Diseases of the lungs Flashcards
1
Q
what is Asthma
A
Chronic inflammatory, obstructive airway disease (obstruction in the conductive airway), primary of the small airways (ex. segmental bronchi and bronchioles).
2
Q
Risk factors of asthma
A
atopy- exaggerated IGE immune response.
atopy conditions- atopic dermatitis (eczema), allergic rhinitis, asthma, nasal polyps.
3
Q
what are the two categories of asthma
A
Extrinsic (atopic) and intrinsic (non atopic)
4
Q
Pathophysiology of extrinsic asthma
A
hypersensitivity reaction to an extrinsic antigen or allergen. Ex dust mites, pollen, mold, animal dander.
5
Q
Early phase response (extrinsic asthma)
A
- broncho-constriction and some inflammation within 10-12 minutes of exposure.
- allergen exposure- IGE coated mast cells rapidly release histamine and cytokines which leads to bronchial wall edema + increase mucus secretion + stimulation of the parasympathetic receptors to cause broncho-constriction.
CAN BE TREATED WITH B2 AGONISTS!!
6
Q
Late phase response (extrinsic asthma)
A
- inflammation that peaks within 12-24 hrs.
- continued release of inflammatory mediators from mast cells and other inflammatory cells which leads to airway epithelial injury + decreased mucocillary function + increase bronchospasm
7
Q
Pathophysiology of intrinsic (non atopic asthma)
A
hypersensitivity reaction to an intrinsic trigger.
Ex. respiratory viruses-damage epithelium and stimulate IGE
-exercise- induces tachypnea, not allowing for proper warming of air
-cold air- induce mast cell release in the airway
-aspirin/ NSAIDs- complex, not well understood.
8
Q
Clinical manifestation of Asthma
A
- Wheezing with a prolong expiratory phase
- SOB and chest tightness- because of air trapping. increase residual volume. breathing in air fine but have trouble exhaling.
- cough.
9
Q
clinical manifestation of status asthmaticus (acute severe asthma)
A
- increase accessory muscle use
- Tachypnea
- Anxiety, diaphoresis
- Pulse ox <90%, respiratory acidosis (high co2)
- can only speak in short sentences
- Silent chest. Bradypnea, absent/ diminished breath sounds on auscultation.
10
Q
what is the best way to Diagnose of Asthma?
A
Spirometry/ pulmonary function test before and after administration of short acting bronchodilator.
- obstructive pattern: FEV1/FVC<70%, reversible with bronchodilators.
- FEV1 decreases
- FVC is normal/ slightly decreased.
11
Q
what is the 2nd way to diagnose of asthma
A
- Bronchial provocation test. performed if spirometry is inconclusive.
- The test is positive if methacholine (cholinergic that induces broncho-constriction) is administered and it leads to a drop in FEV1.
- A NEGATIVE TEST STRONGLY RULES OUT ASTHMA.
12
Q
the third way to diagnose asthma
A
Peak expiratory flow meters (Peak flow).
- is a hand held device, perfect as a monitoring tool.
- a CXR is not needed unless you are looking for other cause of symptoms/ exacerbation, eg. pneumonia.
13
Q
treatment for asthma: acute exacerbations
A
- short acting beta 2 agonists (SABA):
-ALBUTEROL, levalbuterol, terbutaline
EVERYONE WITH ASTHMA SHOULD HAVE A RESCUE ALBUTEROL INHALER PRL!!!!!
14
Q
MOA for short acting beta 2 agonist
A
beta 2 agonism->broncho-dilation, fast acting, most effective.
S/E- tachycardia and tremors.
-This is the mainstay of rescue therapy for acute asthma exacerbations, not meant for daily use.
15
Q
2nd treatment for asthma
A
short acting anti-cholinergic:
-ipratropium (blocks muscarinic receptors).
16
Q
what is the MOA of short acting anti-cholinergics
A
-inhibit vagallly mediated bronchospasm, used in acute exacerbations.
GIVE IN CONJUNCTION WITH ALBUTEROL!!!!
17
Q
3rd treatment for acute asthma exacerbation
A
Systemic corticosteroids:
-methylprednisolone, prednisone, prednisolone.
MOA- anti-inflammatory via decrease transcription of inflammatory cytokines (oral and IV have similar outcome, onset 6hrs).
18
Q
side effects of systemic corticosteroids
A
- hyperglycemia, Cushing syndrome, immunosuppression, osteoporosis, impaired wound healing, avascular necrosis
19
Q
Other treatments for acute exacerbation
A
- Magnesium Sulfate IV- improves airflow, reduces hospitalization rates in ER.
