Clin Med Exam 2 Flashcards
Coin Lesion
<3 cm SMALL well defined bordered lung lesion- completely surrounded by pulmonary parenchyma
Coin lesion
<3 cm
not assoc w/ infiltrate, atelectasis, or adenopathy
Most BENIGN
smooth edges
dense central calfification
Coin Lesion (SPN)
<3 cm
most common are infectious granulomas
Mass
> 3 cm
more likely Cancerous
After what age, chance of an SPN being malignant increases to 50%?
60 or older!!
Risk factors for SPN being malignant
Obvious ones: tobacco, family hx, previous CA, asbestos
ALSO:
Female> Male, emphysema
SPNs in AZ
good chance it is Cocci 60% are
1st step approach to SPN
Review old films
Malignant nodules usually double in 1-13 months
Minimal growth of SPN
minimal in 2 years suggests BENIGN lesion
Calcification of SPN
usually benign
No calcification of SPN
bad sign
Increase risk of Malignancy
Size of lesions
<3cm is considered Small Pulm Nodule (SPN)
IF 5 cm or greater = 90% CA
Preferred imaging for SPN
Helical CT WITHOUT contrast with low dose radiation
Helical CT without contrast details:
thin 1 mm sections
Most reliable for: nodule size, growth, lobar location, density and borders
Solid nodule > 8mm and Low probability, what next?
CT at 3 months
no growth: another CT at 9-12 and 18-24
growth: pathologic eval
Solid nodule > 8mm and Intermediate probability, what next?
FDG PET/CT and or Biopsy
CT again at 3, 9-12, and 18-24 months
Solid nodule >8mm and High probability, what next?
Biopsy or excision!!! not only CT in this case- need to do more
Staging with PET/CT may be helpful
Solid nodule 6-8 mm
Follow w CT at 6-12 months, repeat as indicated
Solid nodule < 6mm
does not require f/u
CT at 12 months is optional (pt dependent)
Indications for Referral
New/enlarging lesion
Lesion is, unstable, not calcified, irregular shape, >3cm
Lesions are are indeterminate
Small cell CA is associated with
SIADH, Cushings syndrome, Eaton Lambert Synd, and Mets to BRAIN
Staging of Small Cell
Limited (to ipsilateral hemithorax) vs Extensive (extends beyond hemithorax, includes pleural effusions)
Staging of Non Small Cell
“T-N-M”
T: primary tumor
N: nodal involvement
M: distant Mets
Performance status
0: fully active
1: strenous PE restricted, but able to carry out light work
2: capable of all self care, but unable to carry out work activities, about 50% of waking hours
3: capable of only light, limited self care
confined to bed >50% of waking hours
4: completely disabled, cannot carry out any self care
If FEV1 is <60% and Lung CA
<60 is the strongest indicator of post-op complications
What is used in PET scans
FDG
Fluorodeoxyglucose
Downfall of PET scan
does not detect all CA (i.e. bronchoalveolar CA)
Air is
Black on X Ray
Bone is
White on X Ray
Fluid is
Grey on X Ray
PA (posterior anterior view)
Good for X Ray bc it doesn’t falsely enlarge the heart
Systematic approach for reading CXR
A-airway (trachea midline?) B- bones (fracture) C- cardiac outline D- diaphragm (free air?) E- edges (pleural plaques, effusion? F- fields (infiltrates, nodules?)
PA and Lateral view of CXR allow us to see
structures behind the heart and diaphgram
PA and Lateral decubitis CXR
good to evaluate for PNA vs effusion
with effusion (Fluid) will lay out when person lies down
Pulmonary infarct
“Hamptons hump” on CXR
CT
a bunch of cross sectional slices thru body
a bunch of X ray slices
Indications for CT
Clarify abnormal CXR Characterize pulm nodules Assist in dx of clinical sx Detect and Stage CA Evaluate suspected mediastinal or hilar mass
Conventional CT scan
10 mm slice
Step and shoot
25-30 min
Helical (spiral) CT
Faster
Continuous
<5 minutes
HRCT
1mm slice
best detail
Low dose CT
LDCT
Used for Screening
less detail
CT angiography
CTPA
Special populations to consider with CT scans
Peds- more radiosensitive than adults, inc risk of leukemia and brain tumors, radiation risk compounded d/t lifespan
Pregnant- in utero exposure linked to pediatric CA mortality
CT WITH contras
Iodine
When is contrast needed with a CT?
