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Pulmonology > Diseases of the lungs > Flashcards

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).

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2
Q

Risk factors of asthma

A

atopy- exaggerated IGE immune response.

atopy conditions- atopic dermatitis (eczema), allergic rhinitis, asthma, nasal polyps.

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3
Q

what are the two categories of asthma

A

Extrinsic (atopic) and intrinsic (non atopic)

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4
Q

Pathophysiology of extrinsic asthma

A

hypersensitivity reaction to an extrinsic antigen or allergen. Ex dust mites, pollen, mold, animal dander.

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5
Q

Early phase response (extrinsic asthma)

A
  1. broncho-constriction and some inflammation within 10-12 minutes of exposure.
  2. 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!!
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6
Q

Late phase response (extrinsic asthma)

A
  1. inflammation that peaks within 12-24 hrs.
  2. continued release of inflammatory mediators from mast cells and other inflammatory cells which leads to airway epithelial injury + decreased mucocillary function + increase bronchospasm
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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.

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8
Q

Clinical manifestation of Asthma

A
  1. Wheezing with a prolong expiratory phase
  2. SOB and chest tightness- because of air trapping. increase residual volume. breathing in air fine but have trouble exhaling.
  3. cough.
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9
Q

clinical manifestation of status asthmaticus (acute severe asthma)

A
  1. increase accessory muscle use
  2. Tachypnea
  3. Anxiety, diaphoresis
  4. Pulse ox <90%, respiratory acidosis (high co2)
  5. can only speak in short sentences
  6. Silent chest. Bradypnea, absent/ diminished breath sounds on auscultation.
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10
Q

what is the best way to Diagnose of Asthma?

A

Spirometry/ pulmonary function test before and after administration of short acting bronchodilator.

  1. obstructive pattern: FEV1/FVC<70%, reversible with bronchodilators.
    - FEV1 decreases
    - FVC is normal/ slightly decreased.
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11
Q

what is the 2nd way to diagnose of asthma

A
  1. 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.
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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.
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13
Q

treatment for asthma: acute exacerbations

A
  1. short acting beta 2 agonists (SABA):
    -ALBUTEROL, levalbuterol, terbutaline
    EVERYONE WITH ASTHMA SHOULD HAVE A RESCUE ALBUTEROL INHALER PRL!!!!!
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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.

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15
Q

2nd treatment for asthma

A

short acting anti-cholinergic:

-ipratropium (blocks muscarinic receptors).

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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!!!!

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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).

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18
Q

side effects of systemic corticosteroids

A
  • hyperglycemia, Cushing syndrome, immunosuppression, osteoporosis, impaired wound healing, avascular necrosis
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19
Q

Other treatments for acute exacerbation

A
  1. Magnesium Sulfate IV- improves airflow, reduces hospitalization rates in ER.
  2. Epinephrine- non selective B agonist for status asthmaticus (silent chest).
  3. Heliox- mixture of oxygen and helium. Easily passes through constricted airways.
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20
Q

treatment of asthma: Controller Medications

A
  1. 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
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21
Q

2nd treatment for asthma: Controller Medications

A

Long acting beta 2 agonists (LABA):
-salmeterol, formoterol- lasts 12 hrs.
Not for acute exacerbation.

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22
Q

other treatments of asthma: controller medications (less used)

A
  1. long acting anticholinergic: tiotropium bromide
  2. leukotriene modifiers- montelukast, zileuton (good for patient with exercise and aspirin induced asthma.
  3. Anti- IGE monoclonal antibodies: omalizumab (very expensive drug)
    CROMOLYN- good for exercise- induced asthma as prophylaxis. inhibits mast cell degranulation by stabilizing membrane potential.
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23
Q

what is COPD

A

chronic, progressive inflammatory ,obstructive airway disease.

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24
Q

What are the risk factors of COPD

A
  1. Smoking (MC),

2. Genetic- alpha 1 antitrypsin deficiency.

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25
Q

what are the two categories of COPD

A

Emphysema and Chronic bronchitis

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26
Q

Pathophysiology of emphysema

A
  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!
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27
Q

Causes of emphysema

A
  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.
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28
Q

Pathophysiology of chronic bronchitis

A
  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

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29
Q

Long term effects of chronic bronchitis

A

hypoxic vasoconstriction of pulmonary arteries which leads to pulmonary HTN.

