Final Flashcards
Time difference b/t Acute and Chronic Cough
Acute cough < 3 wks
Chronic cough > 3 wks
Be sure to consider non-pulmonary manifestations, particularly alarming sx like weight loss / fatigue / appetite loss.
Also, be sure to do a thorough exam of lung fields to listen for adventitious or absent sounds.
Acute cough DDX:
Viral infection:
Viral infection:
- Rhinoviruses, coronaviruses, RSV (Respiratory syncytial virus) all most frequent.
- Cough typically starts day 4 or 5
- CXR is a low-yield screen, reserve for elderly or immunocompromised.
Acute cough DDX:
COPD and asthma exacerbations:
Viral/bacterial/allergic/pollution & Pertussis
COPD and asthma exacerbations:
- Viral/bacterial/allergic/pollution
- Consider tx w/ abx only if bad SOB, change in amt or character of sputum
- Allergic rhinitis leading to post-nasal drip
Pertussis in children:
What to look for?
- Suspect (and test for) pertussis in children with barking cough and/or vomiting after cough episode
- Check w/ local health dept to see if there is a current outbreak
kids with lingering wet cough (3-4 wks):
What to look for?
*Lingering wet cough (3-4 wks), suspect bacterial etiology
In particular, non-B Hemophilus influenza is a common contributor (Pediatrics, 2012)
Non-B Hemophilus influenza
Kids w/Lingering wet cough (3-4 wks),
Common suspect in bacterial etiology
Acute cough DDX:
- Viral infection
Rhinoviruses, coronaviruses, RSV most frequent
Cough typically starts day 4 or 5
CXR is a low-yield screen, reserve for elderly/immunocompromised - Allergic rhinitis leading to post-nasal drip
- COPD and asthma exacerbations
viral/bacterial/allergic/pollution
Consider tx w/ abx only if bad SOB, change in amt or character of sputum - Pertussis
Chronic cough DDX:
- Note that occult lung CA rarely presents w/ cough
- Up to 60% have multiple etiologies
- Postnasal drip: Most common cause in adults
- Asthma: Most common cause in children
- GERD: The first three = 90% of non-smokers w/ cough
- Chronic bronchitis
- ACE inhibitors
- Bronchiectasis: 4% or less of cases
- Note that occult lung CA rarely presents w/ cough
- Up to 60% have multiple etiologies
Most common cause of Chronic cough in adults?
Postnasal drip: Most common cause in adults
Most common cause of Chronic cough in children?
Asthma: Most common cause in children
T/F: Occult lung CA presents w/ cough.
False: Occult lung CA rarely presents w/ cough
Dx of a solitary pulmonary nodule definition and Clinical dilemma.
*Discrete, well-marginated, rounded opacity <= 3 cm in diameter (must be > 1 cm to be visualized by CXR)
- Completely surrounded by lung parenchyma
- W/o atelectasis or pleural effusion
- Patient is asymptomatic
- Clinical dilemma: is the nodule benign (like the majority) or malignant
- If malignant, survival at 5 yrs from early surgery is 70% or greater
*Risk of malignancy increases w/ age < 40: 3% 40-49: 15% 50-59: 43% 60+: >50%
Pulmonary nodules
Age Risk?
Increased and decreased risk of malignancy?
*Risk of malignancy increases w/ age < 40: 3% 40-49: 15% 50-59: 43% 60+: >50%
Increases risk of malignancy:
Hx of other cancers (so for metastatic spread)
Hx of smoking
Occupational risks (e.g., asbestos)
Decreases risk of malignancy:
Hx of TB
Hx of pulmonary mycosis
Residence in or travel to area with high prevalence of either condition
Pulmonary nodules:
Using imaging to ddx Benign vs. Malignant
- Benign: Calcification or cavitation
- ——–(> 18 mos is probably benign)
- Malignancy: Irregular border
- ———(> 4 cm very likely to be malignancy)
Infectious: Doubling Time (growth of 26%) in less than one mo.
PET scan may be used to confirm:
Has low sensitivity for slow growing cancers
Pulmonary nodules biopsies:
*Bronchoscopy
Less invasive
Often inconclusive, esp w/ smaller lesions
*Transthoracic needle aspiration
More likely (but still misses frequently) gets a definitive dx
Rate of pneumothorax is 25%.
