Pulmonology Flashcards

1
Q

FRV1/FVC

A

ratio of air volume expired in 1 second to FVC.
80% is normal,
and this ratio helps us to understand whether the patient has obstructive or restrictive lung disease

80% is +/- restrictive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Total lung capacity

A

increased in obstructive lung disease

decreased in restrictive lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Functional vital capacity (FVC)

in obstructive versus restrictive lung disease

A

FVC is the air volume that can be inspired and then expired

decreased in obstructive lung disease because you can’t move air out very well

decreased in restrictive lung disease because you can’t move air in very well

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

FEV1 in obstructive versus restrictive lung disease

A

decreased in obstructive as well as in restrictive lung disease

In obstructive lung disease, FEV decreases even more than FVC, so with obstructive lung disease the FEV1/FVC ratio drops more than 70%

In restrictive lung disease the FEV1/FVC ratio is normal or increased because the FEV1 and FVC decrease at a similar rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

DLCO

A

relative measure of ability to transfer air from pulmonary alveoli to capillary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Alveolar-arterial gradient

What’s a normal value?
When would A-a gradient be increase?

A

Compares O2 status of alveoli to arterial blood

Normal= 5-15 mmHg
Increased Aa gradient indicates pulmonary embolism, pulmonary edema, right-to-left shunt, higher concentration of inspired oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Aa gradient equation

A

PAO2-PaO2

(Atmospheric air pressure x FiO2) - (PaCO2/0.8) - (PzO2)= (713nnHg) * (0.21 PaCO2/0 .8)-(PaO2)= 5-15mmHg is considered a normal A-a gradient

PAO2= alveolar O2 content
PaO2= Arterial O2 content
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Common cold (viral rhinitis)

A

inflammation of the upper airways

Causes: rhinovirus, coronavirus, adenovirus

H and P: nasal and throat irritation, sneezing, rhinorrhea, nonproductive cough
(Productive cough tends to be more indicative of PNA or bronchitis)

Treatment: supportive, rest, analgesia, hydration, NO antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pharyngitis

A

Inflammation of the throat

viruses: rhinovirus, coronavirus, adenovirus
bacteria: group A beta-hemolytic streptococci (strep pyogenes)

Symptoms: sore throat, lymphadenopathy, nasal congestion
fever, HA, GI symptoms
Red and swollen pharynx
Tonsillar exudates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pharyngitis diagnosis- Centor criteria

A
Add one point if:
Fever
Tonsillar exudates
Tender anterior cervical adenopathy
Absence of cough
44yo subtract a point
Cough (absence of)
Exudates
Nodes
T (temperature)
OR (plus or minus one point for age)

0-1 points= no antibiotic/no throat culture
2-3 points= throat culture/treat if positive
4-5 points= treat empirically

Treatment: self- limited
antibiotics to prevent ARF
(post-strep glomerulonephritis risk does not change with antibiotic use)

Use beta-lactam antibiotics (penicillin, amoxicillin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What nonbacterial infections present with tonsillar exudates?

A

infectious mononucleosis

strep pharyngitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Tonsillar infections

A
Streptococcal pharyngitis symptoms
Ear pain
Difficulty swallowing
High fever
Tonsillar exudates

Treatment: beta- lactam antibiotics (penicillin, amoxicillin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the diagnostic features of peritonsillar abscess? What is the treatment?

A

Infection between the tonsil and pharyngeal constrictors caused by streptococcus pyogenes, staphylococcus aureus, and/or bacterioides spp.

Severe sore throat, fever, muffled “hot potato” voice

Classic diagnostic feature is obvious abscess on the tonail or deflection of the uvula to the opposite side

Other signs and symptoms include trismus (“lockjaw”) and drooling

Treatment:
Needle aspiration or I&D
Pain meds and antibiotics: amoxicillin/clavulanate, clindamycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Viral influenza

A

H and P: arthralgias, myalgias, nasal congestion, nonproductive cough, high fevers, lymphadenopathy

Flu swab
Treatment: symptomatic treatment, fluid intake, zanamivir and oseltamivir which will decrease severity of symptoms

Annual flu vaccine (especially elderly patients, healthcare workers, immunocompromised, lung disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sinusitis- acute

A

streptococcus pneumoniae
haemophilus influenzae
moraxella catarrhalis
viral infection

associated with barotrauma, allergic rhinitis, prolonged gastric tube placement, asthma and other chronic resp infection

Complications- may spread to CNS and cause meningitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Sinusitus- chronic

A

usually caused by sinus obstruction and anaerobic infection

DM predisposes to mucor mycosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Sinusitis H and P

A

sinus pain, purulent nasal discharge, maxillary tooth pain, sinus tenderness to palpation, illumination test (unreliable)

CT sinuses for severe sinusitis
Treatment: 
nasal irrigation
analgesics
oral decongestants
intranasal steroids
amoxicillin- clavulanate, doxycycline, or levofloxacin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the complications of strep pharyngitis, and which can be prevented with antibiotics?