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30
Q

clinical manifestation of COPD

A
  1. Both SOB and chest tightness; tripod position.
  2. Small volume hemoptysis (coughing up blood).
  3. wheezing
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31
Q

clinical manifestation of COPD : emphysema predominant

A

Pursed lip breathing, Barrel chest, pink puffers (pink because they are still oxygenated).

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32
Q

Clinical manifestation of COPD: Bronchitis predominant

A
  1. chronic productive cough lasting more than 3 months.
  2. Hypoxic/cyanotic, edematous
  3. Blue bloaters (only when right HF develops)
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33
Q

COPD diagnosis

A
  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.
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34
Q

Complications of COPD

A
  1. Acute COPD exacerbations- often associated with acute bronchial infection.
    Pulmonary HTN which can leads to Cor pulmonale (right HF).
  2. Cardiac arrhythmia eg. multifocal tachycardia
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35
Q

Management for COPD: acute exacerbation

A
  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.
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36
Q

management for COPD: chronic management

A
  1. Long acting Beta agonists (LABA)- salmeterol
  2. Long acting anticholinergic: Tiotropium
  3. corticosteroids: add on to bronchodilators for more severe disease.
  4. GOLD STAGING OF COPD- allows for staging as well as medication recommendations.
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37
Q

other managements of COPD

A
  1. STOP SMOKING!
  2. oxygen therapy.
  3. surgery- lung transplant
  4. vaccinations
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38
Q

Beta blockers

A

1- SHOULD BE AVOIDED IN PTS WITH ASTHMA AND COPD EXACEBATIONS.
they block the beta receptors causing increased broncho constriction.

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39
Q

Pneumonia

A
  • acute infection of the lung parenchymal tissue.

- MC bacterial

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40
Q

What are the risk factors for pneumonia

A

Elderly, smoking, alcohol use, COPD, asthma, cystic fibrosis, CHF, immunocompromised and viral respiratory infection.

41
Q

classification of pneumonia

A
  1. Community acquired pneumonia (CAP)- acquired outside of a health care setting.
    2, Nasocomial pneumonia- acquired in the hospital
42
Q

microbiology of pneumonia (CAP). typical

A
  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
Q

microbiology of pneumonia: Nosocomial pneumonia

A
  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
Q

there bacteria that causes pneumonia

A
  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
Q

Viruses that cause pneumonia

A
  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
Q

pneumocystis Jirovecii

A

fungus that causes pneumonia in HIV and other immunocompromised patients.

47
Q

clinical manifestations of typical pneumonia

A
  • 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
Q

clinical manifestation of atypical pneumonia

A
  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
Q

clinical manifestation of nosocomial pneumonia

A

similar to typical pneumonia.

  • pseudomonas- green sputum with fruity smell.
  • staph aureus- lung abscesses/cavitations.
  • CXR- lobar consolidations
50
Q

clinical manifestations of klebsiella

A

similar to typical CAP.

  • currant jelly sputum.
  • CXR- RUL consolidation, +/- cavitations
51
Q

clinical manifestations of viral pneumonia

A

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
Q

clinical manifestation of aspiration pneumonia

A

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
Q

clinical manifestations of PCP pneumonia

A

caused by pneumocystis jirovecii.
- CXR- diffuse interstitial infiltrates.
TREATMENT IS BACTRIM (HIV patients with low CD4 count).

54
Q

Diagnosis of pneumonia

A
  1. CHEST X RAY confirms diagnosis of pneumonia.
55
Q

common CXR patterns for pneumonia

A

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
Q

other ways to diagnose pneumonia

A
  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
Q

supporting diagnosis of pneumonia

A
  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
Q

management for pneumonia (CAP)

OUTPATIENT!!

A
  1. if outpatient- MACROLIDE OR DOXYCYCLINE (1st line).
    - clarithromycin, azithromycin, doxycycline .
    * ***Augmentin + azithromycin is the go to **
59
Q

management for pneumonia (CAP)

INPATIENT!!

A
  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
Q

management of nosocomial pneumonia

A
  • *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
Q

Complications of pneumonia

A
  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
Q

assessing the severity of pneumonia: admit or discharge

                                     CURB-65
A

“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
Q

vaccinations that help prevent pneumonia

A
  1. Prevnar (PCV13)- childhood vaccination against various strains of s. pneumoniae.
  2. Pneumovax (PPSV23)- adult vaccination against various strains of s. pneumoniae.
64
Q

Acute bronchitis

A

acute inflammation of bronchi, most commonly from a viral infection (influenza, A/B, parainfluenza, rhinovirus.