- Epinephrine- non selective B agonist for status asthmaticus (silent chest).
- Heliox- mixture of oxygen and helium. Easily passes through constricted airways.
20
Q
treatment of asthma: Controller Medications
A
- inhaled corticosteroids:
Beclomethasane, budesonide, flunisolide.
-MOA- anti-inflammatory (not for acute exacerbation).
=THIS IS THE FIRST LINE ADD ON FOR PERSISTENT ASTHMA, FOR DAILY USE.
-S/E- oral thrush
21
Q
2nd treatment for asthma: Controller Medications
A
Long acting beta 2 agonists (LABA):
-salmeterol, formoterol- lasts 12 hrs.
Not for acute exacerbation.
22
Q
other treatments of asthma: controller medications (less used)
A
- long acting anticholinergic: tiotropium bromide
- leukotriene modifiers- montelukast, zileuton (good for patient with exercise and aspirin induced asthma.
- Anti- IGE monoclonal antibodies: omalizumab (very expensive drug)
CROMOLYN- good for exercise- induced asthma as prophylaxis. inhibits mast cell degranulation by stabilizing membrane potential.
23
Q
what is COPD
A
chronic, progressive inflammatory ,obstructive airway disease.
24
Q
What are the risk factors of COPD
A
- Smoking (MC),
2. Genetic- alpha 1 antitrypsin deficiency.
25
what are the two categories of COPD
Emphysema and Chronic bronchitis
26
Pathophysiology of emphysema
1. Destruction of alveolar walls (parenchyma) and elastin which leads to enlargement of alveoli which causes hyper inflated lungs. (flatten diaphragm).
2. flatten diaphragm causes air trapping.
NO HYPOXIA!
27
Causes of emphysema
1. Smoking- causes the release of elastase and other proteases that destroys elastin and alveolar wall integrity.
2. Hereditary alpha anti-trypsin deficiency- often younger patients who doesn't smoke.
28
Pathophysiology of chronic bronchitis
1. airway obstruction of both the large and small airways.
| 2. mucus producing cells , productive cough. Mucus acts as a breeding ground for recurrent bacterial infections
29
Long term effects of chronic bronchitis
hypoxic vasoconstriction of pulmonary arteries which leads to pulmonary HTN.
30
clinical manifestation of COPD
1. Both SOB and chest tightness; tripod position.
2. Small volume hemoptysis (coughing up blood).
3. wheezing
31
clinical manifestation of COPD : emphysema predominant
Pursed lip breathing, Barrel chest, pink puffers (pink because they are still oxygenated).
32
Clinical manifestation of COPD: Bronchitis predominant
1. chronic productive cough lasting more than 3 months.
2. Hypoxic/cyanotic, edematous
3. Blue bloaters (only when right HF develops)
33
COPD diagnosis
1. spirometry/ pulmonary function test.
obstructive pattern: FEV1/FVC<70%. THIS IS IRREVERSIBLE with bronchodilator.
- increase residual volume and total lung capacity from air trapping.
- respiratory acidosis because of hypercapnia
- CXR is not needed but it shows hyper inflation of lungs seen in emphysema.
34
Complications of COPD
1. Acute COPD exacerbations- often associated with acute bronchial infection.
Pulmonary HTN which can leads to Cor pulmonale (right HF).
3. Cardiac arrhythmia eg. multifocal tachycardia
35
Management for COPD: acute exacerbation
1. Short acting bronchodilators
- SABA (albuterol)
- Short acting anticholinergic (Ipratropium)
2. systemic corticosteroids.
3. Antibiotics- treatment if pt has dyspnea with increase sputum production. Azithromycin is the best, doxycycline and augmentin.
36
management for COPD: chronic management
1. Long acting Beta agonists (LABA)- salmeterol
2. Long acting anticholinergic: Tiotropium
3. corticosteroids: add on to bronchodilators for more severe disease.
3. GOLD STAGING OF COPD- allows for staging as well as medication recommendations.
37
other managements of COPD
1. STOP SMOKING!
2. oxygen therapy.
3. surgery- lung transplant
4. vaccinations
38
Beta blockers
1- SHOULD BE AVOIDED IN PTS WITH ASTHMA AND COPD EXACEBATIONS.
they block the beta receptors causing increased broncho constriction.