A

ARF and glomerulonephritis

ARF can be prevented

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Signs of a peritonsillar abscess

A

deviated uvula
trouble opening mouth
muffled “hot potato” voice

look for a bulge in the back of the throat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

murmurs that decrease with squatting

A

HOCM and MVP, because the valve leaflets are further apart with greater afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Acute bronchitis

A

trachea and bronchi
difficult to differentiate from URI in the first few weeks. Generally a clinical diagnosis because the symptoms and radiology are nonspecific. If high fever then evaluate for PNA, and consider influenza

productive cough
shortness of breath
wheezing

sputum culture in persistent cases

Rads- CXR rules out PNA, shows mild congestion

Viruses- MCC
Mycoplasma pneumoniae
Streptococcus pneumoniae
Haemophilus influenzae

Treatment- symptomatic, self- limited
Abx if increased risk of bacterial infection (other lung disease, smokers, elderly)
fluoroquinolones
tetracycline
erythromycin
azithromycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

PNA

A

inflammation in the alveoli

  • CAP
  • HAP

Clinical manifestations can break down into typical and atypical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Features of typical PNA presentation

A
fever
cough
malaise
purulent sputum
chest pain
SOB

on xray, lobar infiltrate

common organisms:
streptococcus pneumoniae
staphylococcus aureus
haemophilus influenzae
GBS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Features of atypical PNA presentation

