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*USMLE* > Pulmonary > Flashcards

Pulmonary Flashcards

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USMLE® Step 1 flashcards
1
Q

Silicosis

sx, cxr and biopsy

disease associations

A

a pneumoconiosis from mineral dust inhalation

often no sx; dyspnea on exertion + productive cough 10-20 years after 1st exposure

cxr shows MANY BILATERAL NODULES, mostly APICAL + calcified hilar nodes

biopsy of CALCIFIED HILAR NODE shows birefringent particles surrounded by WHORLED collagen fibers + dusty macrophages

assoc. with TBC risk via impaired macrophage function

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2
Q

Asbestosis

sx, cxr, biopsy

A

dyspnea on exertion

cxr shows interstitial involvement in LOWER zones +/- PLEURAL PLAQUES

histo shows FERRUGINOUS bodies (fusiform rod with translucent asbestos center + iron coating)

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3
Q

Berylliosis

sx, cxr, biopsy

A

dyspnea

cxr shows ill-defined nodular + irregular opacities

histo shows NON-CASEATING GRANULOMA with associated particles (diff from HS pneumonitis)

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4
Q

Coal Pneumoconiosis

sx, cxr, biopsy

A

exertional dyspnea

cxr shows nodular interstitial opacities

histo of node/perinodal lung shows COAL-LADEN MACROPHAGES (“coal macules”)

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5
Q

Hypersensitivity Pneumonitis

sx, cxr, histo, associations

A

exertional dyspnea

cxr shows diffuse nodular interstitial infiltrate

histo shows NON-CASEATING GRANULOMA (no particles as on berylliosis)

assoc. with bird/birdcage contact, Aspergillus fumigatus and other organic dusts (T2/T3 HS rxns)

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6
Q

ARDS

causes + pathogenesis

A

Sepsis, pneumonia
Trauma
Pancreatitis

direct or indirect pulmonary insult (irritants, trauma, aspiration, pancreatitis, sepsis) causes CYTOKINE release > endothelial activation > increased permeability > NEUTROPHIL activation + degranulation plus alveolar edema with hyaline formation and atelectasis

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7
Q

ARDS

clinical features, effects on various breathing parameters

distinguishing feature from cardiogenic pulmonary edema?

A

hypoxia
CXR shows bilateral infiltrates

decreased compliance, increased work of breathing
V/Q mismatch via inadequate perfusion

ARDS has NORMAL pulmonary capillary wedge pressure (6-12 mmHg) which would be increased in cardiogenic causes of pulmonary edema

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8
Q

FRC

what is it? how does it change in COPD

A

FRC = ERV + RV

ERV = expiratory reserve volume = the amount that can still be exhaled after expiration of tidal volume

RV = residual volume

FRC will INCREASE in COPD (ERV decreases but RV increases greatly)

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9
Q

Categorization / mechanisms of OCCUPATIONAL ASTHMA (2 categories)

A

Immunologic - usual Th2 asthma mechs; often has LATENT period before sx during sensitization; causes include cereals, latex and chemicals (formaldehyde, amines, dyes)

Non-immunologic - aero-irritants cause airway denudation > persistent inflammation; usually after accidents involving CHLORINE/AMMONIA; sx onset is sudden + severe

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10
Q

Mechanisms in Oxygen-Induced Hypercapnia in COPD patients (3)

A
  1. V/Q MISMATCH - pulmonary vessels normally constrict in poorly ventilated areas; upon giving high concentration O2, vasodilation in poorly ventilated areas shunts blood away from well ventilated areas (incr. physiological dead space)
  2. HALDANE EFFECT - oxygenation of blood displaces CO2 from Hb; in hypoxic state Hb carries CO2 well > administer high conc. CO2 and Hb does not rid body of excess CO2 well
  3. DECREASED MINUTE VENTILATION - in chronic hypercapnia, hypoxia becomes major driving force for respiration with PERIPHERAL CHEMORECEPTORS; administer O2 and this driving force diminishes
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11
Q

Oxygen Toxicity

why + when does it happen? s/s?

A

increased ROS production can damage airways + lung parenchyma

within 24 hrs of breathing pure O2 > SUBSTERNAL HEAVINESS, PLEURITIC chest pain, cough + dyspnea

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12
Q

Fusion protein in some cases of NSCLC

what is it? who has it?

A

EML4-ALK fusion protein (inversion of 2p)

causes constitutive activation of a kinase (like in CML)

usually young non-smokers with adenocarcinoma lacking EGFR or K-Ras mutations

(echinoderm microtubule-associated protein-like 4 and anaplastic lymphoma kinase)

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13
Q

Mesothelioma

early presentation? histo? IHC? EM?

