Pulmonary Flashcards

1
Q

COPD general info

A

two types: chronic bronchitis and emphysema
CB - clinical dx; chronic, productive cough with sputum for at least 3 months per year for at least two consecutive years.
E - pathologic dx w permanent enlargement of air spaces d/t destruction of alveolar walls
Both often coexist, pure dz of either rare
COPD 4th leading cause of death of US

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2
Q

COPD risk factors and causes

A
Tobacco smoke (90% of cases)
alpha 1 antitrypsin deficiency - risk worse w smoking
environmental factors (2nd hand smoke)
chronic asthma
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3
Q

COPD pathogenesis

A

Chronic bronchitis - excess mucus productions narrows airways (productive cough); inflammation and scarring in airways, enlargement in mucous glands, smooth muscle hyperplasia lead to obstruction.
Emphysema - destruction of alveolar walls d/t relative excess in protease (elastase) activity or relative deficiency of anti-protease (alpha 1 antitrypsin) activity in lungs. PMNs + macrophages release elastase and digest human lung.
Tobacco smoke increases # of activated PMNs and macrophages, inhibits antitrypsin, and incr oxidative stress on lung by free radical production.

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4
Q

COPD clinical features

A

Any combo of cough, sputum production, dyspnea, some patients may live sedentary lifestyles with few complaints, avoiding exertional dyspnea.
prolonged expiratory time
end-expiratory wheezes on forced expiration, decr breath sounds, inspiratory crackles
tachypnea, tachycardia
cyanosis
accessory respiratory muscle use
hyper-resonance on percussion
signs of cor pulmonale
chronic resp acidosis + compensatory metabolic alkalosis

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5
Q

COPD diagnosis

A

PFT - definitive diagnostic test
obstruction evident - decr FEV1, decr FEV1/FVC ratio < 0.70; incr TLC + incr residual vol + incr FRC = air trapping; decr vital capacity
GOLD staging: FEV1 => 80 of predicted value is mild disease.
FEV1 50% - 80% = moderate disease
30% - 50% = severe disease
< 30% = very severe disease

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6
Q

COPD HPI tips

A

Hx cardiopulmonary diseases
smoking history ( duration, intensity, current smoker)
family history (COPD, heart disease, asthma)
occupation (industrial dusts, fumes)
overall health
history of resp infections (frequency, severity)
pulmonary medications

pulmonary sxs: dyspnea, cough, sputum production, wheezing

clinical monitoring: serial FEV1, pulse ox, exercise tolerance

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7
Q

COPD treatment

A

smoking cessation most important - improvement in sxs, slows rate of decline, prolongs survival, does not completely reverse
1. inhaled anticholinergic drugs (ipratroprium bromide): bronchodilators
2. inhaled B agonists (albuterol): bronchodilators, provide sx relief, long-acting (salmeterol) for pts using frequently
OR combo of the two above
3. inhaled corticosteroids (budesonide, fluticasone): anti inflammatory
4. theophylline - controversial
5. oxygen therapy - improves survival and quality of life for those with chronic hypoxemia (PaO2 55 mmhg or O2 sat < 88% or PaO2 55-59 + polycythemia or cor pulmonale, despite max med therapy)
6. pulm rehab
7. vaccination
8. surgery

give systemic steroids and abx for acute exacerbations
BBs contraindicated in acute COPD

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8
Q

COPD tx guidelines

A

mild - mod dz: bronchodilator MDI +- low dose inhaled glucocorticoids
severe dz: above + continuous O2 (if hypoxemic), pulm rehab, triple inhaler therapy (long-acting B agonist, long-acting anticholinergic, inhaled glucocorticoid)
acute COPD exacerbation: bronchodilators, IV methylprednisolone then taper with oral once improved, abx (azithro, levoquin, doxy), supp O2 (90-93% goal), NPPV, intubate or mechanical vent if above doesn’t stabilize (incr RR, incr PaCO2, worsening acidosis)

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9
Q

COPD complications

A

acute exacerbations (d/t infxns, cardiac dz, noncompliance)
secondary polycythemia
pulm HTN and cor pulmonale