A

less severe symptoms
nonproductive cough
headache fatigue

On CXR, diffuse patchy infiltrates

Common organisms:
mycoplasma pneumonia
legionella pneumophila
chlarmydophila pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Viral causes of PNA
``` influenza parainfluenza adenovirus cytomegalovirus RSV (MCC viral PNA in children) ```
26
Streptococcus pneumonaie PNA
MCC PNA in adults sickle cell patients high fevers, pleuritic pain, productive cough, rust- colored sputum ``` Treatment: cephalosporins respiratory fluoroquinolones beta- lactams macrolides preferred- amoxicillin unless you have resistance ```
27
Haemophilus influenzae
COPD SCD slower onset of symptoms ``` Treatment: beta- lactams fluoroquinolones doxycycline macrolides ```
28
staph aureus PNA
- Nosocomial pneumonia in immunocompromised patients - Seen in higher rate in patients with influenza - Abscess formation Treatment: beta lactams, MRSA coverage (incase resistant)
29
Klebsiella pneumoniae
Alcoholics, aspiration, hospitalized, sickle cell, currant- jelly sputum Treatment: cephalosporins aminoglycosides
30
pseudomonas aeruginosa PNA
chronically ill, immunocompromised, cystic fibrosis, chronic ventilator, nosocomial pneumonia, rapid onset of symptoms (very sick, high mortality) start empiric antibiotics immediately - piperacillin- tazobactam - ceftazidime - cefepime - imipenem - meropenem - doripenem (beta- lactams) - ciprofloxicim, levofloxacin (fluoroquinolones) - aminoglycosides
31
GBS PNA
neonates and infants respiratory distress and lethargy Treatment: beta- lactams ampicillin and gentamicin
32
Enterobacter spp.
Nosocomial pneumonia elderly patients 3rd generation cephalosporins -carbapenem
33
Mycoplasma pneumoniae
walking PNA MCC in young adults diffuse bilateral infiltration on CXR Pt doesn't appear ill less severe sx rash positive cold- agglutinin test (IgM) Treatment- macrolides
34
Legionella pneumophila
aerosolized water, and can be passed from person to person slow onset nausea, diarrhea confusion, ataxia Treatment: macrolides, fluoroquinolones
35
Chlamidophile pneumoniae
another atypical pneumonia - mycoplasma pneumoniae - legionella pneumophila - chlamydophila pneumoniae Very common in the very young and very old - slow onset of symptoms - frequent sinusitis - Treatment with doxycycline, macrolides
36
Empiric therapy for PNA (cover s. pneumoniae and atypical organisms)
Note: resistance to macrolides is growing 1. Resp fluoroquinolone like levofloxicin, moxi, gemifloxifin alone 2. or combine a beta-lactam with doxycycline or a macrolide
37
Most common PNA agent in children
RSV
38
Most common PNA agent in adults
strep pneumo
39
PNA with Higher rate after influenza
s. aureus
40
PNA with currant jelly sputum
klebsiella
41
PNA with associated with CF
pseudomonas
42
PNA MC in neonates
GBS
43
PNA Associated with elderly
enterobacter (Gram negative)
44
PNA common in young adults
mycoplasma
45
PNA associated with aerosolized water
legionella
46
Neonates (first 28 days of life) most common causes of PNA
1. GBS is most common 2. E. Coli 3. Chlamydia trachomatis (long incubation, sx appear 12 weeks later) 4. Herpes simplex virus
47
MCC PNA in children
RSV Strep pneumoniae chlamidophila pneumoniae in older children, think about mycoplasma pneumoniae
48
MCC PNA in adults
``` Streptococcus pneumoniae Haemophilus influenza Mycoplasma pneumoniae Chlamydophila pneumoniae Influenza ```
49
MCC PNA in elderly
``` Streptococcus pneumoniae Haemophilus influenzae Influenza Staphylococcus aureus Anaerobes Gram- negative rods ```
50
What are the indications for pneumococcal vaccination in adults?
1. age 65 and older 2. Serious long-term health problems such as heart disease, sickle cell disease, alcoholism, leakage of cerebrospinal fluid, lung disease, diabetes, or cirrhosis 3. resistance to infections if lowered due to Hodgkin disease, multiple myeloma, cancer treatment with xrays or drugs, treatment with long-term steroids, bone marrow or organ transplant, kidney failure, HIV/AIDS, lymphoma, leukemia, other cancer, nephrotic syndrome, damaged spleen or no spleen 4. Cigarette smokers age 19-54
51
PNA and gram-positive cocci in clusters
s. aureus
52
gram- positive cocci in pairs in the context of PNA
s. pneumoniae
53
gram- negative rods in 80 year-old with PNA
e. coli
54
gram positive cocci in neonate PNA
GBS
55
gram neg rods in neonate PNA
e. coli
56
Fungal PNA with PMHx of travel to SW US
coccidiomycosis
57
Fungal PNA with PMHx of caves, spelunking, bats
histoplasmosis
58
Fungal PNA with PMHx of trave l to eastern North America
blastomycosis
59
Fungal PNA with PMHx of travel to s. America