Pulmonary nodules Management:
*Lesions w/ typical benign features:
Calcification patterns, lack of growth over 2+ yrs
No further workup
*Lesions w/ high suspicion for malignancy
> 4 cm, clear evidence for growth, previous malignancy
Refer for immediate surgical excision
Croup (laryngotracheitis) : Key features
- Inspiratory stridor
- Cough - described as “seal’s bark” or “brass bell”
- —-> = hallmark among infants and young children! - Hoarseness = predominates in older children and adults (Less bark bc airway is larger)
- Subglottic swelling
Croup (laryngotracheitis ) Causes:
Mostly Viruses:
Most common:
Parainfluenza virus 1-2—>Fall
Parainfluenza virus 3 —->Spring
Frequent:
Influenza A & B -»» Winter
RSV (Respiratory syncytial virus)—–> Winter & Spring
( RSV more common in Bronchiolitis)
Croup (laryngotracheitis) Age of onset:
- 3 mo to 3 years of age (After = more hoarseness)
- Most common age of peak incidence: 6-24 months
* ***Rare beyond 6 years of age
*Smaller airways are prone to greater degrees of obstruction from any inflammation of the lining membranes
“Bacterial croup” (Bacterial Tracheitis)
Age 4-8 yo
(Entire respiratory tube involved-DANGER)
Bacterial infection of the subglottic trachea, resulting in a thick, purulent exudate»_space; symptoms of upper airway obstruction
Croup PE (laryngotracheitis)
- Inspiratory stridor
- Retractions: Intercostal, Suprasternal, supraclavicular, substernal
- Respiratory distress
- Inc RR, (no more than 50bpm)
* bronchiolitis = resp. 80-90bpm** - Auscultation: Prolonged inspiration, coarse crackles; ———->Expiration: wheezing & rhonchi
- Cyanosis of the lips and nail beds
- No imaging or Labs
Croup (Naturopathic support)
- Humidifier, steamy bathroom (15 min.)
- Cool air: drive in car w/windows open, walk outside, stand in front of freezer.
- Vitamin C 50 mg x age in years, twice a day
- Immune modulators, antivirals, expectorants:
(sambucus, Echinacea, astragalus, lobelia, glycerrhiza, melissa, viburnum, verbascum, inula, hyssop) - Homeopathic Tx (Spongia, Pulsatilla, Drosera, Ant-t)
Conventional Treatment For Croup
No A/b=virus
- Corticosteroids->Given when Barking & showing accessory muscle use. (Oral)
- Nebulized epinephrine (Very severe cases in ER while waiting for Oral steroids to take effects)
Bronchiolitis Presentation
- M/C season?
- Upper or Lower?
- Age?
- Infxn = seasonal (outbreaks = primarily from November to April (Winter and Spring), (peak in January or February)
- Acute viral LOWER resp. tract illness of children
* *****(Vs. Croup or epiglottitis = UPPER resp. tract) - Children < 2 years old
Bronchiolitis sx’s
More than 2yo , won’t have these signs
Symptoms from acute inflammation of the airways:
- Acute onset of wheezing
- Hyperinflation
- Tachypnea (almost always present in bronchiolitis)
Younger than two months: >60 breaths/min
Two to 12 months: >50 breaths/min
One to 5 years: >40 breaths/min
≥5 years: >20 breaths/min
Etiology of Bronchiolitis
virus type?
Duration?
Peak incidence?
