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STEP2 > Pulmonology > Flashcards

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

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2
Q

Total lung capacity

A

increased in obstructive lung disease

decreased in restrictive lung disease

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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

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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

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5
Q

DLCO

A

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

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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

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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
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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

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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

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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)

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11
Q

What nonbacterial infections present with tonsillar exudates?

A

infectious mononucleosis

strep pharyngitis

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12
Q

Tonsillar infections

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

Treatment: beta- lactam antibiotics (penicillin, amoxicillin)

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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

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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)

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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

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16
Q

Sinusitus- chronic

A

usually caused by sinus obstruction and anaerobic infection

DM predisposes to mucor mycosis

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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
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18
Q

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

A

ARF and glomerulonephritis

ARF can be prevented

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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

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20
Q

murmurs that decrease with squatting

A

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

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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
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22
Q

PNA

A

inflammation in the alveoli

  • CAP
  • HAP

Clinical manifestations can break down into typical and atypical

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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
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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

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25
Q

Viral causes of PNA

A 
influenza 
parainfluenza
adenovirus
cytomegalovirus
RSV (MCC viral PNA in children)
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26
Q

Streptococcus pneumonaie PNA

A

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
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27
Q

Haemophilus influenzae

A

COPD
SCD
slower onset of symptoms

Treatment: 
beta- lactams
fluoroquinolones
doxycycline
macrolides
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28
Q

staph aureus PNA

A
  • Nosocomial pneumonia in immunocompromised patients
  • Seen in higher rate in patients with influenza
  • Abscess formation

Treatment: beta lactams, MRSA coverage (incase resistant)

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29
Q

Klebsiella pneumoniae

A

Alcoholics, aspiration, hospitalized, sickle cell, currant- jelly sputum

Treatment:
cephalosporins
aminoglycosides

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30
Q

pseudomonas aeruginosa PNA

A

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
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31
Q

GBS PNA

A

neonates and infants
respiratory distress and lethargy

Treatment:
beta- lactams
ampicillin and gentamicin

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32
Q

Enterobacter spp.

A

Nosocomial pneumonia
elderly patients

3rd generation cephalosporins
-carbapenem

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33
Q

Mycoplasma pneumoniae

A

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

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34
Q

Legionella pneumophila

A

aerosolized water, and can be passed from person to person

slow onset
nausea, diarrhea
confusion, ataxia
Treatment: macrolides, fluoroquinolones

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35
Q

Chlamidophile pneumoniae

A

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
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36
Q

Empiric therapy for PNA (cover s. pneumoniae and atypical organisms)

A

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
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37
Q

Most common PNA agent in children

A

RSV

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38
Q

Most common PNA agent in adults

A

strep pneumo

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39
Q

PNA with Higher rate after influenza

A

s. aureus

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40
Q

PNA with currant jelly sputum

A

klebsiella

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41
Q

PNA with associated with CF

A

pseudomonas

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42
Q

PNA MC in neonates

A

GBS

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43
Q

PNA Associated with elderly

A

enterobacter (Gram negative)

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44
Q

PNA common in young adults

A

mycoplasma

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45
Q

PNA associated with aerosolized water

A

legionella

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46
Q

Neonates (first 28 days of life) most common causes of PNA

A
  1. GBS is most common
  2. E. Coli
  3. Chlamydia trachomatis (long incubation, sx appear 12 weeks later)
  4. Herpes simplex virus
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47
Q

MCC PNA in children

A

RSV
Strep pneumoniae
chlamidophila pneumoniae

in older children, think about mycoplasma pneumoniae

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48
Q

MCC PNA in adults

A 
Streptococcus pneumoniae
Haemophilus influenza
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Influenza
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49
Q

MCC PNA in elderly

A 
Streptococcus pneumoniae
Haemophilus influenzae
Influenza
Staphylococcus aureus
Anaerobes
Gram- negative rods
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50
Q

What are the indications for pneumococcal vaccination in adults?

