel permeability in acute inflammation
2. Examples-pneumonia, tuberculosis, infarction, metastasis

Front 355

What does chylous exudate causing pleural effusion mean? What are causes? How is it diagnosed?

Back 355

1) Indicates interruption of the thoracic duct
2) Malignancy (most common)
a. Blocks lymphatic drainage
3) Trauma
a. Iatrogenic tear during surgery or pathologic
4) Turbid, milky appearance
a. Due to chylomicrons (diet-derived triglyceride)
b. Chylomicrons form a supranate in a test tube after refrigeration.
5) PF triglyceride > 110 mg/dL is diagnostic

Front 356

What does psuedochylous exudate causing effusion mean? What are causes? How is it diagnosed?

Back 356

1) Turbid, milky appearance
2) Caused by inflammation with increased amount of necrotic debris
a. PF has increased cholesterol
3) Most commonly caused by rheumatoid lung disease

Front 357

What tests are useful for distinguishing transudate vs exudate? How does the pH vary between the two?

Back 357

1) PF and serum concentrations of lactate dehydrogenase (LDH) and protein are most useful.
a. Ratios of PF protein and LDH to serum protein and LDH increase test sensitivity and specificity.
b. Test sensitivity is 99% and specificity is 98% if at least one of the three criteria for an exudate is present.
2) Additional criteria
a. pH > 7.4 indicates a transudate.
b. pH < 7.4 indicates an exudate

Front 358

Clinically what is seen with a pleural effusion?

Back 358

1) Dullness to percussion
2) Absent breath sounds
3) Absent vocal tactile fremitus
4) Contralateral shift of the mediastinum
a. Only large effusions

Front 359

Chest x-ray of a pleural effusion would show what?

Back 359

1. Blunting of the costophrenic angle
2. Obscuration of the diaphragm

Front 360

Who does spontaneous pneumothorax occur in? Who is at increased risk?

Back 360

1. More common in men than women
2. Commonly seen in tall, thin, young men 20 to 40 years of age
3. Risk increases with smoking
4. Approximately 25% recurrence rate within 2 years

Front 361

What are causes of a spontaneous pneumothorax?

Back 361

1) Primary (idiopathic; most common)
2) Chronic obstructive lung disease
3) Marfan syndrome
4) Scuba diving
5) Insertion of subclavian catheter

Front 362

why do the ventricular muscle cells contain invagination of surface membranes ( transverse tubules) and how is this different from skeletal muscles

Back 362

transverse tubules allow deep access of interstial fluid into the cardiac muscle fiber. The cardiac muscle t-tubules has a larger diameter and is filled with glycocalyx (which is full of negative charges, there4 can hold Ca2+ close for when need it for Ca2+ triggered-Ca2+ release)

Front 363

The most common secondary cause of spontaneous pneumothorax is?

Back 363

Paraseptal emphysema

Front 364

Pathologically what occurs in a spontaneous pneumothorax? What is lost?

Back 364

1. Rupture of a subpleural or intrapleural bleb produces a hole in the pleura.
2. Pleural cavity pressure is the same as the atmospheric pressure.
3. Loss of the negative intrathoracic pressure
4. Causes a portion of lung or the entire lung to collapse

Front 365

clinically how will someone with a spontaneous pneumothorax present?

Back 365

1. Sudden onset of dyspnea with pleuritic type of chest pain (90%)
2. Physical examination
a. Tympanitic percussion note
b. Absent breath sounds
c. Trachea deviated to the side of the collapse if there is total lung collapse

Front 366

What does a chest x-ray show in someone with spontaneous pneumothorax?

Back 366

1. White visceral pleural line
2. Absence of vessel markings peripheral to line
3. elevated diaphragm ipsalaterally
4. tracheal shift ispsalaterally

Front 367

How is a spontaneous pneumothorax treated?

Back 367

1) Observation alone if asymptomatic and pneumothorax < 15%
2) One hundred percent oxygen administration
a. Reduces partial pressure of nitrogen; hence, increasing rate of pneumothorax absorption
3) Chest tube insertion or thoracoscopy may be required

Front 368

What causes tension pneumothorax?

Back 368

penetrating trauma to lungs; check valve type of pleural tear

Front 369

Pathologically what is occurring in a tension pneumothorax?

Back 369

1) Flap-like pleural tear (check valve) allows air into the pleural cavity but prevents its exit.
a. Similar in concept to filling a tire up with air
2) Increased pleural cavity pressure with each breath
3) Produces compression atelectasis

Front 370

Clinically and on physical exam what is seen in someone with tension pneumothorax?

Back 370

1) Sudden onset of severe dyspnea and pleuritic chest pain
2) Physical examination
a. Tympanitic percussion note and absent breath sounds
b. Trachea and mediastinal structures deviate to contralateral side if large tension pneumothorax
3) Compromised venous return to the heart, if the pneumothorax is located on the left side

Front 371

How is a tension pneumothorax treated?

Back 371

(1) Relieve pressure first.
a. Insert a needle into the second intercostal space on the midclavicular line.
(2) Insert a chest tube.

Front 372

What are the following values for a pleural transudate?
PF protein/serum protein
PF LDH/serum LDH
PF LDH

Back 372

1) <0.5
2) <0.6
3) <200 U/L

Front 373

What are the pleural fluid values for an exudate?
PF protein/serum protein
PF LDH/serum LDH
PF LDH

Back 373

1) >0.5
2) >0.6
3) >200 U/L