39
Pneumonia
- acute infection of the lung parenchymal tissue.
| - MC bacterial
40
What are the risk factors for pneumonia
Elderly, smoking, alcohol use, COPD, asthma, cystic fibrosis, CHF, immunocompromised and viral respiratory infection.
41
classification of pneumonia
1. Community acquired pneumonia (CAP)- acquired outside of a health care setting.
2, Nasocomial pneumonia- acquired in the hospital
42
microbiology of pneumonia (CAP). typical
1. Streptococcus pneumoniae aka strep pneumo (MC)
| 2. Haemophilus influenzae- 2nd MC- more commonly seen in its with underlying pulmonary disease( COPD, cystic fibrosis)
43
microbiology of pneumonia: Nosocomial pneumonia
1. Staphylococcus aureus- seen in post influenza pneumonia. Can cause abscesses. (gram positive).
2. pseudomonas aeruginosa- green sputum and fruity smelling odor. (gram negative)
44
there bacteria that causes pneumonia
1. Klebsiella pneumoniae- more commonly seen in alcohol abuse (the formation of cavitary lesions and abscesses.
2. Anaerobes- concern in aspiration pneumonia.
3. Atypical bacteria- mycoplasma pneumoniae- MC of atypical/walking pneumonia.
4. Legionella- acquired from contaminated water supply. Associated with outbreaks. (not person to person transmission).
45
Viruses that cause pneumonia
1. Influenza- most common viral cause of pneumonia in ADULTS. It can lead to a super imposed bacterial infection with staph aureus.
2. RSV- most common viral cause of pneumonia in YOUNG KIDS.
3. SARS-CoV2- most common viral cause of pneumonia in the early 2020.
46
pneumocystis Jirovecii
fungus that causes pneumonia in HIV and other immunocompromised patients.
47
clinical manifestations of typical pneumonia
- dyspnea, tachypnea, PLEURITIC chest pain, cough, FEVER, TACHYCARDIA.
- s.pneumoniae normally see RUSTY COLORED SPUTUM AND RIGORS.
- crackles/rales, dull percussion, CXR shows lobar consolidation.
48
clinical manifestation of atypical pneumonia
1. URI symptoms- cough, sore throat, myalgias, headache
2. Mycoplasma- bulbous myringitis.
3. Legionella- nausea/vomiting, diarrhea.
- CXR- diffuse, patchy infiltrates or interstitial pattern, may look normal.
49
clinical manifestation of nosocomial pneumonia
similar to typical pneumonia.
- pseudomonas- green sputum with fruity smell.
- staph aureus- lung abscesses/cavitations.
- CXR- lobar consolidations
50
clinical manifestations of klebsiella
similar to typical CAP.
- currant jelly sputum.
- CXR- RUL consolidation, +/- cavitations
51
clinical manifestations of viral pneumonia
vague and diffuse like atypical.
1. URI symptoms- cough, sore throat, headache, MYALGIAS.
2. Influenza- fever, tachycardia.
- Auscultation is often normal.
- CXR-diffuse, patchy infiltrates or interstitial pattern, may look normal.
52
clinical manifestation of aspiration pneumonia
Similar to typical CAP, might only present with AMS.
1. increase incidence in patients with dysphagia, AMS
2. PURID ODOR TO SPUTUM.
CXR- RLL consolidation with possible abscess formation.
53
clinical manifestations of PCP pneumonia
caused by pneumocystis jirovecii.
- CXR- diffuse interstitial infiltrates.
TREATMENT IS BACTRIM (HIV patients with low CD4 count).
54
Diagnosis of pneumonia
1. CHEST X RAY confirms diagnosis of pneumonia.
55
common CXR patterns for pneumonia
lobar consolidation: CAP or Nosocomial
1. RU lobe- klebsiella
2. RL lobe- typical but consider anaerobes.
3. Abscess formation- anaerobes, klebsiella, staph aureus
4. diffuse patchy- atypical and viral pneumonias
5. diffuse interstitial- PCP
56
other ways to diagnose pneumonia
1. Chest CT- sensory but not necessary
2. sputum gram stain and culture
3. legionella urinary antigen
4. rapid influenza antigen test
5. COLD AGGLUTININ TEST- quick test for mycoplasma
57
supporting diagnosis of pneumonia
1. CBC- leukocytosis
2. arterial blood gas- only if the patient is hypoxic
3. blood cultures- performed for admitted patients.
4. PROCALCITONIN- high levels indicates bacterial etiology.
58
management for pneumonia (CAP)
| OUTPATIENT!!
1. if outpatient- MACROLIDE OR DOXYCYCLINE (1st line).