paracoccidiomycosis
60
Antifungals used to treat fungal PNA
Amphotericin B Ketoconazole Itraconazole Fluconazole
61
Pneumocystic jiroveci (PCP)
Immunocompromise -HIV patients (CD4 count220 (rising LDH despite appropriate treatment portends a poor prognosis) What is the usual treatment: 21 days of antibiotics with choices including -TMP-SMX (IV or PO) -Pentamidine (IV) -Primaquine (PO) + clindamycin (IV or PO)
62
Tuberculosis (primary and secondary)
mycobacterium tuberculosis Primary TB: person who has never been infected with TB contracts disease Symptoms vary widely: fever, CP, cough common CXR: hilar lymphadenopathy, or normal, possible Ghon complex Body often heals from the primary infection by primary fibrosis, allowing the person to move on to latent TB (asymptomatic), which can possibly last for years
63
Ghon focus vs Ghon complex. Both associated with primary tuberculosis
primary TB focus in a small area of lower lung, granulomatous inflammation visible on CXR once it has calcified If seen in combination with hilar lymphadenopathy, a Ghon focus is called a Ghon complex
64
How do you interpret a positive PPD?
current infection past exposure vaccination
65
5mm PPD is considered positive in
highest risk pop HIV+ Close contact with TB CXR findings suggestive of TB
66
10mm PPD is considered positive in
``` homeless immigrants IV drug users chronically ill healthcare workers recently incarcerated ```
67
15mm PPD is considered positive in
anyone, including low-risk | 15mm is always considered positive
68
Significance of negative PPD skin test
``` negative no infection anergic malnutrition immunocompromise sarcoidosis ```
69
Secondary TB
reactivation of dormant tubercles fibrocaseous cavitary lesions symptoms: fever, hemoptysis, weight loss, night sweats ``` complications: parenchymal tuberculoma (brain grey matter) Meningitis Pott's disease (vertebral bodies) lymphadenitis renal disease GI disease miliary TB ```
70
Labs to confirm TB
sputum culture takes 2-4 weeks Acid-fast sputum stain every morning for 3 days negative- probably not TB, discharge, follow up with cultures positive= TB
71
Treat TB
``` Latent- INH (6-9 months) Primary or secondary TB- RIPE Rifampin INH (with B6 to prevent peripheral neuropathy) Pyrazinamide Ethambutol ```
72
BCG vaccine
varying efficacy can have a false positive PPD in the 1st year of life, after 10 years, should be PPD negative
73
Causes of ARDS
sepsis, shock, near-drowning, trauma, aspiration, drug overdose, lung infection, etc ``` Aspiration Acute pancreatitis Air or amniotic embolism Radiation Drug overdose Diffuse lung disease DIC Drowning Shock Sepsis Smoke inhalation ```
74
Symptoms and Signs of ARDS
refractory hypoxemia, decreased lung compliance, pulmonary edema look for a history of acute dyspnea and pulmonary decompensation, cyanosis, tachypnea, wheezing, rales, rhonchi labs: respiratory alkalosis, decreased O2, decreased CO2, PCWP200
75
Treat ARDS
Treat underlying diseases, support in ICU Mechanical ventilation with low tidal volumes (to minimize injury), and adequate PEEP (to recruit collapsed alveoli) Conservative fluid management to reduce pulmonary edema. Goal CVP 4-6mmHg. (Furosemide and albumin may also be helpful to prevent pulmonary edema) Prone positioning improves oxygenation but does not improve survival Minimize oxygen consumption by preventing fever (antipyretics), minimizing anxiety and pain (sedatives and analgesics), and limiting respiratory muscle use (paralytics), particularly in cases of asynchrony of the ventilator and patient's efforts Transfuse blood only if hemoglobin drops below 7g/dL, as transfusion may increase risk of death in ARDs patients
76
What percentage FiO2 does a nasal cannula provide?
24-40% FiO2 (FiO2 increases 3% for every 1L/min up to 6L/min)
77
What percentage FiO2 does a face mask provide?
50-60% FiO2
78
What percentage FiO2 does a non-rebreather provide?
60-95% FiO2
79
What percentage FiO2 does a CPAP provide?
80% FiO2
80
What perventage FiO2 does mechanical ventilation provide?
up to 100% FiO2
81
Asthma
reversible airway obstruction secondary to bronchiolar hyperactivity, etc. Triggers: allergens, illness, exercise, cold temperatures, stress, beta blockers, aspirin (rare), sulfites (rare) Risk factors: family history, allergies, atopic dermatitis, low socioeconomic status, Churg-Strauss vasculitis History and physical: cough, dyspnea, wheezing, chest tightness, tachypnea, tachycardia, prolonged expiratory duration, decreased breath sounds, accessory muscle use, pulsus paradoxus, cyanosis, decreased O2 saturation, difficulty talking Labs: decreased PEFR (pulm exp flow rate), decreased FEV1, ABG shows hypoxemia, respiratory alkalosis normal CXR, maybe mild hyperinflation