- RSV (Respiratory syncytial virus)- accounts for 60-85% of bronchiolitis cases (Bronchiolitis)
***(Parainfluenza virus 3 - next M/C (Usually in CROUP)
- Sx’s resolve over 1-2 weeks (Median duration = 12 days)
- Peak incidence = 6-12 mo (less than 1 yr of age = most severely affected)—> 80% of bronchiolitis occurs within the 1st year
Bronchiolitis Risk Factors:
- Peak: January/February
- Boys 1.5x more likely
- Pre-maturity most common risk factor
- Congenital heart defect
Bronchiolitis Clinical findings:
Hx & PE
History:
- Community outbreak of RSV
- < 12 months old
- No prior episode of wheezing
- Risk factors (prematurity, CardioV or Lung dz, immunodeficiencies)
PE:
- Rhinorrhea,
- nasal congestion,
- low grade fever 50% children,
- cough,
- tachypnea,
- tachycardia,
- nasal flaring,
- expiratory grunting,
- chest retractions, or
- accessory muscles for respiration,
- hyperinflation of the lungs (Increased diameter of chest,
- hyper resonance on percussion)
Bronchiolitis Radiographs
- Patchy atelectasis
- B/L peribronchial infiltrations w/Air bronchographs
- Hyper-inflation of the lungs w/flateening of diaphragm
Management of Bronchiolitis
- The AAP recommends bronchodilators should not be routinely used in the management of bronchiolitis,
- –>but a carefully monitored trial of alpha- or beta-adrenergic agents is an option (but they are very commonly used—I use them as well) - Supportive care
- Nasal suctioning (Nose Frida)
- Positioning of the infant upright
- Adequate rest
- Hydration
Conventional treatment of Bronchiolitis
- Corticosteroids—if airway inflammation is severe
- Anti-virals (Inhaled ribavirin)–>RSV
- PREVENTION- ‘Synagis’ Vaccine for high risk premature infants (Cost is $900 per dose->monthly)
Bronchiolitis Naturopathic support
Same as Croup:
1. Humidifier, steamy bathroom (15 min.)
2. Cool air: drive in car w/windows open, walk outside, stand in front of freezer.
3. Vitamin C 50 mg x age in years, twice a day
4. Immune modulators, antivirals, expectorants:
(sambucus, Echinacea, astragalus, lobelia, glycerrhiza, melissa, viburnum, verbascum, inula, hyssop)
5. Homeopathic Tx (Spongia, Pulsatilla, Drosera, Ant-t)
Bronchiolitis sequelae
IF they are hospitalized->Airway have been remodeled->May develop Asthma
A frequent sequelae of bronchiolitis, especially that caused by RSV, is recurrent wheezing, which occurs in 30-50% of children who are hospitalized for bronchiolitis.
Probiotic effects in kids w/cold sx’s
Children age 3-5 were given probiotics twice daily for 6 months
- fever incidence reduced by 72.7%
- coughing incidence reduced by 62.1%
- rhinorrhea incidence reduced by 58.8%
- Fever, coughing, and rhinorrhea duration was decreased significantly, relative to placebo, by 48%
- Antibiotic use incidence was reduced, relative to placebo, by 84.2%
Pertussis epidemiology:
Vaccines:
Morbidity:
DTaP under age 7,
TDaP for older 7yo
Infants younger than 6 months (90% of deaths-morbidity)
Conclusion: Tdap protection wanes within 2 to 4 years. Lack of long-term protection after vaccination is likely contributing to increases in pertussis among adolescents.
Younger the better! (vaccine efficacy-bad in teens)
3 stages of pertussis
First: Catarrhal stage (Most spreading-no big signs)
- 7-20 days after exposure
- Nonspecific URI sxs: rhinorrhea, lacrimation, mild cough, conjunctival injection
- This stage lasts approximately 2 weeks
Second: Paroxysmal stage (Sig cough-spastic cough)
- Characteristic intermittent dry hacking cough, with repetitive forceful coughs, inspiratory whoop
- Between attacks, patient seems comfortable
- Younger infants: gagging, gasping, apnea, bradycardia, cyanosis
Third: Convalescent stage
Diminishing severity and frequency of paroxysms
Intermittent coughing x weeks-months
Pertussis:
Clinical picture in infants < 6 months old
- Catarrhal
- Paraxysmal
- Complication
- Short or absent catarrhal stage:
- —-> Infant can appear deceptively well w/no fever, watery coryza, sneezing, and a mild cough - Paroxysmal stage:
- —->Characterized by gagging gasping, eye bulging, vomiting, cyanosis & bradycardia or tachycardia if illness is severe
- —->(cough may or may not be paroxysmal) - Complications:
- —->Apnea, seizures, respiratory distress, pneumonia and pulmonary hypertension, hypotension/shock, renal failure, and death - Hx of close contact (usually a family member, often the mother) with a prolonged cough and no fever
Pertussis:
Contagiousness
- Most contagious during the catarrhal stage and during the first two weeks after the onset of coughing.