A
  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
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51
Q

PNA and gram-positive cocci in clusters

A

s. aureus

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52
Q

gram- positive cocci in pairs in the context of PNA

A

s. pneumoniae

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53
Q

gram- negative rods in 80 year-old with PNA

A

e. coli

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54
Q

gram positive cocci in neonate PNA

A

GBS

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55
Q

gram neg rods in neonate PNA

A

e. coli

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56
Q

Fungal PNA with PMHx of travel to SW US

A

coccidiomycosis

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57
Q

Fungal PNA with PMHx of caves, spelunking, bats

A

histoplasmosis

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58
Q

Fungal PNA with PMHx of trave l to eastern North America

A

blastomycosis

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59
Q

Fungal PNA with PMHx of travel to s. America

A

paracoccidiomycosis

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60
Q

Antifungals used to treat fungal PNA

A

Amphotericin B
Ketoconazole
Itraconazole
Fluconazole

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61
Q

Pneumocystic jiroveci (PCP)

A

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)

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62
Q

Tuberculosis (primary and secondary)

A

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

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63
Q

Ghon focus vs Ghon complex. Both associated with primary tuberculosis

A

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

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64
Q

How do you interpret a positive PPD?

A

current infection
past exposure
vaccination

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65
Q

5mm PPD is considered positive in

A

highest risk pop

HIV+
Close contact with TB
CXR findings suggestive of TB

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66
Q

10mm PPD is considered positive in

A 
homeless
immigrants
IV drug users
chronically ill
healthcare workers
recently incarcerated
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67
Q

15mm PPD is considered positive in

A

anyone, including low-risk

15mm is always considered positive

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68
Q

Significance of negative PPD skin test

A 
negative
no infection
anergic
malnutrition
immunocompromise
sarcoidosis
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69
Q

Secondary TB

A

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
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70
Q

Labs to confirm TB

A

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

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71
Q

Treat TB

A 
Latent- INH (6-9 months)
Primary or secondary TB- RIPE
Rifampin
INH (with B6 to prevent peripheral neuropathy)
Pyrazinamide
Ethambutol
72
Q

BCG vaccine

A

varying efficacy
can have a false positive PPD
in the 1st year of life, after 10 years, should be PPD negative

73
Q

Causes of ARDS

A

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
Q

Symptoms and Signs of ARDS

A

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
Q

Treat ARDS

A

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
Q

What percentage FiO2 does a nasal cannula provide?

A

24-40% FiO2 (FiO2 increases 3% for every 1L/min up to 6L/min)

77
Q

What percentage FiO2 does a face mask provide?

A

50-60% FiO2

78
Q

What percentage FiO2 does a non-rebreather provide?

A

60-95% FiO2

79
Q

What percentage FiO2 does a CPAP provide?

A

80% FiO2

80
Q

What perventage FiO2 does mechanical ventilation provide?

A

up to 100% FiO2

81
Q

Asthma

A

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
Q

Pulsus paradoxus

A

deep inspiration causes SBP to drop at least or more than 10mmHg

83
Q

Definition of mild intermittent asthma

A

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
Q

Definition of mild persistent asthma

A

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
Q

Definition of moderate persistent asthma

A 
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
Q

Definition of severe persistent asthma

A

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
Q

Rapid- acting beta2 agonists

A

bronchodilators
rapid onset of action

albuterol, levalbuterol

88
Q

Long- acting beta2 agonists

A

salmeterol, fometerol

bronchodilators, gradual onset, sustained activity

89
Q

Inhaled corticosteroids

A

decreased cells involved with airway inflammation, mild persistent and onward, often combined with rapid- acting beta2 agonists

90
Q

Leukotriene inhibitors

A

montelukast, zafirlukast, ziluton

block activity or production of leukotrienes (inflammation and bronchospasm), useful in patients with rhinitis- like sx

91
Q

Mast cell stabilizing agents

A

cromolyn, etc

stabilizes mast cells
anti-inflammatory prophylaxis
not useful acutely, not used much at all
dosed 3-4 times per day

92
Q

Theophylline bronchodilator

A 
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
Q

Anticholinergic agents

A

block vagal- mediated smooth muscle contraction

used as adjunctive therapy in moderate-to-severe asthma

94
Q

acute asthma- treatment

A

3 doses albuterol back to back, ipratropium

95
Q

systemic steroids

A

corticosteroids
decreased cells involved with airway inflammation
stronger effect than inhaled preparation
take 4 hours to kick in

