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CVPR > Pulm Week 3 > Flashcards

Pulm Week 3 Flashcards

1
Q

Pneumonia

A

inflammation of the parenchyma of the lung (alveoli) and accumulation of abnormal alveolar filling with fluid of lung tissue

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2
Q

Physical exam findings of pneumonia

A

1) Fever, chills
2) SOB, tachypnea
3) crackles, rhonchi
4) evidence of consolidation (bronchial breath sounds, egophony dullness to percussion)
5) pleuritic chest pain
6) productive cough (bacterial) or unproductive (atypical, viral)

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3
Q

Who should get blood and sputum cultures?

A

Get blood and sputum cultures for inpatients or patients with healthcare associated risk factors

-Treat out patients empirically and follow for improvement

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4
Q

Pathogenesis of pneumonia

A

Most commonly caused by infection + inhalation of infectious particles or microaspiration

Pulmonary parenchymal inflammation due to infection (bacterial, fungal, viral) in which purulence develops and fills the alveoli

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5
Q

Community acquired pneumonia (CAP)

A

begins outside hospital

  • Diagnosed less than 48 hours after hospital admission
  • Patient not a resident in long-term facility for > 14 days or more before onset of symptoms
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6
Q

Hospital (Nosocomial) acquired pneumonia (HAP)

A

PNA > 48 hrs after hospital admission

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7
Q

Ventilator associated pneumonia (VAP)

A

PNA > 48-72 hrs after endotracheal tube intubation

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8
Q

Healthcare-associated pneumonia (HCAP)

A

PNA in a non-hospitalized patient with extensive healthcare contact

Hemodialysis, nursing home, IV therapy, wound care, IV chemo

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9
Q

Typical bacteria that cause community acquired pneumonia (7)

A

1) Streptococcus Pneumoniae (30-60% of CAP)
2) Haemophilus influenzae
3) Moraxella catarrhalis
4) Staphylococcus aureus
5) Group A streptococci
6) Anaerobes
7) Aerobic gram-negative bacteria

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10
Q

Atypical bacteria that cause community acquired pneumonia (3)

A

10-20% of CAP

1) Legionella species
2) Mycoplasma pneumoniae
3) Chlamydia pneumoniae

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11
Q

Characteristics of HAP/VAP/HCAP Organisms

A
  • Organisms that colonize the oropharynx
  • Enter lower respiratory tract by micro or macro aspiration
  • Frequently polymicrobial in origin
  • Vary based on antimicrobial practices in hospital
  • Tend to be multidrug resistant (MDR)
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12
Q

Gram negative (5) and gram positive (1) pathogens that cause HAP/VAP/HCAP

A

Gram negative pathogens: “SPACE”

1) Serratia
2) Pseudomonas
3) Acinetobacter
4) Citrobacter
5) Enterobacter or Escherichia coli

Gram positive pathogens:
1) MRSA

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13
Q

Outpatient treatment of CAP duration and abx (3)

A

5 day therapy

Macrolide (azithromycin) or Doxycycline

Respiratory fluoroquinolone (levofloxacin)

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14
Q

Inpatient, Non-ICU treatment of CAP (2)

A

Respiratory fluoroquinolone
or
Beta-lactam + Macrolide

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15
Q

Inpatient, ICU treatment of CAP (2)

A

Beta-lactam + Macrolide
or
Beta-lactam + Respiratory fluoroquinolone

Consider anti-MRSA therapy

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16
Q

HCAP/VAP/HAP Treatment duration

A

7-8 day therapy (longer for pseudomonas/MRSA)

Critical to de-escalate therapy based on culture data and clinical response in 48-72 hours

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17
Q

HCAP/VAP/HAP Treatment: ______ + _______ + ________

A

Antipseudomonal Agent:

1) Beta-Lactam + Beta-Lactamase inhibitor
2) 4th Gen Cephalosporin
3) Carbapenem

Plus 1 of the following:

1) Antipseudomonal fluoroquinolone
2) Anti-gram negative aminoglycoside

Plus 1 anti-MRSA medication:

1) Linezolid
2) Vancomycin

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18
Q

Epidemiology of influenza

A

Distinct outbreaks every year, nearly every year

Begin abruptly over a 2-3 week prior and last 2-3 months

Usually infects 10-20% in general population and can exceed 50% in pandemics

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19
Q

Transmission and incubation of influenza

A

close contact with infected individual via exposure to respiratory secretions

Incubation period 1-4 days, onset of illness within 3-4 days

Virus shed from infected individuals 24-48 hours prior to onset of illness and can continue for 10 days (longer in at risk populations)

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20
Q

Pathogenesis of influenza

A

Hemagglutinin (surface glycoprotein) binds to sialic acid residues on respiratory epithelial cell surface glycoproteins and starts infection

→ viral replication, progeny virions bound to host cell membrane

→ Neuraminidase cleaves link between virion and host, and liberates new virions

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21
Q

Influenza A

A

(H1,2,3 + N1,2) has more antigenic shift (major changes in glycoproteins)

Antigenic shift → epidemics and pandemics

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22
Q

Influenza B

A

only has antigenic drifts (minor changes in glycoproteins)

Antigenic drift → localized outbreaks

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23
Q

Clinical features of influenza infection

A

Abrupt onset of fever, headache, myalgias and malaise
Cough, nasal congestion, sore throat
Pharyngeal hyperemia, lymphadenopathy

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24
Q

Complications associated with influenza infection (4)

A

Primary IFN Pneumonia
Secondary bacterial pneumonia
Myositis, rhabdomyolysis
CNS involvement

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25
Q

Treatment of influenza

A

Give within 48 hours of illness (neuraminidase inhibitors - oseltamivir, zanamivir)

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26
Q

Starling resistor model in upper airway collapse

A
  1. P-upstream > P-downstream > P crit then there is no flow limit and tube will stay open
  2. Pus > Pcrit> Pds → point of narrowing but not complete collapse
    a. Physics of snoring
  3. Pcrit > Pus > Pds → collapse of airway no matter what the pressure inside airway
    a. Upstream pressure always > downstream pressure because you are taking a breath in
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27
Q

Effect of obesity on upper airway

A

fat deposition in tongue itself and neck → narrowing of oropharynx (only becomes a problem during sleep)

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28
Q

Effect of sleep on upper airway

A

lose a lot of protective mechanisms when you sleep (decreased tonic output, decreased output from inspiratory premotor neurons, and decreased reflex stimulation, higher threshold)

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29
Q

Defense against airway collapse (3)

A
  1. Upper airway recruitment threshold: stimuli (intra-airway pressure becomes negative enough, increased CO2, decreased O2) recruit upper airway dilator muscles to adequately overcome Pcrit
    a. Airway narrowing → increased resistance → increased muscular EMG activity
    b. High upper airway recruitment threshold → increased duration of obstructive events
  2. Arousal threshold: negative pressure needed in order to trigger arousal
    a. Low arousal threshold → frequent arousals → hyperventilation → hypocapnia → decreased ventilation and upper airway muscle tone
  3. Loop gain: magnitude of ventilatory response to stimuli
    a. High loop gain → greater sensitivity to CO2 and O2 → hyperventilation → hypocapnia → decreased upper airway muscle tone
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30
Q

Prevalence of snoring in men and women

A

44% men 28% women

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31
Q

Prevalence of upper airway resistance syndrome

A

9% in population

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32
Q

Prevalence of sleep apnea syndrome

A

a. 4% of men, 2% of women
b. Obstructive: 85%
c. Mixed or Complex: 14%
d. Central: less than 1%

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33
Q

Cheyne-Stokes respiration

A

a. 40-50% of patients with heart failure
b. 10% of patients with stroke
c. Greater sensitivity to CO2 → hyperventilation and “overshooting” of PaCO2 below the apneic threshold → reduces drive to breathe
d. Arousals generally occur at peak of ventilation