- Protracted illness: Contagious (less) for at least 21 days —–>or until 1 wk after antibiotics initiated—i.e. can go back to school after that time.
Pertussis:
treatment
- Early treatment (e.g., during the first seven days of sx’s) may decrease the severity of sx’s
- —>Most patients don’t seek med. care until the paroxysmal phase, which occurs 1-2 weeks after onset.
**Antibiotics still necessary to stop the spread of the illness, but will not change the clinical course when started in the paroxysmal phase
Pertussis Testing:
PCR test (Nasalpharyngeal swab-in an inch thru their nose-20 seconds) In office
*Better than culture
Pertussis Clinical diagnosis:
Pertussis can be diagnosed as “probable pertussis” w/o lab testing in pts w/cough illness lasting ≥ 2 weeks w/o a more likely dx & at least one of the following sx’s:
- Paroxysms of coughing
- Inspiratory whoop
- Post-tussive vomiting
- Apnea, with or without cyanosis (Infants <1 year only)
***“Confirmed” if pt had contact w/a lab-confirmed case of pertussis & “probable” if pt has not had such contact.
Suspect pertussis (regardless of vaccination status):
Infants < 4 mo’s w/a cough illness, usually w/o sig. fever, who have:
- Cough that is not improving (of any duration); the cough may or may not be paroxysmal
- Rhinorrhea w/nasal discharge remains watery
- Apnea, seizures, cyanosis, vomiting, or poor weight gain
- Leukocytosis with lymphocytosis (WBC count ≥20,000 cells/microL with ≥50 percent lymphocytes)
- Pneumonia
Suspect pertussis (regardless of vaccination status):
Infants ≥ 4 mos & kids w/a cough illness, usually without sig. fever who have:
- Paroxysmal nonproductive cough of ≥ 7 days duration (with or without a whoop or post-tussive vomiting)
- Cough illness associated with rhinorrhea in which the nasal discharge remains watery
- Cough illness with whoop
- Cyanosis
- Sweating episodes b/t paroxysms
Why give Tdap in pregnancy for pertussis?
- Bc majority of infants w/pertussis are exposed from parents.
- Greatest morbidity & mortality occurs in infants that are either too young to get the DTaP vaccine, or have not completed the series yet.
- Transplacental transmission of pertussis antibodies provides “passive protection” against pertussis for the first few months of a baby’s life.
- Vaccination in the third trimester provides the highest level of antibodies for baby.
- Cord blood tested in infants whose mother received a Tdap 2 or more years before delivery had minimal antibody levels.
- The recommendation is that all pregnant women receive a Tdap vaccine in EACH pregnancy
Pulmonary Embolus:
Classic presentation:
S/Sx: dyspnea, pleuritic chest pain, apprehension, cough, tachypnea, rales, fever
Patients may complain of vague sx for weeks prior to death from PE
Pulmonary Embolus Risks:
Inherited vs. Acquired
- Inherited: Factor V leiden mutation, prothrombin mutation, deficiency of protein C or S
- Acquired: age, malignancy, anti-phospholipid abs, meds (OCP/HRT), DVT, surgery, trauma, pregnancy
Pulmonary Embolus:
“Well’s PE score”
Clinical signs--->3 Alt. Dx Unlikely-->3 Hrt rate >100-->1.5 Immobilization prev. 4 days--->1.5 Prev. DVT/PE--->1.5 Hemoptysis--->1 Malignancy (tx last 6 mo)--->1 ------------------------------------------------------------------------------- PE less likely = less than 4 pts PE likely = More than 4 pts
Pulmonary Embolus Diagnosis
- CT pulmonary angiography is gold standard
**V/Q (ventilation/perfusion) diagnostic:
Inc’d ventilation relative to perfusion = alveolar deadspace -respiration/cardio – PE, capillary prob, pneumothorax, shock
Decreased VQ indicates shunting - Resp etiology– COPD, asthma, atelectasis, ARD
**Can see abnormalities on CXR: wedge shaped infiltrate
Pulmonary Embolus Management
- Over 5 on dx algorithm: immediate urgent workup
- <4, r/o DVT, run D-dimer
Anti-coagulant: Min. 3 mos w/rev. risk,
- —>6 mos for first event,
- —>12 mos for recurrent event, inherited
Pulmonary hypertension:
Elevation of blood pressure in the pulmonary vasculature.