Vessels
Malignancy
Trauma
3 main risk of Iodine contrast with a CT scan
- Allergic rxn
- Contrast induced Nephropathy (kidney)
- Lactic acidosis (if taking glucophage/Metformin)
Allergic rxn to Radiocontrast
5-60 min after exposure
Risk factors: prior rxn, hx of Asthma or Atopy
Pre-tx with Prednisone and Diphenhydramine (benadryl)
CIN- Contrast Induced Nephropathy
Increased serum creatinine >/ -.5 or >/ 25 % from baseline
1-2 day after exposure, peaks at 3-5 days
Usually reversible
Caution using contrast in pts with impaired kidney fx
Creat > 1.5
GFR <60
Use alternative (CT without contrast, MRI without gadolinium, or US)
Check Renal fx prior to giving contrast IF
>60 YO Renal dz HTN on meds Diabetes Taking Glucophage
CTPA
replaced conventional catheter directed pulmonary angiography
less invasive, less $, and less time
CTPA
detect PE, Aortic dissection, SVC syndrome
Gold standard in evaluation of PE (even though it is invasive)
Catheter-directed Pulmonary Angiography
Catheter directed pulmonary angiography (invasive)
Needle/catheter is inserted into R femoral or internal jugular vein; into R side of heart and pulmonary arteries
Dye is injected and X rays taken
When is catheter directed pulmonary angiography especially useful?
When V/Q scan or CTPA is inconclusive BUT high clinical suspicion for PE
MRI has limited use in Pulmonary field, BUT use if
Hilar or mediastinal density
Sulcus tumor (pancoast)
Cyst/lesion of chest wall
HIGH QUALITY images of blood vessels
If person is allergic to Iodine (used in CT)
can do MRI with Gadolinium instead
MRI is less detailed for
Lung parenchyma (compared to CT chest)
No bone artifact seen on
MRI
AND no ionizing radiation
Limitations with MRI
Claustrophobia
Nephrogenic Systemic Fibrosis- avoid use of Gadolinium if GFR <30
Possible contra to MRI
Implanted pacemaker/defib
Metal in eye
Aneursym clip in brain
Cochlear implant
V/Q
Evaluate PE and
Pre-op assessment (before lung resection)
V/Q process
IV phase (perfusion): Tach 99 labeled to albumin
Inhalation (ventilation): radio labeled Xenon gas
Test of choice to dx PE in pregnant woman
V/Q scan
V/Q scan is best utilized in:
pts with normal CXR and high suspicion for PE
Absolute contra for V/Q?
