Pulm Week 3 Flashcards
Pneumonia
inflammation of the parenchyma of the lung (alveoli) and accumulation of abnormal alveolar filling with fluid of lung tissue
Physical exam findings of pneumonia
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)
Who should get blood and sputum cultures?
Get blood and sputum cultures for inpatients or patients with healthcare associated risk factors
-Treat out patients empirically and follow for improvement
Pathogenesis of pneumonia
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
Community acquired pneumonia (CAP)
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
Hospital (Nosocomial) acquired pneumonia (HAP)
PNA > 48 hrs after hospital admission
Ventilator associated pneumonia (VAP)
PNA > 48-72 hrs after endotracheal tube intubation
Healthcare-associated pneumonia (HCAP)
PNA in a non-hospitalized patient with extensive healthcare contact
Hemodialysis, nursing home, IV therapy, wound care, IV chemo
Typical bacteria that cause community acquired pneumonia (7)
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
Atypical bacteria that cause community acquired pneumonia (3)
10-20% of CAP
1) Legionella species
2) Mycoplasma pneumoniae
3) Chlamydia pneumoniae
Characteristics of HAP/VAP/HCAP Organisms
- 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)
Gram negative (5) and gram positive (1) pathogens that cause HAP/VAP/HCAP
Gram negative pathogens: “SPACE”
1) Serratia
2) Pseudomonas
3) Acinetobacter
4) Citrobacter
5) Enterobacter or Escherichia coli
Gram positive pathogens:
1) MRSA
Outpatient treatment of CAP duration and abx (3)
5 day therapy
Macrolide (azithromycin) or Doxycycline
Respiratory fluoroquinolone (levofloxacin)
Inpatient, Non-ICU treatment of CAP (2)
Respiratory fluoroquinolone
or
Beta-lactam + Macrolide
Inpatient, ICU treatment of CAP (2)
Beta-lactam + Macrolide
or
Beta-lactam + Respiratory fluoroquinolone
Consider anti-MRSA therapy
HCAP/VAP/HAP Treatment duration
7-8 day therapy (longer for pseudomonas/MRSA)
Critical to de-escalate therapy based on culture data and clinical response in 48-72 hours
HCAP/VAP/HAP Treatment: ______ + _______ + ________
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
Epidemiology of influenza
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
Transmission and incubation of influenza
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)
Pathogenesis of influenza
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
Influenza A
(H1,2,3 + N1,2) has more antigenic shift (major changes in glycoproteins)
Antigenic shift → epidemics and pandemics
Influenza B
only has antigenic drifts (minor changes in glycoproteins)
Antigenic drift → localized outbreaks
Clinical features of influenza infection
Abrupt onset of fever, headache, myalgias and malaise
Cough, nasal congestion, sore throat
Pharyngeal hyperemia, lymphadenopathy
Complications associated with influenza infection (4)
Primary IFN Pneumonia
Secondary bacterial pneumonia
Myositis, rhabdomyolysis
CNS involvement
Treatment of influenza
Give within 48 hours of illness (neuraminidase inhibitors - oseltamivir, zanamivir)
Starling resistor model in upper airway collapse
- P-upstream > P-downstream > P crit then there is no flow limit and tube will stay open
- Pus > Pcrit> Pds → point of narrowing but not complete collapse
a. Physics of snoring - 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
Effect of obesity on upper airway
fat deposition in tongue itself and neck → narrowing of oropharynx (only becomes a problem during sleep)
Effect of sleep on upper airway
lose a lot of protective mechanisms when you sleep (decreased tonic output, decreased output from inspiratory premotor neurons, and decreased reflex stimulation, higher threshold)
Defense against airway collapse (3)
- 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 - 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 - 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
Prevalence of snoring in men and women
44% men 28% women
Prevalence of upper airway resistance syndrome
9% in population
Prevalence of sleep apnea syndrome
a. 4% of men, 2% of women
b. Obstructive: 85%
c. Mixed or Complex: 14%
d. Central: less than 1%
Cheyne-Stokes respiration
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
Complications of sleep disordered breathing
primarily cardiovascular and motor vehicle crash
Clinical deatures of obstructive sleep apnea syndrome
- More common in men and as they age until 60s or 70s
- PMH: chronic rhinitis, acromegaly, neuromuscular disorder, amyloidosis, upper airway anatomic abnormalities, genetic syndromes (e.g. Downs)
- Family History: first degree relative with OSA
- Social history: smoking, alcohol, obesity
- Medications: sedative-hypnotics, opioids
Symptoms of obstructive sleep apnea syndrome
excessive daytime sleepiness, snoring, memory loss, decreased concentration, decreased libido, irritability, attention deficit (children), hyperactivity (children), nocturia or enuresis
Diagnosis of obstructive sleep apnea
- Epworth sleepiness scale