- clarithromycin, azithromycin, doxycycline .
* ***Augmentin + azithromycin is the go to ****
59
management for pneumonia (CAP)
| INPATIENT!!
1. B-lactam + (macrolide or doxycycline) eg. ceftriaxone (covers gram + & -), +azithromycin.
- alternatively, FLUOROQUINOLONE (covers all the major bugs + pseudomonas.
- if aspiration suspected, add CLINDAMYCIN (covers MRS).
60
management of nosocomial pneumonia
* *need two types of pseudomonas covering antibiotics**
1. Zosyn (piperacillin- tazobactam) + gentamicin (covers gram- bacteria)
2. cefepime (4th gen cephalosporin) + levaquin.
* add vancomycin if MRSA is suspected*
3. if legionella is suspected, add anti-atypical (macrolide, levofloxacin).
4. If aspiration is suspected, add clindamycin to cover anaerobes.
61
Complications of pneumonia
1. ARDS- acute respiratory distress syndrome- hypoxic respiratory failure.
2. Bacteremia: spreading of bacteria into the bloodstream.
3. Sepsis
4. Empyema (collection of pus)- pus within pleural cavity.
62
assessing the severity of pneumonia: admit or discharge
CURB-65
"CURB-65"
Confusion, Urea (BUN >20), Respiratory rate >30, Blood pressure <90/60 and 65years and older.
- if patient score 0-2- outpatient management.
- if patient score 2-5- inpatient management.
63
vaccinations that help prevent pneumonia
1. Prevnar (PCV13)- childhood vaccination against various strains of s. pneumoniae.
2. Pneumovax (PPSV23)- adult vaccination against various strains of s. pneumoniae.
64
Acute bronchitis
acute inflammation of bronchi, most commonly from a viral infection (influenza, A/B, parainfluenza, rhinovirus.
65
clinical manifestations of bronchitis
1. COUGH- productive or non-productive.
2. often preceded by URI symptoms (headache, sore throat).
3. SOB & CHEST PAIN USUALLY ABSENT.
4. wheezing or bronchi
66
Diagnosis of acute bronchitis
* clinical*
| - CXR- normal or non specific- not really needed.
67
Management of acute bronchitis
1. *self limited disease*
2. reassurance and symptom control- antitussives (dextromethorphan).
3. Antibiotics are not required in magority of cases except for COPD, cystic fibrosis, or other high risk patients.
68
What is Cystic fibrosis
- a genetic autosomal recessive disease that affects multiple systems.
- affects patients of Northern European descent.
69
Pathophysiology of cystic fibrosis
1. mutation in the cystic fibrosis transmembrane regulator (CFTR) protein.
- CFTR- a membrane chloride channel.
70
cystic fibrosis in the lungs
-thick mucus with inability to clear it (mucus stasis) predisposes the airways to chronic infections, particularly infections caused by pseudomonas and staph.
71
cystic fibrosis in the pancreas
inability to excrete enzymes from exocrine glands will eventually lead to auto- destruction of pancreas. Malnutrition, fatty stools and sit A,D,E,K, deficiency.
72
cystic fibrosis in sweat glands
inability to reabsorb NaCl from sweat produced by eccrine glands ->salty sweat.
73
cystic fibrosis in the intestines
excessive absorption of liquid from the intestines-> GI obstruction (often seen at birth).
74
cystic fibrosis in gonads
congenital absence of the vas deferens-> infertility
75
clinical manifestations of cystic fibrosis:
| Respiratory
- frequent respiratory tract infections (hallmark of the disease).
- Bronchiectasis- sequel of frequent infections and mucus buildup. MC pathogen is pseudomonas (green sputum, staph and h. influenza.
76
clinical manifestations of cystic fibrosis:
| Pancreas
- pancreatic insufficiency: fat/protein malabsorption ->fatty/bulky stools, malabsorption of vit A,D,E,K, malnourishment.
* *CF-induced diabetes mellitus: in older patients, inflammation within the pancreas eventually destroys beta cells.
77
clinical manifestations of cystic fibrosis:
| GI and Reproduction
* GI- In newborns, Meconium ileus- inability to pass stool, abdominal distention and is often first sign of cystic fibrosis.
* infertility in men.
78
Diagnosis of cystic fibrosis
1. Sweat test: elevated sweat chloride >60 meq/L with administration of pilocarpine.
2. DNA ANALYSIS- DEFINITIVE DIAGNOSIS.
79
Management of cystic fibrosis
1. Respiratory- antibiotics for infections (levaquin).
- albuterol PRN, lung transplantation, vaccinations.