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34
Q

Complications of sleep disordered breathing

A

primarily cardiovascular and motor vehicle crash

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35
Q

Clinical deatures of obstructive sleep apnea syndrome

A
  1. More common in men and as they age until 60s or 70s
  2. PMH: chronic rhinitis, acromegaly, neuromuscular disorder, amyloidosis, upper airway anatomic abnormalities, genetic syndromes (e.g. Downs)
  3. Family History: first degree relative with OSA
  4. Social history: smoking, alcohol, obesity
  5. Medications: sedative-hypnotics, opioids
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36
Q

Symptoms of obstructive sleep apnea syndrome

A

excessive daytime sleepiness, snoring, memory loss, decreased concentration, decreased libido, irritability, attention deficit (children), hyperactivity (children), nocturia or enuresis

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37
Q

Diagnosis of obstructive sleep apnea

A
  1. Epworth sleepiness scale
  2. Physical Exam:
    a. Mallampati classification - airway narrowing
    b. Neck circumference > 17 inches (male) or > 16 inches (female) → greater risk
    c. Retrognathia (recessive jaw) → decreases space inside mouth → tongue moves posteriorly and narrows airway diameter
  3. Polysomnography (sleep study):
    a. Full night (diagnostic only)
    b. Split night (diagnostic and therapeutic)
    c. Portable (diagnostic only)
    i. Not for patients with confounding cardiopulmonary abnormalities
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38
Q

Treatment of obstructive sleep apnea (9)

A
  1. general measures- sedative avoidance, smoking cessation
  2. weight reduction
  3. positional therapy
  4. oxygen therapy
  5. pharmacotherapy
  6. PAP
  7. Oral devices
  8. Upper airway surgery
  9. Nerve stimulation
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39
Q

Positive airway pressure (PAP)

A

Mechanical solution to mechanical problem

Helps patient to overcome critical airway pressure

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40
Q

Oral devices (2)

A
  1. Tongue Retainer - holds tongue in anterior (forward) position
    i. For patients with compromised dentition
  2. Mandibular repositioner - advances mandible (and tongue) forward
    i. Contraindications: compromised dentition, TMJ dysfunction
  3. Billy’s penis
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41
Q

Upper airway surgery for obstructive sleep apnea (4)

A
  1. Tracheostomy: percutaneous tracheal opening distal to pharynx to bypass area of upper airway obstruction
    i. Indicated for severe life-threatening OSA
  2. Maxillomandibular advancement: advance both maxilla and mandible, enlarges retrolingual and retropalatal airway

i. Pain and nerve damage possible complications
ii. Effective up to 90% of the time

  1. UvuloPalatoPharyngoPlasty (UPPP): excision of uvula, posterior soft palate, redundant pharyngeal tissue, and tonsils
    i. Rarely effective - high recurrence of OSA
  2. Tonsillectomy and adenoidectomy: remove tonsils and enlarged adenoids (best for children with OSA)
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42
Q

Nerve stimulation for OSA

A

Similar to a pacemaker - box connects to wire that goes to intercostal muscles and tongue

Breath initiated by patient and then box stimulates muscle contraction

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43
Q

Risk factors of lung cancer (8)

A

1) Smoking
2) Environmental risk factors (Second hand smoke, radon gas, asbestos, industrial, polycyclic aromatic hydrocarbons, air pollution, silica, vinyl chloride, TB)
3) COPD secondary to smoking
4) Family history
5) Gender - females > males
6) Sarcoidosis, ILD/pulmonary fibrosis (chronic inflammation)
7) Previous tobacco related cancer - lung cancer, head/neck cancer
8) Sputum cytologic atypia

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44
Q

Non-small cell lung cancer

A

87% of cases

1) Squamous cell carcinoma
2) Adenocarcinoma
3) Large Cell

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45
Q

Squamous cell carcinoma

general info

A

25% of cases

**strongly linked to smoking

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46
Q

Squamous cell carcinoma histopathology (3)

A

1) PROXIMAL/CENTRAL squamous metaplasia of bronchial epithelium
2) Usually >3 cm in diameter
3) Keratin pearls (stain + for keratin)

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47
Q

Squamous cell carcinoma (genetic mutations)

A

p53, Rb, p16

No proven genomically targeted therapies

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48
Q

Adenocarcinoma general info

A

40% of cases

**most common type in women and non smokers

**subclass is bronchioalveolar carcinoma, insitu

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49
Q

Adenocarcinoma histopathology (3)

A

1) PERIPHERAL cancer
2) Cells attempt to form gland like structure
3) stain + for mucin

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50
Q

Adenocarcinoma genetic mutations (3)

A

1) K-Ras
2) EGFR
3) EML-4-ALK

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51
Q

Large cell carcinoma

A

heterogenous group of poorly differentiated tumors, arise in distal airway epithelial cells

  • Present as unresolving infiltrate or nodules
  • does not stain for mucin or keratin
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52
Q

Small cell carcinoma general info

A

13% of cases

  • highly aggressive
  • strongly linked to smoking
  • metastasizes widely (especially to brain)
  • very bad prognosis
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53
Q

Small cell carcinoma histopathology (5)

A

1) small, dark staining cells that form clusters
2) stain + for neuroendocrine markers (NCAM)
3) often presents with hilar and mediastinal lymphadenopathy
4) Bronchial origin (can narrow/obstruct bronchi)
5) CENTRAL lesion

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54
Q

Characteristics that define solitary pulmonary nodules (5)

A

1) Lesion less than 3 cm diameter
2) Round or oval with smooth contour
3) Surrounded by aerated lung
4) No satellite lesions
5) No associated atelectasis, pneumonitis, or regional adenopathy

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55
Q

Goals of solitary pulmonary nodule evaluation (3)

A

1) Expedite resection of potentially curable lung cancer
2) Minimize resection of benign nodules
3) Morbidity and mortality of nodule evaluation is 5-10%

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56
Q

Evaluation of solitary pulmonary nodules

A
  • Size of nodule, age, prior cancer history, smoking, COPD, asbestos
  • Look at previous imaging (stable for > 2 yrs = no evaluation needed)
  • Larger node and higher risk patient is more frequent CTs for screening
  • All resections must include a lymph node dissection
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57
Q

Presenting symptoms of lung cancer

A 
weight loss
cough (or change in chronic cough)
weakness
hemoptysis
pain (local or metastatic disease)
neuro symptoms/signs
lymphadenopathy

*Paraneoplastic symptoms (especially for small cell - ADH, ACTH release, hypercalcemia, gynecomastia)

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58
Q

Tests to diagnose lung cancer (5)

A

1) Blood tests: high alk phos (bone metastasis), high Ca2+, anemia, cytopenias suggest metastases
2) CT/PET scan (solitary pulmonary nodule is common finding)
3) Tissue study (transbronchial biopsy, open lung biopsy, needle biopsy)
4) Cytology
5) mediastinoscopy to assess mediastinal lymph nodes

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59
Q

Staging of small cell lung cancer

A

Limited disease (25-30%) - limited to ipsilateral hemithorax (including contralateral mediastinal nodes)

Extensive disease (70-75%) - tumor extends beyond hemithorax (including pleural effusions)

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60
Q

Staging of NSCLC

A

TMN staging

tumor size, nodal involvement, presence or absence of metastases

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61
Q

T0
Tis
T1a
T1b

A

T0 = no evidence of primary tumor

Tis = carcinoma in situ

T1a = tumor less than 2cm (not in mainstem bronchus)

T1b = tumor > 2-3 cm (not in mainstem bronchus)

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62
Q

T2a

T2b

A

T2a = tumor less than 5 cm, or present in mainstem bronchus (not within 2 cm of carina, no invasion of visceral pleura, atelectasis, or pneumonitis)

T2b = tumor > 5-7 cm

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63
Q

T3

T4

A

T3 = tumor > 7 cm, or invades chest wall, diaphragm, mediastinal pleura, parietal pericardium, less than 2 cm from carina, associated with atelectasis or pneumonitis, or more than 2 malignant nodules in the same lobe