- 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 - 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
Treatment of obstructive sleep apnea (9)
- general measures- sedative avoidance, smoking cessation
- weight reduction
- positional therapy
- oxygen therapy
- pharmacotherapy
- PAP
- Oral devices
- Upper airway surgery
- Nerve stimulation
Positive airway pressure (PAP)
Mechanical solution to mechanical problem
Helps patient to overcome critical airway pressure
Oral devices (2)
- Tongue Retainer - holds tongue in anterior (forward) position
i. For patients with compromised dentition - Mandibular repositioner - advances mandible (and tongue) forward
i. Contraindications: compromised dentition, TMJ dysfunction - Billy’s penis
Upper airway surgery for obstructive sleep apnea (4)
- Tracheostomy: percutaneous tracheal opening distal to pharynx to bypass area of upper airway obstruction
i. Indicated for severe life-threatening OSA - 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
- UvuloPalatoPharyngoPlasty (UPPP): excision of uvula, posterior soft palate, redundant pharyngeal tissue, and tonsils
i. Rarely effective - high recurrence of OSA - Tonsillectomy and adenoidectomy: remove tonsils and enlarged adenoids (best for children with OSA)
Nerve stimulation for OSA
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
Risk factors of lung cancer (8)
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
Non-small cell lung cancer
87% of cases
1) Squamous cell carcinoma
2) Adenocarcinoma
3) Large Cell
Squamous cell carcinoma
general info
25% of cases
**strongly linked to smoking
Squamous cell carcinoma histopathology (3)
1) PROXIMAL/CENTRAL squamous metaplasia of bronchial epithelium
2) Usually >3 cm in diameter
3) Keratin pearls (stain + for keratin)
Squamous cell carcinoma (genetic mutations)
p53, Rb, p16
No proven genomically targeted therapies
Adenocarcinoma general info
40% of cases
**most common type in women and non smokers
**subclass is bronchioalveolar carcinoma, insitu
Adenocarcinoma histopathology (3)
1) PERIPHERAL cancer
2) Cells attempt to form gland like structure
3) stain + for mucin
Adenocarcinoma genetic mutations (3)
1) K-Ras
2) EGFR
3) EML-4-ALK
Large cell carcinoma
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
Small cell carcinoma general info
13% of cases
- highly aggressive
- strongly linked to smoking
- metastasizes widely (especially to brain)
- very bad prognosis
Small cell carcinoma histopathology (5)
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
Characteristics that define solitary pulmonary nodules (5)
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
Goals of solitary pulmonary nodule evaluation (3)
1) Expedite resection of potentially curable lung cancer
2) Minimize resection of benign nodules
3) Morbidity and mortality of nodule evaluation is 5-10%
Evaluation of solitary pulmonary nodules
- 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
Presenting symptoms of lung cancer
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)
Tests to diagnose lung cancer (5)
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
Staging of small cell lung cancer
Limited disease (25-30%) - limited to ipsilateral hemithorax (including contralateral mediastinal nodes)
Extensive disease (70-75%) - tumor extends beyond hemithorax (including pleural effusions)
Staging of NSCLC
TMN staging
tumor size, nodal involvement, presence or absence of metastases
T0
Tis
T1a
T1b
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)
T2a
T2b
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
T3
T4
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
N0
N1
N2
N3
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
M0
M1a
M1b
M0 = no distant metastases
M1a = separate tumor nodules in contralateral lobe, tumor with pleural nodules, or malignant pleural or pericardial effusion
M1b = distant metastasis
Genetic alterations in non-small cell lung cancer (4)
1) Epidermal Growth Factor (EGFR/ERB-1)
2) Her2/neu (ERG-2)
3) Vascular Endothelial Growth Factor (vEGF) over expressed
4) Ras mutations
Epidermal Growth Factor (EGFR) and treatment of EGFR NSCLC
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
Her2/neu (ERB-2) and treatment of Her2 NSCLC
10% NSCLC
Drugs available = trastuzumab (herceptin)
Vascular Endothelial Growth Factor (vEGF) and treatment of vEGF NSCLC
Over expressed
Drugs available = bevacizumab (Avastin)
Ras mutations
2-30% NSCLC, adenocarcinoma
Associated with resistance to tyrosine kinase inhibitors (TKIs, EGFRi)
Hoarseness
abnormal voice changes, breathy, raspy, strained, weak
Dysphonia
general alteration of voice quality (usually laryngeal source)
Dysarthria
defect in rhythm, enunciation, articulation (usually neurological or muscular source)
Stridor
large airway noise from obstruction
Inspiratory vs. Expiratory vs. Biphasic stridor
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
Sertor
snoring sound from nose, nasopharynx, throat
Causes of hoarseness (top 2 plus a few others)
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
When should a patient see an otolaryngologist?