Mean pulm. arterial pressure:
- At rest: >25mmHg
- Exercise: >30mmHg
- Normal is about 15mmHg
Pulmonary hypertension S/sx:
Initially asymptomatic, Dyspnea worse w/exertion, chest pain, palpitations, fatigue, dizziness, syncope
Pulmonary hypertension PE:
assoc conditions: smokers, drug/toxin exposure
Tachycardia, split S2, sternal heave, edema, JVD, clubbing, hepato/splenomegaly, cyanosis
Pulmonary hypertension Poor prognosis:
Untreated median survival 2-3 years,
15% mortality in 1 year with treatment
Sleep Apnea d/t & Untreated risk?
Malfunctions in respiratory control or mechanics lead to disruption in normal pattern
- Central hypoxia = disrupted sleep pattern, hypoxemia, HTN & cognitive impairment
- Untreated = risk for CV disease, stroke
Sleep Apnea S/Sx, Dx & tx?:
S/sx’s=Crescendo snoring followed by waking, Epworth daytime sleepiness scale
Dx: sleep study (at clinic or at home) – >5-15 resp dist/hr (avg at home is 60/hr)
Foundational tx: side-lying, avoid alcohol, sedatives, stop smoking, weight loss, treat nasal allergies, appliances to open airway, CPAP (improves sleep and reduces risk of heart disease/stroke)
Lycopene:
(No provitamin A activity, potent carotenoids, reduces DNA damage & IGF-1…)
Major uses?
- HTN (10/4 drop over 6-8 wks - significant) esp. SBP (Quiz)
- Exercise induced asthma
- Hyperlipidemia (~10% drop in LDL; two raw romas tomatoes/day improved HDL)
Lycopene Dose?
Toxicity?
Dose: 10-30 mg qd (QUIZ->low end = 2 servings), absorption best with fat, can impair absorption of similar nutrients
Toxicity: 2mg assoc w/low birth weight babies, allergy, lycopenodermia
Thiamin:
Major uses:
*Alcoholism, diabetic nephropathy (TQ)
**Benfotiamine is a synthetic thiamin derivative that’s lipid soluble, used when high dose needed
Oxygen Delivery & Nebulizer
Oxygen Masks:
(TQ) Too rapid a rate of administration leads to respiratory depression and hypercapnia
Oxygen Masks:
- Low flow: nasal cannula (each L/min increases O2sat by 4% - up to 5ml/min) or face mask (6-10 L/min)
- High flow: venturi mask (24% to 50% oxygen)
(TQ) Too rapid a rate of administration leads to respiratory depression and hypercapnia
Lung Infections:
Bacterial Pneumonia
(CABP: community acquired bacterial pneumonia)
Clinical features?
Tx?
CABP common causes: strep, HiB, Staph
-Clinical features:
S/Sx: cough, fever, sputum, chest pain, dyspnea
PE: Rales in lateral decubitus position, fever
Imaging: CXR (Mb req. to establish dx of pneumonia)
Tx: Uncomplicated pts, use single beta-lactam x 5 days. **Fluoroquinolone (SE: achillles rupture, renal dz exacerbated) or combined in high-risk pts
Fungal Pneumonia: Hx? Dx? Tx? Etiology?
*Immunocompromised population
Hx: Hx of travel, Dz unresponsive to antimicrobials, eosinophilia, immunocompromised,
Dx: CXR will show patchy infiltrate, adenopathy
Tx: Self-limiting in healthy pop.->Antifungals if needed.
Fungal pneumonia immunocompromised refer to infectious disease specialist
Etiology:
Aspergillis: can form balls in damaged lungs, can cause hypersensitivity rxn
Cryptococcus: usually asymptomatic, can invade CNS
Histoplasma: heavy exposure can cause fulminant infection, can cause cavitation
Coccidiodes: valley fever, coin-like residual lesions
Tuberculosis:
(Transported by airborne particles)
- Primary infection:
- Ghon’s lesions:
- Risks for reactivation:
*Primary infxn-> latency-> reactivation (higher risk of mortality)
*Primary infxn: self-limiting, often undiagnosed.
CXR may show infiltrates in lower or middle lobes.