82
Pulsus paradoxus
deep inspiration causes SBP to drop at least or more than 10mmHg
83
Definition of mild intermittent asthma
2 or less daytime episodes per week 2 or less nighttime episodes per month FEV1 greater than or equal to 80% Treatment: PRN albuterol
84
Definition of mild persistent asthma
3-6 daytime episodes/week 3-4 nighttime episodes/month FEV1 > 80% Management: Treatment with PRN albuterol Low dose inhaled steroid +/- montelukast or cromolyn if pt has high allergy susceptibility
85
Definition of moderate persistent asthma
``` daily daytime episodes greater than 1 nighttime episode/week FEV1 60-80% Treatment: PRN albuterol Low to med-dose inhaled steroid +/- long-acting B2 agonist +/- montelukast, cromolyn, theophylline if everything else is failing ```
86
Definition of severe persistent asthma
continued daytime episodes frequent nighttime symptoms FEV1>60% Treatment: PRN albuterol, High-dose inhaled steroid, long-acting beta2 agonist, daily PO steroid, +/- montelukast, +/- theophylline
87
Rapid- acting beta2 agonists
bronchodilators rapid onset of action albuterol, levalbuterol
88
Long- acting beta2 agonists
salmeterol, fometerol bronchodilators, gradual onset, sustained activity
89
Inhaled corticosteroids
decreased cells involved with airway inflammation, mild persistent and onward, often combined with rapid- acting beta2 agonists
90
Leukotriene inhibitors
montelukast, zafirlukast, ziluton block activity or production of leukotrienes (inflammation and bronchospasm), useful in patients with rhinitis- like sx
91
Mast cell stabilizing agents
cromolyn, etc stabilizes mast cells anti-inflammatory prophylaxis not useful acutely, not used much at all dosed 3-4 times per day
92
Theophylline bronchodilator
``` previously first-line, now replaced in recent years by beta agonists side effects and interactions -hypotension -seizures -tachycardia ``` treat OD with benzodiazepines, dialysis adjunct if severe refractory
93
Anticholinergic agents
block vagal- mediated smooth muscle contraction used as adjunctive therapy in moderate-to-severe asthma
94
acute asthma- treatment
3 doses albuterol back to back, ipratropium
95
systemic steroids
corticosteroids decreased cells involved with airway inflammation stronger effect than inhaled preparation take 4 hours to kick in PO=IV
96
status asthmaticus
prolonged, nonresponsive asthma attack, can be fatal ``` treatment: aggressive bronchodilator therapy corticosteroids O2 intubation ``` keep SpO2>94% normal CO2 signals impending decompensation
97
PCWP cut-off for noncardiogenic pulmonary edema
PCWP18 signals backed up fluids, and this is more likely to be cardiogenic pulmonary edema, or heart failure
98
ARDS
acute onset of respiratory distress | PaO2:FiO2 ratio
99
COPD
pulmonary disease that includes airflow limitation and chronic inflammation in the airways and lungs
100
Chronic bronchitis
chronic productive cough for 3 months
101
Emphysema
permanent enlargement of airspaces distal to the terminal bronchioles due to destruction of the airspace walls
102
Asthma
chronic inflammation of the airways resulting in airway responsiveness, wheezing, and SOB that is reversible
103
COPD H and P, labs
productive cough recurrent respiratory infection dyspnea, wheezing, rhonchi labs: FEV1/FVC
104
COPD GOLD staging
GOLD 1: FEV1>80% predicted (mild) may be a gradual, relatively asx progression leading to late diagnosis in stage 2 Gold 2: FEV1 50-80% (moderate) Gold 3: FEV1 30-50% (severe) Gold 4: FEV1
105
COPD management
smoking cessation in all patients, and give flu and pneumovax vaccines ``` Category A (Gold 1 or 2 with mild or infrequent symptoms) -short-acting bronchodilator- albuterol, atrovent ``` Category B (Gold 1 or 2 with moderate to severe symptoms) - short- acting bronchodilator - long-acting bronchodilator: B2 agonist or anticholinergic (tiotropium, ipratropium) Category C (GOLD 3 or 4 with mild or infrequent symptoms) - short- acting bronchodilator - long-acting bronchodilator - inhaled steroid Category D (Gold 3 or 4 with moderate to severe symptoms) - short- acting bronchodilator - long-acting bronchodilator - inhaled steroids - +/- theophylline - home oxygen if pulse-ox
106
Indications for home oxygen
pulse-ox
107
vaccinations for patients with COPD
yearly influenza vaccine pneomococcal vaccine -all smokers between age 19 and 65 -single revaccination after age 65 if greater than 5 years since initial vaccination
108
Emphysema