T4 = tumor of any size with invasion of mediastinum, heart, great vessels, trachea, esophagus, vertebral body, or carina + malignant nodules in ipsilateral lung

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64
Q

N0
N1
N2
N3

A 
N0 = no nodal involvement
N1 = metastasis to ipsilateral peribronchial or hilar region
N2 = metastases to ipsilateral mediastinal and/or subcarinal lymph nodes
N3 = metastases to supraclavicular or contralateral mediastinal, hilar, or scalene nodes
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65
Q

M0
M1a
M1b

A

M0 = no distant metastases

M1a = separate tumor nodules in contralateral lobe, tumor with pleural nodules, or malignant pleural or pericardial effusion

M1b = distant metastasis

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66
Q

Genetic alterations in non-small cell lung cancer (4)

A

1) Epidermal Growth Factor (EGFR/ERB-1)
2) Her2/neu (ERG-2)
3) Vascular Endothelial Growth Factor (vEGF) over expressed
4) Ras mutations

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67
Q

Epidermal Growth Factor (EGFR) and treatment of EGFR NSCLC

A

50-80% NSCLC (most common in non smokers)

Overexpression of EGFR, associated with poor prognosis

Drugs available = erlotinib, gefitinib, cetuximab, afatinib
VERY expensive

Development of resistant tumor → must move down the line of treatments

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68
Q

Her2/neu (ERB-2) and treatment of Her2 NSCLC

A

10% NSCLC

Drugs available = trastuzumab (herceptin)

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69
Q

Vascular Endothelial Growth Factor (vEGF) and treatment of vEGF NSCLC

A

Over expressed

Drugs available = bevacizumab (Avastin)

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70
Q

Ras mutations

A

2-30% NSCLC, adenocarcinoma

Associated with resistance to tyrosine kinase inhibitors (TKIs, EGFRi)

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71
Q

Hoarseness

A

abnormal voice changes, breathy, raspy, strained, weak

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72
Q

Dysphonia

A

general alteration of voice quality (usually laryngeal source)

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73
Q

Dysarthria

A

defect in rhythm, enunciation, articulation (usually neurological or muscular source)

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74
Q

Stridor

A

large airway noise from obstruction

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75
Q

Inspiratory vs. Expiratory vs. Biphasic stridor

A

Inspiratory → supraglottic, extrathoracic
E.g. epiglottitis, epiglottis cancer

Expiratory → tracheal, large bronchi intrathoracic
E.g. tracheal cancer

Biphasic → laryngeal, immediate subglottis
E.g. subglottic stenosis (due to intubation), laryngeal cancer, croup

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76
Q

Sertor

A

snoring sound from nose, nasopharynx, throat

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77
Q

Causes of hoarseness (top 2 plus a few others)

A

1) Viral laryngitis (acute) - most common cause
2) Laryngeal reflux (chronic)

Other: Vocal abuse, allergies, chronic cough, nodules, polyps, trauma, age, neuro disorders, smoking, malignancies of thyroid, larynx, lungs

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78
Q

When should a patient see an otolaryngologist?

A

Hoarseness lasts longer than 2-3 weeks

Hoarseness associated with:

  • Pain (ear radiation?)
  • Coughing up blood
  • Difficulty swallowing
  • Lump in neck
  • Complete loss or severe change in voice lasting longer than a few days
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79
Q

5 layers of vocal folds

A

1) Epithelium
2) Superficial lamina propria
3) Intermediate lamina propria
4) Deep lamina propria
5) Vocalis muscle (medial thyroarytenoid)

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80
Q

Components of voice production (3)

A

1) Source (pulmonary/infraglottic)
2) Vibratory production (larynx/intrinsic muscles, extrinsic muscles)
3) Resonance (supraglottic and oral phase)

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81
Q

Components that generate source airflow

A

1) diaphragm
2) intercostal muscles
3) tracheobronchial tree, lungs, thorax
4) abdominal support system

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82
Q

Effect of ANS on voice

A

ANS plays role in mucus production, voice stability → B-blockers

Fine muscular control at risk with sympathetic stimulation or when a neurological conditions exists

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83
Q

Diaphragm and voice production

A

inspiratory force and fine regulation of singing

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84
Q

Abdominal muscles and voice production

A

maintains efficient, constant power source and inspiratory-expiratory mechanism

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85
Q

Extrinsic muscles and vibratory production

A
  • maintain position of larynx and neck
  • Essential to consistent sound
  • Change in tension, position, tilt
  • Changes resting length of intrinsic muscles
  • Well trained singer can sing for hours
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86
Q

Cartilages of larynx (3)

A

Thyroid, cricoid (only one that is a complete ring), paired arytenoids

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87
Q

Intrinsic muscles of larynx and their function

A

arytenoid muscle (moves vocal folds)

posterior cricoarytenoid muscle (only muscle that opens your vocal folds)

As larynx descends pitch will drop (e.g. with puberty)

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88
Q

Supraglottic/oral phase and resonance

A

Includes supraglottic larynx lips, teeth, tongue, palate, pharynx, nasal cavity, and sinuses

  • ALL shape the way your voice sounds
  • Can tune our frequencies by changing shape of our vocal tract
  • Vocal tract length effects frequencies → shorter tract = higher frequencies
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89
Q

Central innervation of vocal folds

A

Cerebral cortex:

  • Speech area = temporal cortex
  • Voice area = precentral gyrus

–> Vagus (X) exits medulla –> jugular foramen

→ superior laryngeal nerve (internal branch = sensation, external branch = motor to cricothyroid muscle)

→ *Recurrent laryngeal nerve (all intrinsic muscles but CT)

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90
Q

Major causes of hoarseness: (10)

A

1) Vocal nodules, cysts, and polyps
2) Granulomas
3) Reinke’s edema
4) Vocal fold hemorrhage or tear
5) Presbyphonia and vocal bowing with age
6) Immobile vocal fold
7) Laryngopharyngeal reflux
8) Papilomas
9) Leukoplasia
10) Precancerous/cancerous lesions

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91
Q

Laryngopharyngeal Reflux

A

Escape of stomach acids from stomach into esophagus through laryngoesophageal sphincter

May reach larynx, oral cavity, and lungs

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92
Q

Symptoms of Laryngopharyngeal Reflux

A

hoarseness, chronic cough, foreign body sensation (globus), tracheal stenosis

Bad breath or bitter taste in a.m.

A.m hoarseness or after meals

Sensation of post nasal drip, but no nasal issues

Heartburn not always present

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93
Q

Why do we cough?

A

defense mechanism, clears pathogens, particulares, foreign bodies, and accumulated secretions from the lung airways, larynx, and pharynx

*For cough to effectively clear airway, both afferent and efferent pathways of cough reflex must be intact

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94
Q

Afferent pathway activation of cough

-which 3 types of nerves?

A

cough initiated in areas supplied by vagus nerve (or voluntarily by cerebral cortex)

1) Rapidly adapting receptors (RARs)
2) Slowly adapting stretch receptors (SARs)
3) C-fibers

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95
Q

Rapidly adapting receptors (RARs) and Slowly adapting stretch receptors (SARs)

A

highly sensitive to mechanical stimulation (bronchial obstruction, lung inflation)

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96
Q

C-fibers

A

highly sensitive to noxious chemical stimuli

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97
Q

Efferent pathway of cough (4 phases)

A

1) Inspiratory phase
2) Compressive phase
3) Expiratory phase
4) Relaxation phase

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98
Q

Inspiratory phase of cough

A

inhalation ends before closure of glottis

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99
Q

Compressive phase of cough

A

thoracic and abdominal muscles contract against a fixed diaphragm (e.g. Valsalva) → intrathoracic pressure increases

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100
Q

Expiratory phase of cough

A

glottis opens, air rapidly expelled

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101
Q

Relaxation phase of cough

A

chest wall and abdominal muscles relax

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102
Q

Acute cough

A

lasts less than 3 weeks

-identify if life threatening or not

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103
Q

Life threatening causes of acute cough

A

pneumonia, severe asthma or COPD, pulmonary embolism, heart failure

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104
Q

Non-life threatening causes of acute cough

A

1) Infectious: URI or acute bronchitis (LRI)
2) Exacerbations of pre-existing condition (Asthma, brochiectasis, UACS, COPD)
3) Environmental/Occupational exposure to allergens (pollen, fungi, etc.) and irritants (chemicals, dust)

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105
Q

Upper respiratory tract infection (URI)

-treatment?