*Ghon’s lesions: calcified nodules,
Ranke’s complex: ipsilateral hilar lymphadenopathy
Tuberculosis:
(Transported by airborne particles)
S/sx:
Dx:
CXR:
Tx: (TQ)
Testing: Mantous tuberculin test or serology
Who to test: known exposure, immunocompromised, symptoms of disease, IV drug use
S/Sx: weight loss, fevers, night sweats, fatigue, loss of appetite, cough >3 weeks, hemoptysis, chest pain
Diagnosis: BCG vaccine could cause false positive; screen; PE; PA CXR; sputum smear (acid fast stain)
CXR patterns reactivated TB
- **92% Upper lobe infiltrates
- **8% lower lobe, hilar adenopathy, miliary TB, norm CXR
(TQ) Tx latent TB to control dz spread, reactivated TB requires polypharm to prev further resistance. Lots of AE’s and require monitoring. Drugs dosed daily or weekly for 4-9 mo.
Influenza:
Epidemiology?
Preventing spread?
Vaccine?
Strains A & B can = dz. Flu season Oct-May (Worse=Jan/Feb)
Epidemiology: risk is highest in pregnant women
Preventing spread: sx lag 4 days from exposure, start to shed virus at day 3, done shedding 1 day after fever, keep 6 ft distance to reduce spread, consider masks
Vaccine recommended for people >6 months, if <65 choose live attenuated vaccine, >65 choose high dose trivalent IM vaccine
Influenza:
Conventional treatment?
Tamiflu?
Conventional treatment: vary by flu season, check CDC site, tx more aggressive w/ at-risk, antivirals need to be started w/in 48 hours of onset (safe in PG) – this season only tx high risk with meds, tx presumptively
Tamiflu - While significantly better than placebo, Tamiflu effect is relatively small and tends to shorten duration of disease by about a day. SE: 10% - nausea, vomiting, diarrhea
Lung Infections Pharmacology:
CAP (Community Acquired Pneumonia) empiric therapy:
CAP empiric therapy:
- Healthy outpatient=> macrolide or doxycycline
- Outpatient at risk (like COPD)=> fluoroquinolone or beta lactam + macrolide
- Inpatient=> fluoroquinolone or beta lactam + macrolide
- Inpatient, ICU => beta lactam + azithromycin or beta lactam + fluoroquinolone
Treatment time: 5 days if afebrile by 48-72 hours OR 10-14 days if atypical
Cystic Fibrosis:
Change seen in airway: thick mucus block airway, blood in mucus, bacterial infection
Etiology?
S/Sx?
Etiology: autosomal recessive disease involving: lungs pancreas, sweat glands, intestines, liver, reproductive tract
S/Sx:
- Respiratory: chronic productive cough, sinusitis, bronchiolitis/asthma, staph colonization, digital clubbing
- GI: pancreatic insufficiency, DIOS, CFRD, vitamin deficiencies, prolonged neonatal jaundice, volvulus, rectal prolapse, biliary cirrhosis, portal HTN
- Genitourinary: absence of vas deferens, infertility
Cystic Fibrosis:
Diagnosis criteria?
- One of more of: chronic sinopulmonary disease, GI & nutritional abnormalities, salt lass syndrome, obstructive *azoospermia OR
- History of CF in sibling OR
- Positive newborn screening test PLUS
- Elevated sweat chloride concentration OR
- Identification of mutation in each CFTR gene OR
- In vivo demonstration
Cystic Fibrosis:
Supportive management?
Naturopathic treatment?
Supportive management: chest physical therapy, PEP therapy, huffing, autogenic drainage, exercise
Naturopathic treatment: music therapy, unclear evidence for beta-carotene, borage seed oil, massage, omega 3 FA, safflower, selenium & taurine
Pulmonary Function Testing:
Peak flow meter
*Measures maximal rate of low on forced expiration
*ALL patients w/asthma should have one.
=====> *Reading <80% of max indicate under treatment.
=====> *<50% = crisis & urgent treatment
- To take: zero out meter, stand up, breath in deeply, place in mouth tongue under mouthpiece, blow out as hard as possible, repeat 3x.