Central- from smoking Panacinar- from A1AT deficiency (alpha 1 antitrypsin inhibits elastase, without it the acini get broken down) ``` H&P: dyspnea productive cough morning headache barrel- chested pursed-lip breathing prolonged expiratory duration decreased heart sounds decreased breath sounds wheezing rhonchi accessory muscle use JVD ``` Labs: PFT: decreased FEV1 decreasd FEV/FVC ratio increasd TLC ABG: decreased O2, increased CO2 CXR: hyperinflated lungs, flat diaphragms, decreased vascular markings DLCO: decreased in proportion to severity of emphysema, +/-normal in chronic bronchitis ``` Treatment: inhaled short-acting beta-2 agonist inhaled anticholinergic inhaled corticosteroid alpha- antitrypsin augmentation lung transplantation (severe) home O2 if pulse-ox ```
109
Chronic bronchitis
chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of chronic cough have been excluded - procedes or follows changes in FVC - smoking is often a risk factor -abx on an individual basis azithromycin levofloxacin amoxicillin with clavulanate
110
What are the possible etiologies for bronchiectasis?
unknown etiology in 50% of patients cystic fibrosis immunodeficiency dyskinetic cilia: Kartagener syndrome (dextrocardia, sinusitis, bronchiectasis), autosomal dominant polycystic kidney disease (ADPKD) Pulmonary infections : TB, fungal infection, lung abscess Obstruction: foreign body aspiration, tumor, lymph nodes Other etiologies: Young syndrome, foreign body aspiration, rhematoid arthritis, Sjogren syndrome, allergic bronchopulmonary aspergillosis, cigarette smoking
111
Bronchiectasis H&P, radiology, Treatment, complications
``` persistent productive cough hemoptysis frequent respiratory infections dyspnea copious sputum wheezing, rales hypoxemia ``` Radiology: multiple cysts and bronchial crowding Treatment: Pulmonary hygeine, chest physical therapy, antibiotics, inhaled beta- 2 agonists and corticosteroids, resection of severely diseased regions of the lungs Complications: cor pulmonale massive hemoptysis abcsess formation
112
Asbestosis
plumbers construction workers demolition workers Complications: - malignant mesothelioma - bronchogenic carcinoma - synergistic effect with tobacco
113
Silicosis
sand blasting increased risk of TB progressive fibrosis
114
Coal- worker's disease
progressive fibrosis | does not increase risk of cancer unless there is radon in the mine
115
berylliosis
ceramics, electronics, dye- manufacturing increased risk of lung cancer may need corticosteroid treatment to maintain respiratory function
116
Goodpasture syndrome
progressive autoimmune disease of the lungs and kidney 2/2 anti-glomerular basement membrane antibodies Characterized by intra-alveolar hemorrhage and glomerular nephritis hemoptysis dyspnea recent respiratory infection diagnosed with +anti-GBM antibodies UA: proteinuria granular casts hematuria Renal biopsy: crescent glomerulonephritis IgG deposition along glomerular capillaries Treatment: plasmapheresis corticosteroids immunosuppressive agents
117
Granulomatosis with polyangiitis
kidney, lung, upper airway ``` H and P: hemoptysis dyspnea myalgias chronic sinusitis ulcerations of nasopharynx, saddle nose deformity ``` labs: c-ANCA positive Treatment: cyclophosphamide corticosteroids rapidly fatal if untreated
118
which pneumoconiosis is associated with progressive fibrosis?
Coal worker's silicosis
119
which pneumoconiosis is associated with increased risk of TB?
silicosis
120
which pneumoconiosis is associated with working with electronics, causes increased cancer risk?
berylliosis
121
which pneumoconiosis is associated with malignant mesothelioma and bronchogenic carcinoma
asbestosis
122
Chromosome 22q11 deletion heart defects
truncus arteriosus | tetralogy of fallot
123
tri21 heart defects
endocardial cushion defects, toF, PDA
124
Congenital rubella heart defects
PDA, pulmonary artery stenosis
125
Turner syndrome heart defect
coarctation of the aorta
126
Marfan syndrome heart defect
aortic regurgitation
127
PE risk factors
``` immobilization malignancy recent surgery pregnancy OCP use obesity fractures prior DVT severe burns ```
128
PE- what does it look like?
``` sudden dyspnea pleuritic chest pain cough +/- syncope feeling of impending doom delirium ``` Tachypnea and tachycardia on exam AMS decreased breath sounds
129
What tests are helpful to order in PE?