A

“common cold” (nasal congestion, discharge, sneezing)

-postnasal drip irritates larynx –> cough

→ Do not treat with abx (viral, e.g. rhinoviruses)
-Can use decongestants and cough suppressants

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106
Q

Lower respiratory tract infection (Acute bronchitis)

A
  • 90% viral etiology
  • Cough with or without sputum
  • Distinguish from pneumonia with CXR (no infiltrates)

Treatment:

  • antitussives/support
  • NO ABX
  • ABX if pertussis (whooping cough) or mycoplasma/ chalmydophila pneumonia
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107
Q

Subacute cough

-causes?

A

lasts 3-8 weeks

Post-infectious:

  • Pneumonia
  • Pertussis
  • Bronchitis
  • New onset exacerbation of UACS, Asthma, GERD, Bronchitis

Non-post infectious –> treat as chronic cough

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108
Q

Four most common causes of chronic cough

A

1) Upper Airway Cough Syndrome
2) Asthma
3) GERD
4) Non-Asthma Eosinophilic Bronchitis

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109
Q

Upper Airway Cough Syndrome (UACS)

-mechanism of cough production?

A

most common cause of chronic cough (postnasal drip syndrome)

Mechanism: stimulation of upper airway cough receptors by secretions from nose/paranasal sinuses → direct irritation/inflammation of upper airway cough receptors

110
Q

Signs and Symptoms of UACS

A

Symptoms: “tickle” or something in throat, throat clearing, hoarseness, nasal congestion and drainage, inflamed nasal mucosa, secretions in posterior oropharynx

Signs: cobblestone oropharyngeal mucosa

111
Q

Treatment of UACS

A

first gen antihistamine/ decongestant combination med for more than 2 weeks

112
Q

Asthma

-mechanism of cough production?

A

chronic inflammatory disorder with variable airflow obstruction and airway hyperresponsiveness

Mechanism: stimulation of cough receptors by inflammatory mediators, mucus, bronchoconstriction

113
Q

Signs and Symptoms of asthma?

A

Symptoms:
intermittent wheezing, dyspnea, cough
Cough variant asthma = cough is only symptom

Signs: bilateral, expiratory wheezing (when present)

> 12% and 200ml increase in FEV1 after SABA

Methacholine inhalation challenge positive (20% decline in lung function with low dose of methacholine)

114
Q

GERD

mechanism of cough production (3)

A

backflow of stomach contents into esophagus

Mechanism: stimulation of afferent cough reflex by irritation of:

1) upper respiratory tract
2) lower respiratory tract (by aspiration of gastric contents)
3) Esophagus (esophageal-bronchial cough reflex, esophagus alone triggers cough)

115
Q

Signs and Symptoms of GERD

A

Symptoms: cough with/without phlegm, heartburn, regurgitation, hoarseness (edema and erythema of larynx), sour taste in mouth (cough may be only symptom!)

Signs: none

116
Q

Diagnosis of GERD

A

24 hr esophageal pH monitoring, esophagram

117
Q

Treatment of GERD

A

gastric acid suppression with a proton pump inhibitor for > 2 months + diet and lifestyle modification

118
Q

Non-Asthmatic Eosinophilic Bronchitis (NAEB)

Mechanism of cough stimulation?

A

-eosinophilic airway inflammation similar to asthma, but WITHOUT variable airflow limitation or airway hyperresponsiveness

Mechanism: stimulation of lower airway cough receptors by inflammatory mediators

119
Q

Signs and symptoms of NAEB

A

Symptoms: cough without wheezing or dyspnea

Signs: no wheezing, normal PFTs methacholine challenge

-Induced sputum analysis shows >3% increase in eosinophils

120
Q

Treatment of NAEB

A

inhaled corticosteroid for more than 4 weeks

121
Q

Neuropathic Cough, aka Chronic Cough Hypersensitivity Syndrome

A

Cough triggered by low level stimuli - change in ambient temp, taking a deep breath, etc.

Caused by neural injury from: virus infection, chronic irritation/inflammation, or environmental pollutants

122
Q

Differences of cough in children

A

Most common cause of cough is URI of viral etiology

Chronic cough = cough lasting > 4 weeks

-Common causes: asthma, sinusitis, GERD, inhaled foreign body, cystic fibrosis, second hand tobacco smoke

123
Q

4 sites of action of antihistamines

A

1) H1 receptor blockade (reversible, competitive)
2) Muscarinic receptor block
3) Sodium channel block
4) Adrenergic (a1) receptor block

124
Q

Effects of Muscarinic receptor block by histamines (3)

A

1) CNS side effects
2) prevent nausea and vomiting
3) block secretions –> Side effects: no pee, no see, no spit, no shit (urinary retention, blurred vision, dry mouth, constipation)

2nd generation do NOT block muscarinic receptors

125
Q

Effects of sodium channel blockade by histamines (1)

A

1) local anesthetic effects

126
Q

Effect of adrenergic (a1) receptor block by histamines (1)

A

1) may cause orthostatic hypotension

127
Q

H1 receptor activation –> (5)

A

1) Vasodilation (endothelial cells)
2) Increased capillary permeability (endothelial cells)
3) GI smooth muscle contraction (Cramping)
4) Bronchoconstriction (bronchiolar smooth muscle)
5) Stimulate sensory nerve endings (pain, itching)

128
Q

Treatment of common cold

A

1st gen antihistamine/decongestant (brompheniramine/pseudoephedrine)

+ Naproxen (anti-inflammatory cough suppression)

129
Q

Treatment of UACS

A

1st gen antihistamine/decongestant (brompheniramine/pseudoephedrine)

130
Q

Treatment of NAEB

A

inhaled corticosteroid

131
Q

Treatment of neuropathic cough

A

Amitriptyline-Gabapentin

132
Q

Pathophysiology of the common cold

A

Typically Rhinoviruses → attachment of virus to respiratory cells → inflammation (BRADYKININ release) → symptoms

1) Pain via nociceptors
2) Nasal stuffiness via dilation of blood vessels
3) Nasal fluid hypersecretion via increased capillary permeability
4) Cough via activation of irritant sensory receptors
* Mast cell mediators (histamine) only MINOR role in viral inflammatory response

133
Q

4 names of first gen antihistamines

A

Meclizine
Dimenhydrinate
Bronpheniramine
Diphenhydramine (Benadryl)

134
Q

First generation antihistamines:

Mechanism?
Kinetics?

A

Mechanism: H1 receptor antagonist
-Also blocks muscarinic, Na-channel and adrenergic receptors

Kinetics:

  • Oral (rapid)
  • Last 6-8 hours
  • *CNS penetration
  • CYP3A4 metabolized
135
Q

Major clinical uses of first gen antihistamines (Meclizine/ Dimenhydrinate/Bronpheniramine/ Diphenhydramine) (5)

A 
Allergic rhinitis
Anaphylactic reaction
Motion sickness
Insomnia
Cough suppression
136
Q

Side effects of first gen antihistamines (Meclizine/ Dimenhydrinate/Bronpheniramine/ Diphenhydramine) (5)

A

M3 (muscarinic) block → SEDATION, antiemetic, blurred vision, DRY MOUTH, urinary retention

Na channel block → mild decrease in pain, cough

Adrenergic block → ORTHOSTATIC HYPOTENSION

Possible DDIs (CYP3A4 induction)

Chronic use may diminish effect → switch classes

137
Q

3 names of 2nd gen antihistamines

A

Loratadine (Claritin)
Fexofenadine
Cetirizine

138
Q

2nd gen antihistamine:

Mechanism?
Pharmacokinteics?

