W2 Chronic Cough >8w (Review EOD Tuesday 25th) Flashcards
What are the obstructive diseases? 5
Chronic Bronchitis
Emphysema
Bronchiectasis
Cystic Fibrosis
Asthma
What are the 3 types of airway obstruction ?
Increased resistance to airflow can be caused by conditions
(1) inside the lumen
(2) in the wall of the airway, and
(3) in the peribronchial region
-
Inside the lumen
—The lumen can be partially occluded by excessive secretions.
—Partial obstruction can also occur in pulmonary edema or aspiration of a foreign body. -
In the wall of the airway
—Airway wall can be compromised by contraction of bronchial smooth muscle (asthma), hypertrophy of mucus glands (chronic bronchitis), and inflammation/edema of the wall (asthma and bronchitis) -
In the peribronchial region
—Outside of the airway, destruction of the parenchyma may cause narrowing because it tethers the alveoli open when it’s healthy (emphysema) or can be compressed by an enlarged lymph node or mass (cancer)
Chronic bronchitis
Defined as
Most important causative factor
5 other factors
Acute bronchitis causes by? Name the agents
⭐️chronic cough and sputum production for at least 3 months a year for 2 consecutive years.
—It is a clinical diagnosis.
Most important causative factor:
—🚬cigarette smoke exposure 🚬, active/passive.
Other causes
—Inhaled irritants such as industrial pollutants and airborne chemicals
—Repeated viral infections🦠
—Associated with other respiratory illnesses like cystic fibrosis and bronchiectasis
—Can co-exist with Emphysema
—GERD
Acute bronchitis
Viruses
—🦠influenza A & B
🧫Bacterial:
—Staph
—Strep
— Haemophilus influenzae
— Moraxella catarrhalis
— Mycoplasma pneumonia
repeated exposure = chronic bronchitis
Chronic bronchitis
Pathology
Common symptoms
S/S
PE
What does the patient look like?
PATHOLOGY
—Hypertrophy and hypersecretion of mucous glands (goblet cells) in the large bronchi and
—Chronic inflammatory changes in the small airways
—Exposure to the epithelial cells lining the airway to toxins/infections release inflammatory mediators.
—This results in increased mucus production and decreased mucociliary function.
—Excess mucus narrows the airway, limiting airflow, and accelerating the decline in lung function causing COPD. Cannot exhale as forcefully
SYMPTOMS
—wheezing
—dyspnea
—tight chest
—cough
—and increased mucus production
—⭐️persistent cough for 3 months a year for 2 consecutive years
SPUTUM
—color may vary from clear > yellow/green or even blood tinged.
—Color can be related to a bacterial infection however sputum color can change due to peroxidase released by leukocytes in sputum and is not a definite indicator of bacteria.
PE
—Typically overweight and cyanotic appearing blue bloater
—Tachypnea
—Elevated JVD, peripheral edema
pulmonary vessels undergo vasoconstriction to shunt blood to areas with better gas exchange and away from blocked areas
*if a large portion… increase pulm resistance causing pulm HTN … RV enlargement…”cor pulmonary”
—Use of accessory muscles, prolonged expiration, wheezing, coarse rhonchi, decreased breath sounds
—secondary polycythemia vera d/t low O2 from chronic bronchitis, producing more RBCs
Chronic bronchitis
Diagnosis — what do you see on
PFTs
ABG — 2
Chem panel
CXR
PFTs
—Documentation of airflow obstruction by PFTs is helpful both to the diagnosis a swell as response to inhaled bronchodilator therapy
—Decreased FEV1 and FVC
ABG
—Hypoxemia with concomitant hypercapnia on the ABG
—Mild polycythemia (+++ RBC production)
Chem panel
—elevated serum bicarb to buffer the high CO2
CXR
—correlates poorly with symptoms but some findings include hyperinflation, diaphragmatic flattening, and peribronchial markings
Sputum culture
Procalcitonin
—new biomarker elevated in bacterial pneumonia
—not elevated in chronic bronchitis
FVC: how much you can blow out after a full inhale
Chronic bronchitis
Treatment 2 main, 1 step up or if refractory
Non-Pharm 3
GOALS
—relieving symptoms and slow the progression of disease
—reducing the production of mucous, controlling inflammation, and lowering the cough burden.