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10
Q

CAP gen info

A

Two types: community acquired and nosocomial
CAP
- occurs in community or within 72 hrs of hospitalization
- typical or atypical
MC bacterial pathogen: strep pneumoniae (60%) –> H. flu, reg flu, legionella spp
Nosocomial pna
- occurs during hospitalization after 72 hrs
- MC bacterial pathogen: gram neg rods (Ecoli, pseudomonas) and staph aureus
- if vitals entirely normal in OP, probability of pna < 1%
Two rec prevention methods
- influenza vaccine
- pneumococcal vaccine: >65 yo or young ppl at risk (heart disease, scd, etc)

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11
Q

Typical CAP: common agents, sxs, CXR

A

Common agents

  • strep pneumoniae (60%)
  • H flu (15%)
  • Aerobic gram-negative rods (6-10%) - klebsiella (& other enterobacteriaceae)
  • staph aureus (2-10%)

Symptoms

  • sudden shaking chills followed by fever
  • cough productive of thick, purulent sputum
  • pleuritic chest pain (suggests pleural effusion)
  • dyspnea

Signs

  • tachycardia, tachypnea
  • late inspiratory crackles, bronchial breath sounds, increased tactile and vocal fremitus, dullness on percussion
  • pleural friction rub (a/w pleural effusion)

Chest xray

  • lobar consolidation
  • multilobar consolidation indicates very serious illness

Most cases of CAP result from aspiration of oropharyngeal secretions bc majority of organisms that cause CAP are normal inhabitants of the pharynx.

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12
Q

Atypical CAP: common agents, sxs, CXR

A

Atypical pna - organisms not visible on gram stain & not curable on standard blood agar

Common Agents

  • mycoplasma pneumoniae mc
  • chlamydia pneumoniae
  • chlamydia psittaci
  • coxiella burnetti (Q fever)
  • legionella spp
  • viruses: influenza A or B, adenoviruses, parainfluenza virus, RSV

Symptoms

  • insidious onset - sore throat & headache 1st, fatigue, myalgias
  • dry cough (no sputum production)
  • fevers (chills are uncommon)

Signs

  • pulse-temp dissociation; nl pulse in setting of high fever
  • wheezing, rhonchi, crackles

CXR

  • diffuse reticulonodular infiltrates
  • absent or minimal consolidation
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13
Q

CAP diagnosis

A

1st differentiate lower resp tract infection from upper resp infection and other causes of cough.

  • nasal discharge, sore throat, ear pain predominates –> upper
  • lower tract infection suss –> differentiate btw pna and acute bronchitis (can’t just with clinical features), need CXR.

CXR, labs (cbc diff, BUN, Cr, glc, lytes or CMP) O2 sat, blood cultures, gram stain/culture, abx therapy)

PA and lat CXR required to confirm dx

  • interstitial infiltrates, lobar consolidation, and/or cavitation
  • sensitive; if findings not suggestive of pna don’t treat w abx
  • false negative cxrs w neutropenia, dehydration, infection w PCP, early dz < 24 hrs
  • after treatment, changes on CXR lag behind clinical response (up to 6 wks)

Sputum gram stain (everyone) and culture (hospitalized pts) with cap (low sensitivity + specificity, but done for antimicrobial resistance prob)
- good specimen > 25 [mns and < 10 epithelial cells

Special stains

  • acid-fast stain (mycobacterium spp) if TB suss
  • silver stain (fungi, p.carinii) for HIV/immunocompromised

Urinary antigen assay for legionella

  • very sensitive
  • antigen persists in urine for weeks (even after treating)

Consider two blood cultures

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14
Q

CAP pearls

A

Alcoholics –> klebsiella
Immigrants –> TB
Nursing home residents –> nosocomial pathogen
HIV + –> P. carinii, TB, more likely to have typical infxn
legionella –> organ transplant recipients, renal failure, chronic lung dz, smokers
- presents with GI sxs + hyponatremia

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15
Q

CAP treatment

A

Hypoxic or hypotensive –> hospitalize (can use PSI, CURB-65 admission if at least 2 points)

Uncomplicated CAP in <60yo, no comorbidities –> macrolide (azithromycin, clarithyromycin) or doxycycline first line