PO=IV

96
Q

status asthmaticus

A

prolonged, nonresponsive asthma attack, can be fatal

treatment:
aggressive bronchodilator therapy
corticosteroids
O2
intubation

keep SpO2>94%
normal CO2 signals impending decompensation

97
Q

PCWP cut-off for noncardiogenic pulmonary edema

A

PCWP18 signals backed up fluids, and this is more likely to be cardiogenic pulmonary edema, or heart failure

98
Q

ARDS

A

acute onset of respiratory distress

PaO2:FiO2 ratio

99
Q

COPD

A

pulmonary disease that includes airflow limitation and chronic inflammation in the airways and lungs

100
Q

Chronic bronchitis

A

chronic productive cough for 3 months

101
Q

Emphysema

A

permanent enlargement of airspaces distal to the terminal bronchioles due to destruction of the airspace walls

102
Q

Asthma

A

chronic inflammation of the airways resulting in airway responsiveness, wheezing, and SOB that is reversible

103
Q

COPD H and P, labs

A

productive cough
recurrent respiratory infection
dyspnea, wheezing, rhonchi

labs: FEV1/FVC

104
Q

COPD GOLD staging

A

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
Q

COPD management

A

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
Q

Indications for home oxygen

A

pulse-ox

107
Q

vaccinations for patients with COPD

A

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
Q

Emphysema

A

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
Q

Chronic bronchitis

A

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
Q

What are the possible etiologies for bronchiectasis?

A

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
Q

Bronchiectasis H&P, radiology, Treatment, complications

A 
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
Q

Asbestosis

A

plumbers
construction workers
demolition workers

Complications:

  • malignant mesothelioma
  • bronchogenic carcinoma
  • synergistic effect with tobacco
113
Q

Silicosis

A

sand blasting

increased risk of TB
progressive fibrosis

114
Q

Coal- worker’s disease

A

progressive fibrosis

does not increase risk of cancer unless there is radon in the mine

115
Q

berylliosis

A

ceramics, electronics, dye- manufacturing
increased risk of lung cancer
may need corticosteroid treatment to maintain respiratory function

116
Q

Goodpasture syndrome

A

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
Q

Granulomatosis with polyangiitis

A

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
Q

which pneumoconiosis is associated with progressive fibrosis?

A

Coal worker’s silicosis

119
Q

which pneumoconiosis is associated with increased risk of TB?

A

silicosis

120
Q

which pneumoconiosis is associated with working with electronics, causes increased cancer risk?

A

berylliosis

121
Q

which pneumoconiosis is associated with malignant mesothelioma and bronchogenic carcinoma

A

asbestosis

122
Q

Chromosome 22q11 deletion heart defects

A

truncus arteriosus

tetralogy of fallot

123
Q

tri21 heart defects

A

endocardial cushion defects, toF, PDA

124
Q

Congenital rubella heart defects

A

PDA, pulmonary artery stenosis

125
Q

Turner syndrome heart defect

A

coarctation of the aorta

126
Q

Marfan syndrome heart defect

A

aortic regurgitation

127
Q

PE risk factors

A 
immobilization
malignancy
recent surgery
pregnancy
OCP use
obesity
fractures
prior DVT
severe burns
128
Q

PE- what does it look like?

A 
sudden dyspnea
pleuritic chest pain
cough
\+/- syncope
feeling of impending doom
delirium

Tachypnea and tachycardia on exam
AMS

decreased breath sounds

129
Q

What tests are helpful to order in PE?

A

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
Q

PE treatment:

A 
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
Q

Pulmonary HTN

A

HTN of pulmonary vasc

2/2 PE, valvular disease, left-to-right shunts, COPD

idiopathic pulmonary arterial HTN

high mortality rate

132
Q

Pulmonary HTN- what does it look like?