NONE
PET
Standardized uptake value (SUV)
>2.5 raises possibility of CA
Indications for Ultrasound in the Pulmonary field
Bedside detection of pleural fluid, hemothorax, or pneumothorax
Guide thoracocentesis
Place thoracostomy tubes
Normal lung on US
Positive motion lung beach “seashore sign”
Diseased lung with no chest wall motion (pneumothorax) on US
“Barcode/stratosphere sign”
Bronchoscopy
Diagnostic and therapeutic
Bronchoscopy Dx indications
Evaluate PNA, hemoptysis, cough
Dx tracheoesophogeal fistula/tracheobronchomalacia
Tissue sampling
Bronchoscopy Therapeutic
Remove excess mucus or FB
ET tube placement
Contraindications to Bronchoscopy
Severe hypoxia Bleeding risk Pulm HTN Severe cough/gag Tracheal stenosis
How to perform spirometry
- relax and breathe normally
- deep Inhale
- Forceful exhale
- another deep Inhale
Forced vital capacity on Spirometry
Deep breath in, blow air out as fast as possible = total volume of air with max effort
FEV-1
most useful information for obstructive
FEV1/FVC ratio
Defines severity of obstruction
Diff b/w Obstructive and Restrictive
Ratrio
<0.7 is RESTRICTVE
Bronchodilator reversibility testing
Nebulizer/inhaler 2-4 puffs Hold inhaled med for 5-10 seconds Spirometry test again 15 min after med provided 3-8 rounds of testing
Reversibility is positive IF
FEV1 increases by 12% and 200 ml with Bronchodilator testing
Bronchoprovocation
BUT BE CAREFUL
Dilute solution of Methacholine
Spirometry at 30 and 90 seconds
Positive if FEV1 decreases by 20%
Quality of curve must meet these parameters
curve plateaus
expiration >6 seconds
two best efforts w/in 0.2 L
volume loop free of Artifact
Obstructive
wide and scooped out
Restrictive pattern
Steep and overall less volume
DLCO
ability of lungs to txr gas and Saturate Hgb
misleading if person is anemic
DLCO technique
Pt inhales a single breath of gas with helium and Carbon Monoxide, expires, and measurement of exhalation is taken
Healthy lung: little CO collected (bc most of it was txr in persons lung)
Diseased lung: high levels measured in exhaled gas bc lung txr in persons body is not working well
Obstructive pattern
Can get air in, but cant get it out
High lung volumes
TLC: Increased
Ratio decreased
Restrictive pattern
Trouble getting air IN and OUT
Reduced lung volumed
EVERYTHING: decreased, except
Ratio: normal or increased
Most things we hear about often are Obstructive
Asthma Bronchitis COPD Cystic Fibrosis Emphysema Obstruction
Examples of Restrictive
Pulm Fibrosis Infectious lung dz Thoracic deformity Effusion Tumor Neuromusc dz Obesity
FEV1 value is decreased by more than 15-20% of predicted
OBSTRUCTIVE
FEV1 <80% predicted
OBSTRUCTIVE
With obstructive
FEV1 decreased
but TLC increased (bc person can get air in, trapped, cant get it out)
Ratio <70%
Obstructive
Ratio is normal or increased
Restrictive
How often to take Lung fx tests?
At diagnosis
3-6 months after starting tx (FEV1)
Every 1-2 yrs (more for high risk and children)
Asthma
Chronic inflammation
Intermittent and REVERSIBLE obstruction
Bronchial hyper-responsiveness
Often develop sx before age 5, but misdx
Cough (nocturnal)
Wheezing*- hallmark sx
Wheezing in asthma can be heard with Ins and Exp but usually heard with
EXP due to obstructive pattern
Look for signs of Severe obstruction
Tripod position Tachycardic tachypneic Access muscle use Pulsus paradoxus
ASA Triad/ Samter’s triad
Sinus dz with: Nasal polyps, ASA sensitivity, severe asthma
Atopic triad
Atopic dermatitis –> (food allergy) –> allergic rhinitis –> asthma
Gold standard ratio of COPD for Ratio
<70%
Reversibility bronchodilator test
> 12% adults
>8% in young children
Intermittent Asthma
Sx 2 or less days/wk
No PM awakenings for younger, 2 or less/month for older
FEV> 80%
Ratio: normal
2 or less SABA use
Mild Persistent Asthma
Sx >2 days wk
PM awakenings 1-2/mo for younger, 3-4/mo for older
FEV >80% still
Ratio: normal
>2 days/wk SABA use
Moderate Persistent Asthma
Daily sx
PM awakenings 3-4/mo for younger, once a week for older
FEV 60-80% !!!!
Ratio: reduced!!