A

Mechanism: H1 histamine receptor antagonist ONLY and NOT in brain

Pharmacokinetics:

  • Oral (rapid)
  • Metabolised by liver (CYP3A4)
  • 12-24 hour duration ** longer than first gen
  • Decreased CNS penetration **no sedation, dry mouth, etc.
139
Q

Major clinical uses of 2nd gen antihistamines

A

allergic rhinitis

140
Q

Side effects of 2nd gen antihistamines (3)

A 
Mild sedation
Possible DDIs (CYP3A4 induction)
Chronic use may diminish effect → switch classes
141
Q

2 names of topical decongestants

A

Phenylephrine

Oxymetazoline (Afrin)

142
Q

2 names of oral decongestants

A

pseudoephedrine (Sudafed)

phenylephrine (Sudafed PE)

143
Q

Topical decongestants

benefits
Side effects

A

fast acting, no 1st pass metabolism

Side effects: possible rebound congestion with overuse because it’s so good at helping symptoms

144
Q

Oral decongestants

benefits
side effects

A

longer acting

Affects other vessels to cause headache, dizziness, nervousness, increase BP, palpitations

145
Q

Decongestants (oral and topical)

Mechanism of action
Clinical use

A

Mechanism of Action: stimulate alpha-1 adrenergic receptors, promoting vasoconstriction
→ drainage, improves breathing

Clinical Use: allergic rhinitis AND viral rhinitis

146
Q

2 names of antitussive agents

A

codeine (hydrocodone)

Dextromethorphan (Robitussin)

147
Q

Codeine:

  • Clinical use
  • Mechanism of action
A

Clinical use: oral cough suppressant associated with cold symptoms, allergic rhinitis, asthma, and COPD
*Controlled substance, must be prescribed

Mechanism of action: binds mu-opioid receptors to suppress cough

148
Q

Side effects of Codeine (3)

A

nausea, drowsiness, constipation

149
Q

Dextromethorphan (Robitussin)

Clinical use?
Mechanism of action

A

oral cough suppressants
Most commonly used antitussive

Mechanism of action: binds mu-opioid receptors to suppress cough

150
Q

Dextromethorphan (Robitussin)

side effects (2)

A

drowsiness, GI upset

Can have PCP (phencyclidine) effects at high (50-100x) doses = “Robo-Tripping” via block of NMDA glutamate receptors

151
Q

Diphenhydramine (clinical use, mechanism, side effects)

A

Oral cough suppressants

Mechanism of action: H1 receptor antagonist

Side effects: sedation, antimuscarinic effects

152
Q

Benzonate (Tessalon Perles) (clinical use, mechanism)

A

Oral cough suppressant

Mechanism of action: Tetracaine = local anesthetic to numb the throat

153
Q

Expectorants (Guaifenesin)

A
  • Oral
  • Thought to stimulate secretions in respiratory tract to make more viscous and easier to clear
  • Highly controversial, debatable efficacy → increasing fluid intake or using mist/vaporizer probably more effective
154
Q

Guaifenesin Clinical uses and side effects (1)

A

Clinical uses: encourage ejection of phlegm/sputum → viral cold infections, COPD

Side effects: GI upset

155
Q

Mucolytics: N-Acetylcysteine

mechanism of action

A

splits disulfide bonds to make mucous less viscous

156
Q

Mucolytics: N-Acetylcysteine

adverse reactions

A

may trigger bronchospasm in COPD (give with dilator)

157
Q

Mucolytics: N-Acetylcysteine

Clinical uses

A

viral cold infections, COPD

**Inhaled

158
Q

Defense mechanisms of the lung (3)

A

1) Configuration of the nasopharynx and serial branching of airways —> particle deposition proximal to more vulnerable alveolar structures
2) Mucociliary clearance and cough
3) Alveolar clearance (macrophages + immune response)

159
Q

Mucociliary clearance and cough (4)

A

Large particles (>10um) deposited on mucous coated surfaces of airways

Mucous projected towards pharynx by beating of cilia on epithelial cells

Cleared by coughing, sneezing, and/or swallowing

Part of innate immune system

160
Q

Problems with mucociliary clearance can result from… (3)

A

1) hypersecretion of mucous → chronic bronchitis, COPD, asthma, cystic fibrosis
2) Reduced clearance (air pollution, viral infection, cigarette smoke)
3) Abnormal ciliary function: Primary ciliary dyskinesia (immotile ciliary syndrome)

161
Q

Abnormal ciliary function: Primary ciliary dyskinesia (immotile ciliary syndrome)

A

AR, defect in dynein arm
→ Sinusitis, bronchiectasis, situs inversus, infertility

Kartagener’s syndrome: situs inversus + chronic sinusitis + bronchiectasis

162
Q

Discrimination between harmful and harmless material done by… (3)

A

1) Size and physiochemical property discrimination
2) Presence/Absence of PAMPs
3) Recognition by dendritic cells

163
Q

If a PAMP is present then…

A

Presence of PAMP → activation of innate immunity → stimulate epithelial cells to express chemokines, cytokines, and lipid mediators → recruit neutrophils → DCs traffic to lymph nodes and stimulate T cell proliferation → alveolar macrophages initiate inflammation

164
Q

If a PAMP is absent then…

A

-don’t want to be reacting to everything we breathe in

→ DC cell recognizes it promotes anti-inflammation and tolerance to common antigens

  • inflammation suppressed via tonic signaling of resident alveolar macrophages
  • SIRPa bound to lung specific surfactant proteins (SP-A, SP-D) on alveolar macrophage

–> inhibition of NF-KB –> suppress inflammation in absence of PAMPs

165
Q

How are microbes recognized by resident macrophages? (2)

A

1) Secreted pattern recognition receptors

2) Cellular pattern recognition receptors

166
Q

Immune cells in pulmonary airspaces (normal vs. smoker)

A

Normal: 90-85% macrophages, 5% lymphocytes, 1% eosinophils, 1% neutrophils

Smokers → dramatically increase number of alveolar macrophages, change CD4/CD8 T cell ratio

167
Q

Immune cell progression over time

A

1) Neutrophils
2) Monocytes/Macrophages
3) Lymphocytes

168
Q

Neutrophils in lung defense

A

immediate effector cell

Attracted to lung by chemotactic factors produced by alveolar macrophages and epithelium (IL-8)

Ingest bacteria and fungi that have been opsonized by complement

-Kill by antioxidant production, microbial-cidal proteins and extracellular traps

169
Q

Moncytes/Macrophages in lung defense (5)

A

1) Suppress pro-inflammatory adaptive immune responses
2) Clear particles, pathogens, apoptotic cells, and cellular debris

3) Elicit inflammatory response when appropriate (tonic state vs. presence of PAMPs)
- Alternatively programmed macrophages may generate inflammation that can be harmful (e.g. sarcoidosis, pulmonary fibrosis)

4) Induction of tissue cell repair
5) Activated by PAMPs

170
Q

Resident alveolar macrophages vs. recruited monocytes/macrophages

A

Born with resident alveolar macrophages (from yolk sac and fetal liver), but can call upon migrating monocytes during infection

171
Q

Adaptive immune response in the lung

A

B and T cells

Activated by exposure of DCs to PAMPs and antigens

Provides antigen specificity

Upon re-exposure, immunological memory allows for a more rapid and augmented secondary immune response

172
Q

Primary TB infection

A

Initial infection by Mycobacterium tuberculosis (MTB)

Almost always occurs through the respiratory tract

In immunocompetent individuals, most primary infections do not develop into active disease → latent TB infection, infection cleared spontaneously, or active TB infection (immunocompromised)

173
Q

Stage 1 of TB infection

A

ingestion by resident alveolar macrophages → necrotic death of macrophage → MTB survives and is released extracellularly and taken up by other macrophages

174
Q

Stage 2 of TB infection

A

symbiotic stage

-MTB multiplies and macrophages accumulate

Monocytes migrate from blood into lungs → differentiate to macs
→ continued ingestion but no destruction of MTB
→ MTB multiples within inactivated macrophages
→ formation of early primary tubercle

175
Q

Stage 3 of TB infection

A

migration of T cells to site of infection

T cells begin to activate macrophages to kill and prevent spread of MTB

Granulomas form (MTB unable to multiple within solid caseous material) → infection contained

In AIDS patients granulomas break down → reactivation

176
Q

Stage 4a of TB infection

A

LTBI cellular level

Solid caseous center remains intact

Any bugs that escape ingested by highly activated macrophages

LTBI established if caseation remains solid and does not liquify

177
Q

Stage 4b of TB infection

A

Decline in immunity → reactivation of TB

Immunosuppression (AIFS, cancer, anti-TNFa, aging, malnutrition)

→ Loss of integrity of granuloma
→Liquefaction of caseous material (“caseous necrosis”) provides favorable medium for MTB multiplication
→ Cavity forms → rupture and spread to other parts of lung and to other individuals

178
Q

Latent TB infection:

CXR
PPD
Symptoms?
Virus?