ABG: respiratory alkalosis due to hyperventilation but low PO2 due to hypoxia D-dimer: normal D-dimer makes PE much less likely, and an elevated d-dimer is non-specific US of LE veins to rule out DVT: presence of DVT makes PE more likely, absence of DVT does not rule out PE CXR: usually normal, but may have atelectasis, pleural effusion, or Hampton's hump (wedge-shaped opacification at the distal lung fields) EKG changes: most commonly sinus tachycardia +/- nonspecific ST and T-wave changes, and very rarely the classic S1Q3T3 (wide S in lead I, large Q, inverted T in lead III) V/Q scan: useful and accurate only in confirming low or high clinical probability CT scan with contrast (CT PE protocol or CT pulmonary angiography), most commonly used method to diagnose or rule out a PE, but not 100% accurate Pulmonary angiogram: gold standard but mor invasive and rarely performed
130
PE treatment:
``` start O2 IV fluids or pressors LMWH (initially) warfarin (3-6 months) IVC filter if meds are contra-indicated or high risk of fall +/- thrombolytics if massive PE ```
131
Pulmonary HTN
HTN of pulmonary vasc 2/2 PE, valvular disease, left-to-right shunts, COPD idiopathic pulmonary arterial HTN high mortality rate
132
Pulmonary HTN- what does it look like?
dyspnea, fatigue, chest pain, cough, syncope, cyanosis, clubbing of fingers, loud S2 valves slam shut JVD, hepatomegaly ECG- RVH (cor pulmonale) CXR: congested pulmonary arteries, enlarged right ventricle Echocardiogram is how you make this diagnosis! Monitor pulmonary artery pressure noninvasively
133
Pulm HTN- treatment O2, Vasodilators, Anticoagulants, Diuretics
Treat the underlying condition supplemental O2 vasodilators that decrease pulmonary HTN: Prostanoids: epoprostenol, terprostinil, iloprost Endothelin receptor antagonists: bosentan, ambrisentan Cyclic GMP phosphodiesterase inhibitors:sildenafil CCB: nifedipine Anticoagulants if primary pulmonary HTN, embolic disease, cardiac causes Diuretics: pulmonary congestion, JVD
134
Pulmonary edema:
Increased fluid in lung interstitium (as opposed to in the pleural space as you would see in pleural effusion) caused by left-sided heart failure, MI, valvular disease, arrhythmia, ARDS, wedge pressure 18 think cardiogenic causes
135
What does pulmonary edema look like? symptoms, labs, EKG
``` dypsnea orthopnea paroxysmal nocturnal dyspnea frothy pink sputum tachycardia wheezing ``` labs: BNP might be elevated EKG: T- wave abnormalities, QT prolongation CXR: cephalization of vasculature, kerley B lines (prominent interstitial markings in lower lung fields), diffuse interstitial fluid
136
Treat Pulmonary edema
NO LIP ``` nitrates oxygen until spO2 is in the normal range loop diuretics (go to for PE) inotropic drugs (increase contractility) positioning (legs off the edge of bed to keep fluid out of the chest) ```
137
Pulmonary embolism on CXR
Hampton's hump- wedge shaped pulm infarct
138
Most helpful imaging studies when PE is suspected
spiral CT with IV contrast V/Q perfusion scan Pulmonary angiography
139
Primary drugs for treating pulmonary htn
``` vasodilators prostanoids endothelin receptor antagonists phosphodiesterase inhibitors dihydropyridine calcium channel- blockers ```
140
indications for repair on an abdominal aneurysm
ruptured symptomatic >5.5 cm rapidly enlarging (>0.5cm in 6 months)
141
indications for intubating a child with asthma
unable to speak due to the work of breathing unable to maintain adequate oxygenation despite supplementation AMS "count to 10"
142
What is a pleural effusion?
excess fluid that accumulates in the pleural space presents with SOB, dyspnea on exertion, pleuritic chest pain, fatigue, weakness ``` dullness to percussion decreased breath sounds decreased tactile fremitis egophony tracheal deviation away from the effusion ``` Thoracentesis allows us to analyze the fluid
143
What is egophony?
Egophony: E to A changes
144
Bronchophony:
sounds are louder and clearer
145
Whispered pectoriloquy:
whispered sounds are louder
146
Tactile fremitus
transmitted vibrations (effusions insulate the sounds)
147
pathophysiology of a transudate
increased pressure forces filtration across capillary
148
pathophysiology of an exudate
disruption of lining due to inflammatory process leads to leakage of fluid
149
Common causes of transudate
CHF, cirrhosis, nephrotic syndrome
150
common causes of exudate
cancer, infection, vascullitis
151
Light's criteria
exudate if any one of the following: pleural: serum protein ratio >0.5 pleural: serum LDH ratio >0.6 pleural fluid LDH>2/3 of the upper limit of normal for serum LDH
152
Pleural fluid analysis- what should you order?
``` Glucose pH Amylase Triglycerides cell count gram stain cytology ```
153
How do we treat pleural effusion?
thoracentesis chest tube if there is a large amount of fluid pleurodesis (scarring of the surface of the pleura)
154
Empyema- treatment
chest tube for treatment
155
recurrent malignant effusion
special catheter
156
Pneumothorax, causes