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
5 layers of vocal folds
1) Epithelium
2) Superficial lamina propria
3) Intermediate lamina propria
4) Deep lamina propria
5) Vocalis muscle (medial thyroarytenoid)
Components of voice production (3)
1) Source (pulmonary/infraglottic)
2) Vibratory production (larynx/intrinsic muscles, extrinsic muscles)
3) Resonance (supraglottic and oral phase)
Components that generate source airflow
1) diaphragm
2) intercostal muscles
3) tracheobronchial tree, lungs, thorax
4) abdominal support system
Effect of ANS on voice
ANS plays role in mucus production, voice stability → B-blockers
Fine muscular control at risk with sympathetic stimulation or when a neurological conditions exists
Diaphragm and voice production
inspiratory force and fine regulation of singing
Abdominal muscles and voice production
maintains efficient, constant power source and inspiratory-expiratory mechanism
Extrinsic muscles and vibratory production
- 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
Cartilages of larynx (3)
Thyroid, cricoid (only one that is a complete ring), paired arytenoids
Intrinsic muscles of larynx and their function
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)
Supraglottic/oral phase and resonance
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
Central innervation of vocal folds
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)
Major causes of hoarseness: (10)
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
Laryngopharyngeal Reflux
Escape of stomach acids from stomach into esophagus through laryngoesophageal sphincter
May reach larynx, oral cavity, and lungs
Symptoms of Laryngopharyngeal Reflux
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
Why do we cough?
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
Afferent pathway activation of cough
-which 3 types of nerves?
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
Rapidly adapting receptors (RARs) and Slowly adapting stretch receptors (SARs)
highly sensitive to mechanical stimulation (bronchial obstruction, lung inflation)
C-fibers
highly sensitive to noxious chemical stimuli
Efferent pathway of cough (4 phases)
1) Inspiratory phase
2) Compressive phase
3) Expiratory phase
4) Relaxation phase
Inspiratory phase of cough
inhalation ends before closure of glottis
Compressive phase of cough
thoracic and abdominal muscles contract against a fixed diaphragm (e.g. Valsalva) → intrathoracic pressure increases
Expiratory phase of cough
glottis opens, air rapidly expelled
Relaxation phase of cough
chest wall and abdominal muscles relax
Acute cough
lasts less than 3 weeks
-identify if life threatening or not
Life threatening causes of acute cough
pneumonia, severe asthma or COPD, pulmonary embolism, heart failure
Non-life threatening causes of acute cough
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)
Upper respiratory tract infection (URI)
-treatment?
“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
Lower respiratory tract infection (Acute bronchitis)
- 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
Subacute cough
-causes?
lasts 3-8 weeks
Post-infectious:
- Pneumonia
- Pertussis
- Bronchitis
- New onset exacerbation of UACS, Asthma, GERD, Bronchitis
Non-post infectious –> treat as chronic cough
Four most common causes of chronic cough
1) Upper Airway Cough Syndrome
2) Asthma
3) GERD
4) Non-Asthma Eosinophilic Bronchitis