  • comorbidities –> FQ
  • > 60 yo, comorbidities, or abx tx in last 3 months –> resp FQ (levofloxacin, moxifloxacin) PLUS macrolide or augmentin

OP –> 5 day treatment (don’t stop until patient has been afebrile 48 hrs)
IP –> FQ alone or 3rd gen ceph + macrolide (ceft + azithro)

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16
Q

HAP treatment

A

tx tailored toward gram-neg rods
cephalosporins w pseudomonal coverage: ceftazidime or cefepime
carbapenems: imipenem
Pip tazo

Macrolides not used as single therapy

17
Q

CAP complications

A

Pleural effusion

  • > 50%, empyema infrequent
  • most w uncomplicated course & resolve w reg abx tx
  • thoracentesis if effusion sig > 1 cm on lat decubitus film. Send fluid for gram stain, culture, pH, cell count, glc, protein, LDH levels

Pleural empyema (infected, loculated pleural fluid)

  • 1-2% cases
  • requires chest tube drainage

Acute resp failure

18
Q

Pleural Effusion gen info

A

Caused by one of these mechanisms:

  1. incr drainage of fluid into pleural space
  2. incr production of fluid by cells in pleural space
  3. decr drainage of fluid from pleural space

if patient has minimal lung compromise –> pleural effusions well tolerated vs with lung dz may lead to resp failure.

Transudative effusions - pathophysiology d/t elevated capillary pressure in visceral or parenteral pleura (CHF), or decr plasma oncotic pressure (hypoalbuminemia)
Causes: CHF, cirrhosis, PE, nephrotic syndrome, peritoneal dialysis, hypoalbuminemia, atelectasis

Exudative - pathophys d/t incr permeability of pleural surfaces or decr lymphatic flow from pleural surface bc of damage to pleural membranes or vasculature. Any condition a/w infection or inflamm
- if suss, check pleural fluid for diff cell count, total protein, LDH, glc, pH, amylase, TGs, microbiology, cytology
Causes: bacterial pna, TB, malignancy, metastatic dz, viral infection, PE, collagen vascular dz

19
Q

Light’s criteria

A

Exudative effusions meet at least one of the following (transudates have none):
protein (pleural)/protein (serum) > 0.5
LDH (pleural)/LDH (serum) > 0.6
Pleural LDH > 2/3s ULN serum LDH

20
Q

Pleural effusion causes

A

CHF mc
PNA (bacterial)
Malignancies: lung (36%), breast (25%), lymphoma (10%)
PE
Viral diseases
Cirrhosis with ascites (hepatic hydrothorax)

21
Q

Pleural effusion clinical features

A

Symptoms

  • often asxs
  • dyspnea on exertion
  • peripheral edema
  • orthopnea, PND

Signs

  • dullness to percussion
  • decr breath sounds over effusion
  • decr tactile fremitus
22
Q

Pleural effusion diagnosis

A

Confirm presence/eval size with:

  1. CXR (PA Lat)
    - blunting of costophrenic angle
    - about 250 mL pleural fluid must accumulate before it is detectable
    - lat decubitus - more reliable than PA and lat cxrs for detecting small effusions & determine if free flowing or loculated
  2. CT chest - more reliable
  3. Thoracentesis
    - ind for eval of all new effusions; diagnostic 70%
    - can be therapeutic
    - PTX assoc complication, don’t perform on < 10 mm lat decub
23
Q

Pleural effusion treatment

A

Transudative effusions

  • diuretics and sodium restriction
  • therapeutic thoracentesis - only if massive + causing dyspnea

Exudative effusions - tx underlying dz
Parapneumonic effusions (effusion from pna)
- uncomplicated effusions: abx alone
- complicated or empyema: chest tube drainage, intrapleural inj of fibrinolytic agents (stetokinase, urokinase, TPA, to accelerate drainage)
- surgical lysis of adhesions