A

1) CXR may show Ranke complex = calcified regional hilar and/or mediastinal lymph nodes + calcified lung nodules (Ghon complex)
- May also have a normal CXR

2) Asymptomatic
3) Positive PPD
4) Not shedding virus

179
Q

Active TB infection

CXR
PPD
Symptoms?
Virus?

A

1) abnormal CXR with pneumonia +/- cavitary lesions
2) Symptomatic
3) Shedding virus
4) Positive PPD

180
Q

Disadvantages of TB skin test

A

1) must wait 48-72 hours to read test
2) Can be false positive with BCG vaccination
3) False negativity in people with T cell depletion (AIDS, organ transplant)
4) Not very high sensitivity and specificity

181
Q

A TB test is considered positive for who if the induration is >5mm? (5)

A

1) Recent close contact to an active case of TB
2) HIV positive
3) Apical fibronodular disease consistent with old healed TB
4) Organ transplant
5) Anti-TNFa therapy

182
Q

A TB test is considered positive for who if the induration is >10mm? (4)

A

1) Recent TB skin test converter
2) Immigrants from high prevalent regions for TB
3) Other high risk groups (homeless, jail, healthcare workers)
4) Certain predisposing medical conditions (diabetes, dialysis, etc.)

183
Q

A TB test is considered positive for who if the induration is >15mm?

A

All others - low risk people that shouldn’t have been tested in the first place probably

184
Q

IFNy release assay TB tests (2)

A

1) Quantiferon test

2) T-spot test

185
Q

Quantiferon test

A

blood + antigens specific for MTB → measure IFNy by ELISA

Specifically tests for antigens of MTB, so can differentiate between those who have TB and those who were just vaccinated

186
Q

T-spot TV test

A

assay of IFNy release, each spot = “footprint” of one IFNy producing cell

Better for detection in immunocompromised host

187
Q

Benefits of IFNy assay TB tests (3)

A

1) More sensitive and specific than TST
2) Better positive predictive value than TST for a BCG-vaccinated person
3) Only one visit required

188
Q

BCG scar vs. small pox scar?

A

BCG scar is raised

Smallpox scar is sunken

189
Q

3 options for treatment of latent TB:

A

1) 9 months Isoniazid (INH) daily or twice weekly (BIW)
- Risk of INH associated hepatitis

2) Rifampin daily for 4 months (fewer serious adverse events, better adherence, more cost effective than 9 months on INH)
3) INH + rifampin daily x 3 months ** the best option

190
Q

What’s the link between vitamin D and latent TB reactivation in recent immigrants

A

Vitamin D: suppresses growth of MTB in macrophages

191
Q

Hypoxemic respiratory failure

A

inadequate oxygenation

O2 sat less than 87% or PaO2 less than 55

192
Q

Common causes of hypoxemic respiratory failure? (5)

A

1) Impaired gas diffusion - Alveolar filling (Left HF with pulmonary edema, pneumonia, alveolar hemorrhage, ARDS)
2) Pulmonary vascular disease
3) V/Q mismatch (shunt, dead space)
4) Alveolar hypoventilation
5) High altitude with low inspired O2

193
Q

Hypercapnic Respiratory Failure

A

elevated CO2, or any process that impairs ventilation (can’t breathe or won’t breathe)

194
Q

Typical causes of “Can’t Breathe” in hypercapnic respiratory failure

A

physiological hypoventilation

Asthma, COPD, upper airway obstruction, severe burn (chest wall restriction), neuromuscular

195
Q

Typical causes of “Won’t Breathe” in hypercapnic respiratory failure

A

central hypoventilation

Respiratory drive issues, over sedation, brain injury, seizure

196
Q

Equation for acute respiratory acidosis and change in pH and [HCO3-]

A

increase PaCO2 by 10 mmHg → increase [HCO3-] by 1 mEq/L

Change in pH = 0.008 x (35-PaCO2)

In Denver, where normal CO2 = 35 mmHg

197
Q

Equation for chronic respiratory acidosis and change in pH and [HCO3-]

A

increase PaCO2 by 10 mmHg → increase [HCO3-] by 4 mEq/L

Change in pH = 0.003 x (35-PaCO2)

In Denver, where normal CO2 = 35 mmHg

198
Q

How to determine if respiratory acidosis is acute or chronic?

A

Change in pH/change in pCO2 → either 0.008 (acute) or 0.003 (chronic)
Somewhere in between? → acute on chronic

199
Q

standard notation of ABGs

A

pH/CO2/pO2

200
Q

Determinants of ventilation (2)

A

1) Respiratory Rate
2) Tidal volume

*adjust in case of hypercapnic respiratory failure

201
Q

Determinants of oxygenation (4)

A

1) FIO2
2) Positive End Expiratory Pressure (PEEP)

*adjust in case of hypoxemic respiratory failure

202
Q

Positive end-expiratory pressure (PEEP)

A
  • used to achieve and maintain alveolar recruitment by limiting lung deflation at end expiration
  • Determinant of oxygenation

-Without PEEP patients can develop atelectasis (deflation of alveoli)
→ decreases effective alveolar/capillary surface area

Diffusion capacity and oxygenation directly proportional to SA available for gas exchange

**Used to maintain surface area in hypoxemia: more PEEP, more recruitment (up to a point)

203
Q

4 defining characteristics of ARDS

A

1) Diffuse bilateral pulmonary infiltrates
2) Occurs within one week of known clinical insult or worsening respiratory symptoms
3) Not fully explained by cardiac failure or fluid overload
4) PaO2/FIO2 ratio less than 300

204
Q

Most common causes of ARDS (5)

A

sepsis, pancreatitis, trauma, aspiration, transfusion (also fat embolism, amniotic fluid embolism)

205
Q

Severity of ARDS classified by PaO2/FIO2 with > 5 cm H2O PEEP:

mild, moderate, and severe

A

PaO2/FIO2 = 201-300 → mild, 27% mortality

PaO2/FIO2 = 101-200 → moderate, 32% mortality

PaO2/FIO2 = less than 100 → severe, 45% mortality

206
Q

Pathogenesis of ARDS

A
  • alveolar inflammation with increased permeability of pulmonary capillaries and recruitment of inflammatory cells (PMNs, cytokines)
  • Loss of alveolar/capillary barrier function
  • Loss of surfactant (increased intraalveolar fluid)
207
Q

Histopathology of ARDS

A

1) “hyaline membrane” formation
2) neutrophil influx
3) hemorrhage
4) type II cell hyperplasia
5) alveolar filling with proteinaceous edema
6) systemic inflammation often with extrapulmonary organ dysfunction or failure

208
Q

Treatment strategies to improve survival in ARDS (4)

A

1) Treat underlying cause of ARDS
2) Supportive care
3) Prone positioning in severe disease
4) Ventilator management

209
Q

Best ventilator management

A

survival advantage in ARDS patients ventilated with tidal volumes of 6cc/kg vs. 12cc/kg

Ventilator Induced Lung Injury → high tidal volume ventilation can worsen lung injury and systemic inflammation in ARDS patients

**before increasing a patient’s tidal volume based on ABG analysis, make certain that the patient does not meet criteria for ARDS - could be detrimental to patient

210
Q

Major determinants of site and severity of lung disease (3)

A

1) Dose = duration x concentration
2) Solubility
3) Particle size

211
Q

Effect of solubility on severity of lung disease

A

More water soluble → deposit in upper airway

Less water soluble → affect distal airways/bronchioles

212
Q

Effect of particle size on severity of lung disease

Particles > 10 microns → ?