PHARMACOLOGY:
BRONCHODILATORS:
—short and long acting beta-adrenergic receptor agonists as well as anticholinergics increase the airway lumen, increase ciliary function, and increase mucous hydration
GLUCOCORTICOIDS:
—reduce inflammation and mucous production;
—inhaled corticosteroids reduce exacerbations and improve quality of life
PHOSPHODIESTERASE-4 INHIBITORS:
—apremilast, crisaborole, roflumilast
—decrease inflammation and promote airway smooth muscle relaxation
—last line agent
ABX:
—not indicated for the treatment of chronic bronchitis
—but if needed, according to Chu, in former smokers, Azithromycin
NONPHARMACOLOGIC INTERVENTIONS
—Smoking cessation
—Supplemental O2
—Physiotherapy: pulmonary rehab for patient education, improve exercise tolerance, and assist in sputum clearance
—Avoid Irritants
notes on algorithm below
Just threathlessness and exercise limitation: SABA
Then do PFT and see if > or < 50%
Short acting — as a rescue device
Short actin — maintenance therapy
If on LAMA, you discontinue SAMA
If persistent: LABA + steroid inhaler
Emphysema
How is it characterised
What are the two types?
—chronic obstructive pulmonary disease (COPD) with chronic bronchitis.
—an enlargement of the air spaces distal to the terminal bronchiole with abnormal permanent enlargement of air spaces with destruction of their walls.
—destruction of lung parenchyma with loss of elasticity.
—diagnosis is presumptive and based on radiologic and clinical findings
—increasing due to environmental pollution, increase in cigarette smoking, and decreasing mortality from cardiovascular and infectious diseases.
Types:
1. CENTRIACINAR:
—affects the alveoli and airways in the central acinus, destroying the alveoli in the walls of the respiratory bronchioles and alveolar ducts
2.PANACINAR:
—affects whole acinus
—excessive amounts of the enzyme ⭐️LYSOSOMAL ELASTASE⭐️ are released from neutrophils
—results in the destruction of elastin and subsequently a reduction in the surface area for gas exchange
—antiproteases, such as alpha1-antitrypsin reduce this activity (some people have alpha 1 anti trypsin deficiency so develop emphysema and have never smoked)
Emphysema
What are the causes —2
What can cause a pneumonthorax?
What is the presentation
PE — what does the patient look like?
Auscultation?
Percussion
Skeleton?
Causes:
—Cigarette smoke: cause release of proteolytic enzymes (centriacinar change)
—⭐️Alpha1-antitrypsin deficiency ⭐️
paraseptal changes “bleb” occur in peripheral lungs and as alveoli balloon out, can rupture and cause pneumothorax
Presentation:
—Chronic cough with or without sputum production
—Chronic shortness of breath
—Wheezing
—Loss of weight secondary to inflammation and increased work of breathing, breathless while eating too so only eat a few bites
—Obtain smoking history (current and past) as well as exposure to environmental toxins
PE
—Cachexia
—Pursed-lip exhaling, trying to keep the alveoli open “pink puffers” (prevents airway collapse during expiration)
—Accessory muscle use
—Wheezing
—Hyperresonance to percussion (hyperinflation)
—Decreased breath sounds with poor air movement
—Increased AP diameter
Emphysema
Diagnostic studies
PFT will show?
CXR will show?
ABG will show?
What is FEV1 & for mild, moderate, severe, very severe?
What if panacinar, what are you testing for?
It is a structural disease, so studies diagnose, in comparison to chronic bronchitis which is a clinical diagnosis
PFT:
—mainstay of diagnosis with result of FEV1/FVC < 0.7;
—can stage severity based on GOLD criteria
Chest x-ray
—hyperinflation of the lungs with flattening of the diaphragm in severe disease;
—heart may seem tubular in shape
ABG
—hypoxemia and hypercapnia
If young, test for alpha1-antitrypsin deficiency
CT chest
[SKILLS OSCE]
What is this?
Emphysema
Flat diaphragm
Big back lung volume
Vertical heart
Patient SOB
[SKILLS OSCE]
What is this?
Emphysema
Emphysema
Treatment
Which medical therapy
NO TREATMENT to modify the disease process.
Goal is to slow progression of disease and improve quality of life via risk factor modification and management of symptoms.
Based on the SYMPTOMS and NUMBER OF EXACERBATIONS, emphysema is divided into 4 stages and treated accordingly.
MEDICAL THERAPY includes:
—using a bronchodilator alone or
—in combination with anti-inflammatory drugs (corticosteroids and phosphodiesterase-4 inhibitors)
treatment is essentially the same as chronic bronchitis, but this algorithm is like a questionnaire for the patient to fill out, it doesn’t use FEV1. Then can treat according to what they report. But essentially you start with short or long acting bronchodilator, then corticosteroid, then phosphodiesterase inhibitor. All on MedCalc
Emphysema
Medical therapy
Supportive therapy 2 main ones
BRONCHODILATOR (1st line; inhaled)
—alter smooth muscle tone of airways improving FEV1 and exercise tolerance
¶ Beta-2 Agonist: SABA (short acting) and LABA (long acting):
•promotes smooth muscle relaxation
¶ Anticholinergic/antimuscarinics: SAMA (short acting) and LAMA (long acting)
•NT: ACh > bronchorestriction/mucous production
INHALED CORTICOSTEROIDS (ICS):
—reduce inflammation; add on therapy to bronchodilators
ORAL CORTICOSTEROIDS
—prednisone, 40mg 5-14d
—IV if in hospital or failed oral
ORAL PHOSPHODIESTERASE-4 INHIBITORS:
—reduce inflammation; add on therapy
TRIPLE INHALED THERAPY (LABA + LAMA + ICS)
Supportive Therapy:
Oxygen
—routine use does not improve clinical outcomes or quality of life in stable patients
—Recommended in patients with a PaO2 < 55 mmHg or SaO2 < 88%; oxygen therapy has been shown to increase survival of these patients with resting hypoxemia
Pulmonary Rehab
—Interventional Therapy:
Lung volume reduction surgery
—reduces hyperinflation and improves elastic recoil
Bronchiectasis
What is it?