24
Q

Empyema causes

A

Def: pus within pleural space

  1. untreated exudative pleural effusions
  2. most cases d/t complication of bacterial pna, can be from other foci of infection I.e. mediastinitis, abscess
25
Empyema clinical features
those of underlying disease (pna)
26
Empyema diagnosis
CXR and CT scan
27
Empyema treatment
Aggressive drainage of pleura (thoracentesis) and abx therapy Infection is very difficult to eradicate, recurrence common, requiring repeated drainage For severe, persistent --> rib resection + open drainage
28
Pleural fluid pearls
elevated pleural fluid amylase: esophageal rupture, pancreatitis, malignancy milky, opalescent fluid: chylothorax (lymph) frankly purulent fluid: empyema (pus) bloody effusion: malignancy Exudative effusions primarily lymphotic: TB pH < 7.2: parapneumonic effusion or empyema glc < 60: rheumatoid arthritis, or empyema, TB, esophageal rupture, malignancy, lupus
29
NPPV
NPPV delivered as BiPAP or CPAP BiPAP: can be set at separate inspiratory and expiratory pressures (insp > exp) Both can be given w nasal mask or full-face mask NPPV ind in pts with impending resp failure in an attempt to avoid intubation and mechanical ventilation Success rates highest in pts w hypercapnic resp failure (COPD) NPPV should not be used for life support ventilation, only to temp support the patient's own spontaneous breathing To use NPPV: pt must be neurologically intact, awake and cooperative, able to protect airway, If no improvement seen, bipap should be discontinued and conventional ET intubation and mech vent initiated.
30
Pulmonary hypertension gen info
Def: mean pulmonary arterial pressure > 25 mmHg at rest Can be due to multiple pathophysiologic processes: - passive d/t resistance in pulm venous system (LHF, mitral stenosis, atrial myxoma) - hyperkinetic (L to R cardiac shunts like ASD, PDA) - obstruction (PE, pulm artery stenosis) - pulmonary vascular obliteration (collagen vascular dz) - pulm vasoconstriction (chronic hypoxemia, COPD, OSA) Classification: Group 1: pulmonary arterial hypertension - idiopathic, familial, veno-occlusive dz, connective tissue disorders, congenital shunting, HIV, drugs - abnl incr in pulm arteriolar resistance --> thickening of pulm arteriolar walls --> worsens pulm HTN --> further wall thickening --> vicious cycle - cause is unknown; young or middle-aged women - poor prog; mean survival 2-3 yrs from dx Group 2: left heart disease - 2ry to any cause of LHF; mitral stenosis, MR Group 3: lung disease and/or chronic hypoxemia - ILD, COPD, OSA, etc Group 4: chronic thromboembolic disease - recurrent PE (many pts do not have sx of PE), including non thrombotic etiologies (tumor emboli) Group 5: misc - pulm vascular compression; tumors, lymphadenopathy; sarcoidosis, langerhans cell histiocytosis, etc
31
Pulmonary hypertension clinical features
``` Symptoms DOE Fatigue Chest pain - exertional Syncope - exertional (with severe dz) ``` Signs Loud pulmonic component of 2nd heart sound (P2) and subtle lift of sternum (sign of RV dilatation) RV failure: JVD, hepatosplenomegaly, ascites, peripheral edema
32
Pulmonary hypertension diagnosis
ECG: RV hypertrophy, R axis deviation, R atrial abnl CXR: enlarged pulm arteries w/w/o clear lung fields Echo: dilated pulm artery, dilatation/hypertrophy of RA and RV, abnl movement of IV septum Right heart cath: required for confirmatory dx - incr mean pulm artery pressure > 25 mmHg
33
Pulmonary hypertension treatment
If pulm HTN 2ry to another disease process then tx underlying disease vasoactive agents used in group 1 PAH; right heart cath with trial of vasodilators Vasoactive agents may lower pulm vascular resistance: inhaled NO, pde5 inhibitors (sildenafil), oral CCBs, prostacyclins (epoprostenol), endothelin receptor antagonists (bosentan) Many require home O2, diuretics, +- inotropes (digoxin) Lung transplantation in qualified patients
34
SIRS
SIRS: 2 or more; Fever > 38C or hypothermia <36C Hyperventilation (rate > 20 bpm) or PaCO2 < 32 mmHg Tachycardia > 90 bpm Incr WBC count (>12, <4, or >10% band forms) Sepsis SIRS + suspected source of infection Septic shock hypotension induced by sepsis, persisting despite adequate fluid resuscitation MODS altered organ function in an acutely ill patient, usually leading to death