spontaneous trauma secondary to medical conditions
157
PTX, types
closed (COPD, TB, blunt chest wall trauma, spontaneous PTX) open (iatrogenic, central line placement, lung biopsy, thoracentesis) tension pneumothorax (trauma to the chest wall) H and P: unilateral chest pain, tiredness, weakness, SOB, decreased wall movement, decreased breath sounds, increased resonance to percussion, decreasd tactile fremitus, hypoxia, JVD, decreased BP, tracheal deviation away from side of pneumothorax
158
Treatment for PTX
small (15%, chest tube open PTX: chest tube, occlusive dressing, attempted closure
159
Treat a tension PTX
hypoxia, low BP | needle decompression immediately into 2nd or 3rd intercostal space, midclavicular line
160
Treatment for recurrent PTX
pleurodesis
161
Hemothorax
caused by trauma, malignancy, infection (TB) H and P: dyspnea, fatigue, pleuritic chest pain, dullness to percussion, decreased tactile fremitus Labs: thoracentesis, watch H and H CXR: mediastinal shift Treatment: O2, chest tube, treat underlying cause
162
Complications to hemothorax
clot can harden and scar down, and become harder to remove
163
Malignant mesotheloima
asbestos exposure H and P: chest pain, dyspnea, dullness to percussion, exudative pleural effusion, chest wall mass Treatment: poor prognosis surgery, chemotherapy, radiotherapy, radical surgery
164
What study helps to determine if a pleural effusion is loculated or free- flowing?
upright CXR | lateral decubitus CXR
165
sleep apnea
cessation of breathing for at least 10 seconds 3 types: central obstructive mixed
166
risk factors/ exacerbators for sleep apnea
``` obesity sedatives intoxication alcohol male gender History and physical: excessive sleeping during the day, snores loudly, awakes gasping for air, morning headaches, overweight or obese, short, fat neck, abnormal palate or pharynx, large adenoids ``` Labs: epworth sleepiness scale polysomnography (apnea index) increased H/H (hypoxemia) Treatment for OSA: weightloss avoid alcohol and hypnotic medications continuous positive airway pressure (CPAP) first line, nasal facemask oral appliance (protrude the mandible forward or hold tongue anterior) surgical options (uvulopalatopharyngoplasty) rarely, tracheostomy stimulants -modafinil -armodafinil
167
What is the treatment for central sleep apnea
CPAP BiPAP ASV (adaptive servo- ventilation), which tries to synchronize with the patient's breathing Oxygen supplementation Acetazolamide
168
Atelectasis
``` local collapse of lung often occurs post- surgery anesthesia asthmatics foreign bodies mass effect from tumors various pulmonary lesions can lead to increased work of breathing and hypoxemia, may be symptomatic, if persistent can lead to PNA ``` CXR: fluffy infiltrates, there may be lobar collapse Treatment: IS, post-op ambulation, upper airway suctioning with bronchoscopy
169
Intubation
Pre-oxygenate Pre-treatment: Lidocaine blunts increase in intracranial pressure- good for head trauma Fentanyl blunts pain response Atropine decreases airway secretions, prevents bradycardia Paralysis induction: a. sedatives (etomidate, propofol, midazolam, ketamine) b. paralytics (succinylcholine, rocuronium) protection and positioning placing endotracheal tube (end tidal CO2, auscultate) Complications: tube misplacement vomiting aspiration dental injuries Longterm tracheostomy may be required if the patient has had an ET tube for several weeks
170
Ventilation
inspiration by ventilator expiration spontaneous ventilation is an art
171
Controlled mechanical ventilation
machine controls rate and tidal volume, initiates every breath, patient does not use own energy to breath
172
intermittent mandatory ventilation
machine controls rate and tidal volume Patient is able to breath in between mechanical breaths used when weaning patient off of ventilation
173
Synchronized intermittent mandatory ventilation (SIMV)
synchronizes rate with initiated breaths delivers tidal volume and rate patient breaths in between mechanical breaths used when weaning off mechanical ventilation
174
Assist controlled ventilation (AC)
wait until the patient attempts to breath, then delivers full tidal volume machine sets a baseline rate used when weaning patient off of ventilator
175
Continuous positive airway pressure (CPAP)
positive pressure to keep airway open patient is initiating every breath last step before weaning
176
Extubation- how do you know when the patient is ready?
max inspiratory pressure 10mL/kg Minute ventilation 200 Frequency/tidal volume ratio
177
What substances should be avoided in patients with OSA?
sedatives (benzodiazepines, alcohol, antihistamines)