2. Pancreas/ GI - pancreatic enzyme replacement (vit A,D,E,K).
80
what is bronchiectasis
- congenital or acquired disorder of the bronchi characterized by PERMANENT DILATION and destruction of bronchial walls.
81
Risk factors of bronchiectasis
1. cystic fibrosis accounts for 50% of cases.
| 2. frequent lower respiratory infections.
82
clinical manifestations of bronchiectasis
1. chronic cough with production of copious purulent sputum.
2. hemoptysis (often massive)
3. Dyspnea, wheezing
83
microbiology of bronchiectasis
1. MC shows H.influenzae in non cystic fibrosis patients
| 2. MC shows p. aeruginosa in cystic fibrosis patients.
84
Diagnosis of bronchiectasis
1. Chest CT
| 2. CXR
85
Management of bronchiectasis
1. Daily chest physiotherapy with chest percussion.
2. Bronchodilators
3. Treat the underling cystic fibrosis.
**ANTIBIOTICS in acute infections, guided by sputum:
augmentin for h. influenzae and ciprofloxacin for P. aeruginosa.
86
what causes tuberculosis
- caused by Mycobacterium tuberculosis
microbiology: acid-fast bacilli.
* *TB is common in immigrants, homeless shelters and correctional facilities.
87
Pathophysiology of primary (asymptomatic) TB infection
most patients are asymptomatic during this phase.
88
Pathophysiology of Latent TB infection
1. the ghon complex heals over and calcifies.
2. the host enters into a state of latent TB infection. These patients do not have symptoms, do not have active disease and are not infectious.
89
Pathophysiology of secondary (reactivation) TB infection
1. compromised immune system allows for dormant bacteria to escape from the granuloma and cause active infection.
2. a weaker, slower cell mediated response ensues and the patient develops progressive, chronic symptoms.
90
Pathophysiology of miliary TB
1. in severe immunocompromised patients, the bacteria is able to infiltrate into capillaries/lymphatics within lung interstitial.
2. millet seed shaped granulomas at sites of infection.
3. potts disease - BP changes with position eg sitting to standing.
91
clinical manifestation of TB
1. Primary TB- asymptomatic
2. secondary (reactivation) TB- progressive, chronic symptoms.
- constitutional: fever, night sweats, weight loss, malaise, anorexia.
- Respiratory: chronic cough (hemoptysis).
92
Diagnosis of active TB
1. CXR- upper lobe infiltrate with cavitary lesion (suggest TB but does not confirm).
2. Miliary TB: millet seed shaped lesions throughout lungs.
3. Acid fast bacilli sputum smear- 3 negative AFB smears rule out TB if suspicion is low. A PT WITH LATENT TB WILL NOT TEST POSITIVE WITH AFB SMEAR!!!
93
other diagnosis for TB
1. nucleic acid amplification (NAA). more sensitive and specific than AFB smear.
* **Sputum Culture: Gold Standard, confirms the diagnosis of TB, but it takes 2 weeks.*****
94
management of active TB including Military
1. Isoniazid often given with vitamin B6 (pyridoxine) to prevent neuropathy.
2. Rifampin- S/E include orange colored secretions
3. Ethambutol- S/E include optic neuritis
4. Pyrazinamide- S/E include hepatotoxicity.
* **2 MONTH INITIAL TREATMENT WITH ALL 4 DRUGS, followed by 4 MONTH CONTINUATION PHASE OF ISONIAZID (with vit B6 and RIFAMPIN***
- Direct observed therapy (DOT).
95
Screening for latent TB
1. TB skin test (PPD)- positive means active infection, latent infection or false positive. ALL POSITIVE SHOULD GET CXR!!
* In active TB- CXR would show infiltrates
* in latent TB- CXR may show calcified Ghon complex.
96
Screening of latent TB
* greater than or equal to 5mm- HIV positive and other immunocompromised patients.
* greater than or equal to 10- recent immigrants, homeless shelter.
* greater than or equal to 15- person with no known risk factors for TB.
97
screening of latent TB continued
QuantiFERON Gold (IFN gamma assay). More sensitive and specific, no false positive for BCG vaccination history. One downside is that it does not differentiate active from latent TB.
98
treatment for latent TB
Isoniazid plus pyridoxine (vit B6) times 9 months. This is for patients with positive PPD or QuantiFERON who are likely to have latent TB and who do not have active TB