- ***Record highest reading
Pulmonary Function Testing:
Spirometry
Indications:
Chest pain, cough, dyspnea, orthopnea, phlegm production, wheezing, chest deformity, cyanosis, diminished breath sounds, expiratory slowing, crackles (unexplained), abnormal CXR, hypoxemia, smoking hx
COPD:
Definition: FEV1/FVC <0.7 (includes emphysema, chronic bronchitis, asthma, bronchiectasis)
% of Emphysema vs Chr. bronchitis?
- 15% Emphysema: non uniform enlargement of distal airspaces w/ destruction of acini, loss of elasticity, and absence of fibrosis
- 85% Chronic bronchitis: cough production of at least 2 Tbsp of mucus most days for at least 3 months over at least 2 consecutive years
COPD:
Emphysema Pathophysiology?
Pathophysiology:
loss of elastic recoil=> Inc. total lung volume=> collapse of airways during forced expiration => increased use of accessory muscles in breathing => increased caloric needs.
** blood gases should stay normal until late in disease course. **Measure pulse ox after a short walk
COPD:
Emphysema Types?
Types:
*Centriacinar (centrilobular). Associated w/ smoking, affects upper lungs. Begin in bronchioles peripherally
- Panacinar: Worse in lower lung, seen in alpha-1 antitrypsin deficiency. Uniform alveolus destruction
- Paraspetal (distal acinar): Idiopathic & rare. Airflow preserved but can lead to spontaneous pneumothorax
COPD:
Chronic bronchitis:
Pathophysiology?
Epidemiology?
Pathophysiology: Smoking, irritants, pollutants inflammation capillary permeability fluid & cellular exudate local edema hyper secretion of mucus persistent of cough
Epidemiology:
History of asthma makes COPD 12x more likely
4th leading cause of death in US
COPD:
Chronic bronchitis:
Risk?
Foundational therapy?
Risks:
Smoking 90% of cases, alpha1 antitrypsin deficiency. Other causes: occupational exposure, infections, low birth weight
Foundational therapy:
stop smoking, physical activity (if FEV <50% recommend pulmonary rehabilitation), nutritional status (doing carb rich will increase CO2), deficiencies (Mg, K, P, riboflavin, vitamin D), O2 therapy
COPD Medication:
Management goals?
Management goals:
reduce symptoms, reduce exacerbation frequency/severity, improve exercise tolerance, improve health status
SABA=> LABA or anti-cholinergic=> Steroid=> O2
COPD Medication:
Pharmacotherapy guidelines?
Pharmacotherapy guidelines:
FEV1 >80%: SABA prn
FEV1 50-80%: SABA prn, LABA, rehabilitation
FEV1<30-50%: SABA prn, LABA, rehabilitation, ICS
FEV<30%: SABA prn, LABA, rehabilitation, ICS, O2
Asthma:
Disease of inflammation of the airways. Tends to be episodic & can have periods of low to no symptoms. Exacerbations are often d/t infection, allergen exposure, occupational or environmental exposure. Obstruction d/t bronchiole swelling.
***Pathophysiology?
Pathophysiology:
Bronchoconstriction: IgE or non-IgE mechanisms
Asthma Diagnosis:
Spirometry findings?
- Inc. in FEV1 of > 12% w/ 2-3 puffs of short-acting bronchodilator (may not see in chronic, severe asthma)
- Improvement of FEV >12% w/ bronchodilator
- Obstructive disease (FEV1:FVC < .7)
- Positive metacholine challenge test (>20% improvement of FEV)
Asthma:
Urgent care guidelines?
Acute distress?
Urgent care guidelines:
- Mild (dyspnea w/ activity): PEF >70% care at home, SABA
- Moderate (dyspnea interferes usual activity): PEF 40-69% office or ED, SABA, oral corticosteroids
- Severe (dyspnea at rest, interfere conversation): PEF <40% ED, partial relief w/ SABA, corticosteroids, adjunctive therapies
- Life threatening (cannot speak d/t dyspnea): PEF <25% ED, ICU, no relief from SABA, IV corticosteroids, adjunctive therapy
Acute distress:
- Measure peak flow: 50-80% use SABA/ <50% transport to ER
- Give up to 2 tx w/ SABA 20 minutes apart: PEF >80% continue SABA/ 50-80% continue SABA add steroids/ <50% add steroids, transport to ER