A

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
Q

Pulm HTN- treatment

O2, Vasodilators, Anticoagulants, Diuretics

A

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
Q

Pulmonary edema:

A

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
Q

What does pulmonary edema look like?

symptoms, labs, EKG

A 
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
Q

Treat Pulmonary edema

A

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
Q

Pulmonary embolism on CXR

A

Hampton’s hump- wedge shaped pulm infarct

138
Q

Most helpful imaging studies when PE is suspected

A

spiral CT with IV contrast
V/Q perfusion scan
Pulmonary angiography

139
Q

Primary drugs for treating pulmonary htn

A 
vasodilators
prostanoids
endothelin receptor antagonists
phosphodiesterase inhibitors
dihydropyridine calcium channel- blockers
140
Q

indications for repair on an abdominal aneurysm

A

ruptured
symptomatic
>5.5 cm
rapidly enlarging (>0.5cm in 6 months)

141
Q

indications for intubating a child with asthma

A

unable to speak due to the work of breathing

unable to maintain adequate oxygenation despite supplementation

AMS

“count to 10”

142
Q

What is a pleural effusion?

A

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
Q

What is egophony?

A

Egophony: E to A changes

144
Q

Bronchophony:

A

sounds are louder and clearer

145
Q

Whispered pectoriloquy:

A

whispered sounds are louder

146
Q

Tactile fremitus

A

transmitted vibrations (effusions insulate the sounds)

147
Q

pathophysiology of a transudate

A

increased pressure forces filtration across capillary

148
Q

pathophysiology of an exudate

A

disruption of lining due to inflammatory process leads to leakage of fluid

149
Q

Common causes of transudate

A

CHF, cirrhosis, nephrotic syndrome

150
Q

common causes of exudate

A

cancer, infection, vascullitis

151
Q

Light’s criteria

A

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
Q

Pleural fluid analysis- what should you order?

A 
Glucose
pH
Amylase
Triglycerides
cell count
gram stain 
cytology
153
Q

How do we treat pleural effusion?

A

thoracentesis
chest tube if there is a large amount of fluid
pleurodesis (scarring of the surface of the pleura)

154
Q

Empyema- treatment

A

chest tube for treatment

155
Q

recurrent malignant effusion

A

special catheter

156
Q

Pneumothorax, causes

A

spontaneous
trauma
secondary to medical conditions

157
Q

PTX, types

A

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
Q

Treatment for PTX

A

small (15%, chest tube

open PTX: chest tube, occlusive dressing, attempted closure

159
Q

Treat a tension PTX

A

hypoxia, low BP

needle decompression immediately into 2nd or 3rd intercostal space, midclavicular line

160
Q

Treatment for recurrent PTX

A

pleurodesis

161
Q

Hemothorax

A

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
Q

Complications to hemothorax

A

clot can harden and scar down, and become harder to remove

163
Q

Malignant mesotheloima

A

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
Q

What study helps to determine if a pleural effusion is loculated or free- flowing?

A

upright CXR

lateral decubitus CXR

165
Q

sleep apnea

A

cessation of breathing for at least 10 seconds

3 types:
central
obstructive
mixed

166
Q

risk factors/ exacerbators for sleep apnea

A 
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
Q

What is the treatment for central sleep apnea

A

CPAP
BiPAP
ASV (adaptive servo- ventilation), which tries to synchronize with the patient’s breathing

Oxygen supplementation
Acetazolamide

168
Q

Atelectasis

A 
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
Q

Intubation

A

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
Q

Ventilation

A

inspiration by ventilator
expiration spontaneous

ventilation is an art

171
Q

Controlled mechanical ventilation

A

machine controls rate and tidal volume, initiates every breath, patient does not use own energy to breath

172
Q

intermittent mandatory ventilation

A

machine controls rate and tidal volume
Patient is able to breath in between mechanical breaths
used when weaning patient off of ventilation

173
Q

Synchronized intermittent mandatory ventilation (SIMV)

A

synchronizes rate with initiated breaths
delivers tidal volume and rate
patient breaths in between mechanical breaths
used when weaning off mechanical ventilation

174
Q

Assist controlled ventilation (AC)

A

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
Q

Continuous positive airway pressure (CPAP)

A

positive pressure to keep airway open
patient is initiating every breath

last step before weaning

176
Q

Extubation- how do you know when the patient is ready?

A

max inspiratory pressure 10mL/kg

Minute ventilation 200

Frequency/tidal volume ratio

177
Q

What substances should be avoided in patients with OSA?

A

sedatives (benzodiazepines, alcohol, antihistamines)

STEP2 (34 decks)

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