Daily SABA use
Severe Persistent Asthma
Sx throughout day
PM awakenings once/mo for younger, nightly for older
FEV1 <60%
Ratio reduced
Extremely limited activity
SABA use several times daily
Stage 1 asthma
“Intermittent”
SABA prn
Stage 2 asthma
“Mild persistent”
Low dose ICS daily
OR
LTRA or Cromolyn
Stage 3 asthma
“Moderate persistent”
consider specialist
Medium dose ICS
OR
(Low dose ICS + LABA)
Any time LABA is seen, if you are <5 YO,
replace with LTRA
Stage 4 asthma
“Severe persistent”
definitely refer to specialist
Medium dose ICS and LABA
OR
(Medium dose ICS + LTRA)
Poorly controlled Step 5 asthma
High dose ICS and LABA
Poorly controlled Step 6 asthma
High dose ICS and LABA and Oral steroids
Step 5 and 6 poorly controlled Asthma
Consider adding Omalizumab (Xolair) for ages 12 or greater with allergies
PEFT: Peak Expiratory Flow Rate
> 80% green: good control
50-80% yellow: SABA and med
<50%: Medical alert!!!! ED
Tx for Exacerbation
Oxygen SABA Systemic corticosteroids Abx prn Respiratory monitoring if in ED/inpatient Severe: C-PAP, BiPAP, intubation
How soon to f/u after an Acute Exacerbation of Asthma?
within 1 week!!
Small airway dz vs. Parenchymal destruction
Small airway- inflammation and remodeling
Parenchymal destruction- loss of alveolar attachments and elastic recoil
COPD former terms
Emphysema and Chronic Bronchitis
Emphysema
destruction of alveoli
Chronic Bronchitis
Cough and sputum >3 months in each of past 2 consecutive years
Small airway dz
Inflammation bronchial wall, infiltration of submucosal layer by NEUTROPHILs, bacterial colonization, airway hyper-reactive
Mucous glands enlarge, hypersecretion, loss of ciliary transport, bronchial squamous metaplasia
Parenchymal dz
Destruction of alveolar walls, extensive ELASTASE or ANTITRYPSIN deficiency, reduced alveolar exchange
Parenchymal dz structural change
Decreased elastic recoil
Enlargement of air spaces DISTAL to terminal bronchioles
Systemic effects of COPD
Cor pulmonale Cyanosis Wt gain or loss Resp Acidosis Hypoxemia, Hypercapnia
Sx of COPD (3)
Chronic cough, dyspnea, Sputum production
Sx of CODP
5th or 6th decade
most common early sx: DOE
Elastase and relation to COPD
Degenerative changes in elastin and alveolar structures
Release of cytoxic oxygen radicals from WBC in lung tissue
A-1 Antitrypsin Deficiency
Hereditary
causes premature emphysema
AAT is an inhibitor of Elastase
If not present, elastase does its thing too much
Main sx of COPD
Dyspnea
Cough
Sputum production
PE findings of COPD
Tripod Access muscle usage Pursed lip Cyanosis Tobacco staining S3 gallop or RV lift Muscle wasting Peripheral edema Barrel chest Prolonged expiration Dec breath sounds Wheezing or Rhonchi
Pursed lip breathing
Keeps intrabronchial pressure high during exhalation, keeping bronchi open and allowing more air to be expelled
Most common cause of Cor Pulmonale
COPD
What is required to establish a COPD dx?
Spirometry
What is normal ratio?
70-80% of predicted OR
greater than Lower limit normal which is >5th percentile
Ratio of what confirms obstructive?
<0.7 %
Mild COPD
FEV1 >/ 80%
Moderate COPD
FEV1 50-80%
Severe COPD
FEV1 30-50%
Very severe COPD
FEV1 <30%
As COPD progresses, what is common?
Respiratory acidosis
not able to breathe off CO2
When is Arterial Blood Gas indicated?
FEV1 <50
SPO2 <92
Depressed LOC
Acute exac of COPD
Why do we get BNP
Evaluate suspected Heart Failure
When to get AAT (Alpha-1 Antitrypsin) lab?
sx in a young pt <45
Non smoker
Family hx emphysema
What might you see on CXR of someone with COPD?
Increased AP diameter
Hyperinflation and hyperlucency
Flattened diaphragm
Blebs/ Bullae are pathognomic for on CXR
Emphysema
Perivascular/peribronchial markings on CXR
Chronic Bronchitis