What are the causes — 7
Abnormal, permanently dilated large airways characterized by ⭐️persistent bacterial infection⭐️ an excessive neutrophilic inflammation.
Causes
1. Bacterial Infections
—TB
—Haemophilus Influenzae
—Moraxella catarrhalis
—Streptococcus
—Pseudomonas aeruginosa
—staphylococcus
—HIV
—and mycoplasma)
2.Viral Infections
—RSV
—measles
3.Fungal Infections
4.Bronchial Obstruction
—foregin body
—tumor
—mucus plug
—hilar lymphadenopathy
5.Congenital
—cystic fibrosis
6.Rheumatic
—RA
—Sjogren syndrome
—ulcerative colitis
7.Pulmonary diseases
—COPD
—pulmonary fibrosis
—asthma
—bronchomalacia
Pathophysiology:
1. Recurrent infections
2. Airway obstruction
3. Peribronchial fibrosis
—Neutrophils cause airway inflammatory cell infiltration and increased mucus and exudate.
—Results in cartilage destruction, fibrosis, impaired mucociliary clearance, and bacterial colonization.
Bronchiectasis
Demographic
Presentation
PE findings
Patients have:
—⭐️daily copious sputum/cough ⭐️
—recurrent chest infections
—impaired health related quality of life
— +/- congenital (cystic fibrosis) or acquired
—most prevalent in women and > 60 y/o
—prevalence is increasing
PRESENTATION:
—⭐️Chronic cough (98%) with copious amounts of sputum (78%) ⭐️
—Wheezing, hemoptysis (56%)
—Shortness of breath (62%)
—Recurrent respiratory infections
—Weight loss and fatigue
PHYSICAL FINDINGS:
—nonspecific but can include
—crackles (75%)
—wheezing (22%)
—and clubbing (2%)
Bronchiectasis
Diagnostics — which one?
What are you measuring?
Defining characteristics
Diagnostics:
—⭐️ CT scan ⭐️
—Internal diameter of a bronchus is > 1.5X the diameter of the pulmonary artery
—Bronchial wall thickening
Tree in bud appearance:
1. Failure of bronchial tapering
2. Crowding of bronchi with lobar volume loss
3. Thickening and plugging of small airways
4. Cysts with definable borders
[SKILLS OSCE]
What is this?
For the same disease, what would you see on CXR?
What is the gold standard DX? And what would you measure?
What is the treatment? (Abx)
Bronchiectasis
Notice lack of bronchial tapering where the arrows are
CXR: tram tracks or “plate-like” scarring
Gold standard = CT scan: internal diameter of bronchus 1.5x diameter of the pulmonary artery
ABX: augmenting/amoxi/doxi
Also: PT, bronchodilators, flutter, bronchoscopy etc
Cystic fibrosis
What is it?
What is the patho
Which organs affected and how
—Autosomal recessive disorder that affects the CFTR protein (cystic fibrosis transmembrane conductance regulator, allows Cl- to exit and water so keeps mucous watery not sticky and viscous)
—resulting in diminished chloride secretion as well as increased sodium absorption.
—This removes water from secretions of EXOCRINE (mucus and sweat) glands; viscous mucus forms that then obstructs glands and ducts.
—Thick mucus results in obstruction: gland dilation, inflammation, infection, and tissue damage.
—Most common cause of severe chronic lung disease in young adults
—Affects multiple organ systems:
Lungs
—Thick mucus is unable to clear debris from the airway; provides an environment ideal for bacterial growth
—Causes obstructive disease (inability to push air out of the lung) ….hyperinflation and bronchiectasis
—Chronically, destruction of lung tissue will occur resulting in a restrictive disease atop an obstructive one
Pancreas:
—Prevents enzymes from producing enzymes resulting in abnormal fat digestion …. weight loss, excess fat in stool (abnormal, putrid smell)
—difficulty absorbing protein and vitamins A, D, E K
—diabetes
—pancreatic damage, pancreatic and cyst formation (how it was named)
Intestines:
—Obstruction (meconium ileus)
—FTT
Infertility in men
—lack of vas deferens