65
Q

clinical manifestations of bronchitis

A
  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
Q

Diagnosis of acute bronchitis

A
  • clinical*

- CXR- normal or non specific- not really needed.

67
Q

Management of acute bronchitis

A
  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
Q

What is Cystic fibrosis

A
  • a genetic autosomal recessive disease that affects multiple systems.
  • affects patients of Northern European descent.
69
Q

Pathophysiology of cystic fibrosis

A
  1. mutation in the cystic fibrosis transmembrane regulator (CFTR) protein.
    - CFTR- a membrane chloride channel.
70
Q

cystic fibrosis in the lungs

A

-thick mucus with inability to clear it (mucus stasis) predisposes the airways to chronic infections, particularly infections caused by pseudomonas and staph.

71
Q

cystic fibrosis in the pancreas

A

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
Q

cystic fibrosis in sweat glands

A

inability to reabsorb NaCl from sweat produced by eccrine glands ->salty sweat.

73
Q

cystic fibrosis in the intestines

A

excessive absorption of liquid from the intestines-> GI obstruction (often seen at birth).

74
Q

cystic fibrosis in gonads

A

congenital absence of the vas deferens-> infertility

75
Q

clinical manifestations of cystic fibrosis:

Respiratory

A
  • 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
Q

clinical manifestations of cystic fibrosis:

Pancreas

A
  • 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
Q

clinical manifestations of cystic fibrosis:

GI and Reproduction

A
  • GI- In newborns, Meconium ileus- inability to pass stool, abdominal distention and is often first sign of cystic fibrosis.
  • infertility in men.
78
Q

Diagnosis of cystic fibrosis

A
  1. Sweat test: elevated sweat chloride >60 meq/L with administration of pilocarpine.
  2. DNA ANALYSIS- DEFINITIVE DIAGNOSIS.
79
Q

Management of cystic fibrosis

A
  1. Respiratory- antibiotics for infections (levaquin).
    - albuterol PRN, lung transplantation, vaccinations.
  2. Pancreas/ GI - pancreatic enzyme replacement (vit A,D,E,K).
80
Q

what is bronchiectasis

A
  • congenital or acquired disorder of the bronchi characterized by PERMANENT DILATION and destruction of bronchial walls.
81
Q

Risk factors of bronchiectasis

A
  1. cystic fibrosis accounts for 50% of cases.

2. frequent lower respiratory infections.

82
Q

clinical manifestations of bronchiectasis

A
  1. chronic cough with production of copious purulent sputum.
  2. hemoptysis (often massive)
  3. Dyspnea, wheezing
83
Q

microbiology of bronchiectasis

A
  1. MC shows H.influenzae in non cystic fibrosis patients

2. MC shows p. aeruginosa in cystic fibrosis patients.

84
Q

Diagnosis of bronchiectasis

A
  1. Chest CT

2. CXR

85
Q

Management of bronchiectasis

A
  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
Q

what causes tuberculosis

A
  • caused by Mycobacterium tuberculosis
    microbiology: acid-fast bacilli.
  • *TB is common in immigrants, homeless shelters and correctional facilities.
87
Q

Pathophysiology of primary (asymptomatic) TB infection

A

most patients are asymptomatic during this phase.

88
Q

Pathophysiology of Latent TB infection

A
  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
Q

Pathophysiology of secondary (reactivation) TB infection

A
  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
Q

Pathophysiology of miliary TB

A
  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
Q

clinical manifestation of TB

A
  1. Primary TB- asymptomatic
  2. secondary (reactivation) TB- progressive, chronic symptoms.
    - constitutional: fever, night sweats, weight loss, malaise, anorexia.
    - Respiratory: chronic cough (hemoptysis).
92
Q

Diagnosis of active TB

A
  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
Q

other diagnosis for TB

A
  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
Q

management of active TB including Military

A
  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
Q

Screening for latent TB

A
  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
Q

Screening of latent TB

A
  • 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
Q

screening of latent TB continued

A

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
Q

treatment for latent TB

A

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

Pulmonology (3 decks)

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