Particles less than 10 microns → ?

Particles less than 2.5 microns → ?

A

Particles > 10 microns → filtered by upper airway

Particles less than 10 microns → respirable, penetrate deeply into lung

Particles less than 2.5 microns → affect small airways and alveoli

213
Q

What is the most important tool for evaluating occupational lung disease?

A

OCCUPATIONAL HISTORY

(chronology of jobs, location, name, years of employment)

job titles
specific exposures
specific duties
use of PPE
similar symptoms in co workers
214
Q

Two major categories of occupational lung disease

A

1) Airways diseases (obstructive)

2) Interstitial diseases (restrictive)

215
Q

Four types of airways disease

A

1) Occupational Asthma (immunologic)
2) Irritant Asthma aka Reactive Airways Dysfunction Syndrome (RADS)
3) Occupational Emphysema/COPD
4) Bronchiolitis (obstructive/constrictive)

216
Q

Occupational (Immunologic) Asthma

Presentation
Causes

A

**Isocyantaes (spray paint/autobody painting)

**Onset may be months to years after initial exposure

*Isocyanate exposure → new onset respiratory symptoms → high index of suspicion for occupational asthma

217
Q

Irritant asthma (Reactive Airways Dysfunction Syndrome, RADS)

Causes
Presentation

A

Causes: **Strong acids and bases (e.g. alkaline world trade center dust)

Presentation: **NO LATENCY - symptom onset within 24-48 hours of exposure

218
Q

Occupational Emphysema/COPD is typically caused by…

A

coal mine dust

silica (sand blasting)

219
Q

Five types of ILD

A

Pneumoconioses:

1) Asbestos related lung disease
2) Silicosis
3) Coal workers pneumoconiosis (black lung)

Other ILDs:

4) Chronic beryllium disease
5) Hypersensitivity Pneumonitis (Farmer’s Lung)

220
Q

Asbestos related lung disease

exposed groups?
signs on CXR?

A

Exposed groups: construction workers, shipyard/dock workers, mechanics

Malignant (mesothelioma)

**Non-malignant asbestos-related lung disease → pleural effusion, pleural thickening/calcifications/plaques
**CXR with PLEURAL PLAQUES → ASBESTOS
(WILL BE ON TEST)

221
Q

Silicosis

causes
presentation

A

Progressive, massive fibrosis

**Causes: mining, foundry work, sandblasting, oil and gas industry workers

Presentation: long latency (unless high-grade exposure), cough, SOB

222
Q

Chronic beryllium disease

A

*Granulomatous lung disease (indistinguishable from sarcoidosis) except that it is due to exposure and subsequent immune response to beryllium

223
Q

In regards to PIO2, what changes occur at high altitude

A

Higher altitude → lower barometric pressure

i. PB on everest is 253 → PaO2 = 25 mmHg → SaO2 = 50%
ii. Compared to PB of 630 in Denver and 760 and sea level

224
Q

Acute ventilator and cardiac compensation to high altitude (3)

A

Minutes-> hours
1. Increase CO, increase HR

  1. Increase VE (hyperventilation → decrease PaCO2)
    a. MOST USEFUL short term adaptive response to high altitude (increases hemoglobin saturation)
  2. Decrease SVR - systemic and brain vasodilation, pulmonary vasoconstriction ( → transient pulmonary HTN
225
Q

Chronic ventilator and cardiac compensation to high altitude (5)

A
  1. Increase VE (chronic reduced PaCO2 levels)
  2. Increase [Hb] - increase EPO, increase RBC mass (increase O2 carrying capacity)
  3. Structural change in Hb → altered affinity for O2 and left shift due to respiratory alkalosis → increases Hb O2 saturation
  4. Increase CO2 ventilatory response
    a. Acclimatized individuals have augmented hypoxic drive to breathe
  5. Increase capillary density and myoglobin in muscles
226
Q

Adaption to high altitude

A

genetic event that occurs over generations

1.Maximizes delivery of oxygen to tissues

227
Q

Major illnesses associated with high altitude (4)

A
  1. Acute mountain sickness
  2. High altitude cerebral edema (HACE)
  3. High altitude pulmonary edema (HAPE)
  4. Chronic Mountain Sickness (CMS)
228
Q

Acute mountain sickness

A
  1. Headache + at least 2 other symptoms after rapid ascent (fatigue/weakness, insomnia, poor appetite/nausea, malaise)
  2. Common at CO ski resorts
  3. “Tight box theory” - brain edema with hypoxia due to increased cerebral blood flow in restrictive box (skull)
229
Q

Treatment of acute mountain sickness

A

Symptoms usually resolve in uncomplicated AMS without treatment, can use analgesics to help headache

Symptomatic AMS → oral dexamethasone (corticosteroid) or oral acetazolamide (diuretic that causes respiratory alkalosis)

230
Q

Prevention of acute mountain sickness

A

a. Start day before, continue 1-2 days after ascent to high altitude
b. Acclimatize at lower altitude first!
c. Dexamethasone → steroid that blunts hypoxic induction of brain vessel permeability-inducing proteins
d. Acetazolamide → bicarbonate diuresis → metabolic acidosis) → increase VE → respiratory alkalosis
e. Ibuprofen → decrease headache

231
Q

High altitude cerebral edema

A

severe AMS, medical emergency

  1. Uncommon, but can recur so pt must avoid altitude
  2. AMS with ataxia or mental status change
232
Q

Treatment of HACE

A

Supportive: oxygen, descent, mechanical ventilation

b.IV dexamethasone

233
Q

High altitude pulmonary edema

A

noncardiogenic pulmonary edema, life-threatening form of AMS

  1. +/- signs of AMS
  2. Exuberant pulmonary HTN in response to acute hypoxia, lung capillary breakdown, with plasma/blood leakage into alveoli
    a. People who increase their pulmonary artery pressures more than others with exercise are more prone to HAPE
234
Q

Symptoms of HAPE

A

onset on 2nd day at altitude, rapid progression

a. Cough (pink frothy sputum)
b. SOB
c. Fatigue
d. Hypoxia, rales, infiltrates

235
Q

Treatment of HAPE

A

a. Immediate descent, supplemental O2
b. Vasodilators (lower PAP) - nifedipine, sildenafil, tadalafil
c. NOT DIURETICS

236
Q

Prevention of HAPE

A

a. Avoid high altitude
b. Pulmonary vasodilators (nifedipine, Tadalafil/Sildenafil)
c. Bronchodilatory, LABA (salmeterol) - increases clearance of water out of alveoli
d. Dexamethasone

237
Q

Chronic Mountain Sickness

A

polycythemia + pulmonary HTN/RV failure

  1. Occurs at > 10,000 feet
  2. Increase risk of stroke and heart failure
  3. Poor concentration
  4. Infants → lower birth weights, higher mortality, mothers also have increased rates of preeclampsia
238
Q

Diseases that cause problems at high altitude (3)

A

i. Lowered PaO2 at rest: Lung disease (not asthma), CHF, hypoventilation
ii. Limited minute volume: COPD, pulmonary fibrosis, morbid obesity
iii. Existing pulmonary HTN or left heart failure

239
Q

Clinical Syndromes Associated with Diving/Breath holding/Compressed gas breathing: (4)

A
  1. Pulmonary barotrauma
  2. decompression sickness (bends)
  3. Nitrogen narcosis
  4. Shallow water blackout
240
Q

Pulmonary barotrauma

A

increased pressure in airways can lead to extravasation of air along bronchial tree → Pneumomediastinum, Pneumothorax, Air embolism

241
Q

Pulmonary barotrauma is more common in (3)

A

a. Asthma increases risk of barotrauma because alveolar units that exhale more slowly expand and rupture during ascent
b. Anyone with lung blebs/cysts
c. Free dives (single breath, quick/deep)

242
Q

Decompression sickness

A

occurs with too rapid an ascent

1.Gas in supersaturated tissues can form bubbles as pressure decreases with surfacing → bubbles expand in tissues/blood causing organ dysfunction

243
Q

Symptoms of decompression sickness

A

confusion, MSK pain, dyspnea, stroke, coma, seizures, paralysis, death

244
Q

Treatment of decompression sickness

A

recompression or hyperbaric chamber) to drive gases back into dissolved state

245
Q

Nitrogen narcosis

A

occurs when diver breathes compressed air (>79% N2) at depths > 100 ft → increased N2 in tissues (including brain)

246
Q

Symptoms and treatment of nitrogen narcosis

A

Symptoms: bizarre behavior, unconsciousness, euphoria, confusion

2.Use helium at dives > 100 ft

247
Q

Shallow water blackout

A

hyperventilate to increase PaO2, and blow down PaCO2 before submerging → hypoxemia causes unconsciousness before dyspnea occurs

248
Q

Physics of diving

A

increase pressure with depth

  1. Lungs and the air in them are compressed with dive
    a. → increased density of gas due to compression → **increased resistive work of breathing
    b. → problem for people with existing airflow limitation (COPD, moderate/mild asthma exacerbation)
  2. Increased blood return to lungs (from squeezed limbs/abd) → decreased compliance, → increase in CO and central filling pressures
    a. increased pressure = decreased volume
    b. “Squeeze” = tissues displaced into space gas occupied at surface
    c. → Heart failure patients should avoid diving
  3. Increased depth = increased dissolved gases in tissues
    a. Inert gases (N2, helium) can form bubbles
249
Q

Differences between adult and pediatric pulmonary physiology (3)

A

1) Infant’s larynx and trachea are significantly smaller than an adult
2) Children have weaker muscles and different anatomy
3) Pediatric signs of respiratory distress are different

250
Q

Size of pediatric vs. adult airway

A

Infant’s larynx and trachea are significantly smaller than an adult

Narrowest part of pediatric airway just below vocal cords at level of cricoid cartilage (only complete ring of cartilage)

Narrowest part in adults is vocal cords

Decreases in airway radius results in significant increase in resistance and reduction in cross sectional area of pediatric airway

251
Q

Differences between adult and children pulmonary anatomy (5)

A

1) Children have weaker muscles (flat diaphragm, weak intercostals)
2) Larynx higher and more anterior
3) Epiglottis is floppy, large, touching soft palate
4) infants primarily breath through nose (facilitate suck/swallow/breathe)
5) Tongue is relatively large

252
Q

Pediatric signs of respiratory distress (4)

A

1) Lethargy
2) poor feeding
3) grunting
4) trouble gaining weight (due to chronic respiratory disease causing increased work of breathing)

253
Q

Signs/Symptoms of upper respiratory airway obstruction (5)

A

Stridor
+ 4 D’s of SEVERE obstruction = drooling, dysphagia, dyspnea/distress

NOT hypoxemia (because if you do, then it is because you are hypoventilation, and that is really bad)

254
Q

Laryngomalacia is the most common cause of _______ due to a problem during the _______ phase that causes what?

A

chronic stridor

Embryonic phase

→ cartilaginous support for supraglottic structures is underdeveloped

255
Q

Clinical features of laryngomalacia

A
  • Extrathoracic obstruction
  • Usually presents by 6 weeks
  • Worse with eating, crying, activity
  • Better prone
  • Often outgrown by 1-2 years old
  • If severe, requires surgery
  • Can cause OSA
256
Q

Tracheobronchomalacia is caused by a problem in the _______ stage resulting in what?

A

pseudoglandular stage (wk 6-16)

Intrathoracic obstruction

Cartilage of trachea is extra soft and collapses with expiration → problem with breathing out

257
Q

Symptoms of tracheobronchomalacia

A

Recurrent wheeze and hoarse, wet cough, recurrent illness

258
Q

Viral croup is the most common cause of…

Typically caused by what virus?

A

acute airway obstruction in children

Inflammation of entire airway and edema in subglottic space (larynx)

parainfluenza

259
Q

Symptoms of viral croup (4)

A

1) Barking cough
2) Stridor

3) *Fever (typically low grade)
4) *Cough in ABSENCE OF DROOLING favors dx of viral croup over epiglottitis

260
Q

Epiglottitis

A

Almost always caused by H. influenzae B

Inflammation and swelling of supraglottic structures (epiglottis, arytenoids) can develop rapidly and lead to life-threatening upper airway obstruction

261
Q

Signs/Symptoms of epiglottitis (5)

A

Sudden onset of:

1) high fever
2) dysphagia
3) drooling
4) inspiratory retractions
5) cyanosis

262
Q

Bacterial tracheitis

A

severe, life-threatening form of viral croup

Usually viral infection –> bacterial infection caused by staph aureus

Localized mucosal invasion of bacteria in patients with primary viral croup → inflammatory edema, purulent secretions, pseudomembranes

263
Q

Signs/symptoms of bacterial tracheitis

A

1) usually older kids
2) high fever
3) normal epiglottis with copious purulent tracheal secretions
4) unresponsive to croup therapy

264
Q

Bronchiolitis is the most common cause of…

typically caused by what virus?

A

lower airway obstruction

RSV

265
Q

Why is bronchiolitis worse in kids that are premature?

A

Premature kids →
1) decreased SA for gas exchange –> increased need for O2

2) thickened interstitium → decreased compliance → more significant complications

266
Q

Signs/Symptoms of bronchiolitis in kids

A

1) expiratory wheezing and crackles
2) acute onset tachypnea (rapid, shallow respirations)
3) retractions (to increase TV)
4) Grunting (attempt to keep airways open)
5) fever
6) hyperinflation

267
Q

Asthma in kids

A

1 reason for peds ER visits and hospitalizations

90% of the time is allergic

Diagnosis:
Recurrent symptoms of airway obstruction (cough, SOB, chest tightness)

Partial reversal of bronchospasm/symptom relief with bronchodilator

268
Q

Treatment of bacterial pneumonia in children:

0-3 months

3 months-5 years

> 5 years

A

0-3 months → IV ampicillin or aminoglycosides + hospital admission

3 month-5 years → oral amoxicillin

> 5 yrs → macrolide, amoxicillin or penicillin G

269
Q

Bronchopulmonary dysplasia

A

ARDS in first weeks of life –> decreased surface area for gas exchange

  • require O2 and mechanical ventilation
  • can cause persistent respiratory abnormalities
270
Q

Vicious cycle of bronchopulmonary dysplasia

A 
Insufficient functional surfactant
\+ Insufficient antioxidant defense mechanisms
\+ Structural immaturity
\+ Atelectasis
\+ Pulmonary edema

–> require mechanical ventilation

BUT mechanical ventilation can make this all worse

271
Q

Long term complications of bronchopulmonary dysplasia (4)

A

1) Abnormal oxygenation and ventilation at baseline
2) Trouble with viral illness or exercise
3) Possible need for oxygen/ventilation long term
4) Limited activity

272
Q

Findings in children with cystic fibrosis (7)

A

1) Greasy, bulky, malodorous stools
2) Failure to thrive
3) Focal sclerosis in liver
4) Failure of vas deferens to develop
5) Recurrent respiratory infectious (bronchiectasis, bronchiolitis)
6) Digital clubbing on exam
7) Sweat chloride > 60 mmol/L

CVPR (12 decks)

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