A

early - multiple nodules on parietal pleura grow + encase parenchyma; EFFUSIONS +/- HEMORRHAGE; sx include slow progressive dyspnea, cough, chest pain and weight loss

histo - cuboid/flattened cells (epithelium-like) or SPINDLE cells (stromal-like)

IHC - almost all CYTOKERATIN-positive; many CALRETININ positive

EM - polygonal cells with long, slender MICROVILLI and TONOFILAMENTS

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14
Q

4 asbestos related lung conditions

A
  1. pleural plaques
  2. asbestosis - parenchymal scarring
  3. bronchogenic carcinoma
  4. malignant mesothelioma
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15
Q

Lung tumors:

type, incidence, location + associations

A

ADENOCARCINOMA - up to 50%; PERIPHERAL; clubbing + hypertrophic osteoarthropathy; non-smoker women

SQUAMOUS CELL - up to 25%; CENTRAL with necrosis + cavitation; hypercalcemia; smokers

SMALL CELL - up to 15%; CENTRAL; Cushing, SIADH, or Lambert-Eaton; smokers

LARGE CELL - up to 10%; PERIPHERAL; gynecomastia + galactorrhea (large polygonal cells; mix of squamous + adeno characteristics)

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16
Q

Pulmonary Fibrosis

imaging? s/s? pulmonary function testing?

A

CXR - bilateral, diffuse, RETICULONODULAR opacities mostly in lung BASE

sx - gradual-onset progressive dyspnea; dry cough; fatigue; eventual weight loss/failure to thrive

signs - END-INSPIRATORY CRACKLES at base

RESTRICTIVE function - decr. volumes, decreased FEV1 and FVC with normal/high Tiffeneau and decreased CO diffusion

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17
Q

Drugs causing pulmonary fibrosis

3 categories, 3/1/2 examples

A

immunosuppressants - MTX, cyclophosphamide, sulfasalazine

Antiarrhythmics - amiodarone

Chemo - MTX, bleomycin

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18
Q

Centriacinar vs. Panacinar Emphysema

causes? location?

A

CENTRIACINAR - via smoking, mostly UPPER lobes (higher V/Q ratio)

PANACINAR - via a1-antitrypsin defic.; mostly LOWER lobes (more Q > more neutrophil elastase); family history of liver/lung disease

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19
Q

Protease - Antiprotease balance in lung

which cells release proteases?
what inhibits the proteases?
other proteases + inhibitors present?

A

Neutrophils - neutrophil elastase; inhib. by a1-antitrypsin

Macrophages - macrophage elastase; inhib. by TIMP (tissue inhibitors of metalloproteinases)

Other proteases - Cathepsin G and MMPs
Other inhibitor - alpha-2 macroglobulin

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20
Q

What and where are club cells?

A

nonciliated cells in the terminal parts of bronchioles

secrete CLUB CELL SECRETORY PROTEIN which protects against airway inflammation and oxidation, as well as surfactants that prevent bronchiolar collapse

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21
Q

Chronic Lung Transplant Rejection

histo?
causes what?
presentation?

A

first - lymphos destroy small airway epithelium

then - fibrinopurulent EXUDATE and GRANULATION tissue in BRONCHIOLI > fibrosis, obliteration

called BRONCHIOLITIS OBLITERANS

within 5 YEARS of transplant, dyspnea, dry cough and DECREASED FEV1 and tiffeneau

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22
Q

ABG changes in pulmonary embolism

Compensation? when does it occur?

A

Decreased Q to certain lung region > “dead space ventilation” > redistribution of flow

Central respiratory drive increases (via dyspnea + inflammatory mediators > HYPERVENTILATION

LOW PAO2 - Hb is nearly fully saturated already, so faster breathing can’t help

LOW PACO2 - carbon dioxide removal more dependent on breathing rate > hypocapnia via hyperventilation

RESPIRATORY ALKALOSIS
with renal compensation

at first: NORMAL BICARB
after 48 hours: LOW BICARB

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23
Q

CXR differences in…

pleural effusion vs. mainstem bronchus obstruction

A

both can cause hemithorax opacification (1 via fluid, other via atelectasis)

diff by TRACHEAL DEVIATION

effusion - deviates AWAY from effusion due to compression

bronchus obstruction - deviates TOWARD obstruction due to collapse of lung

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24
Q

Hyperacute Lung Transplant Rejection

onset? etiology? pathophys?

A

minutes to hours

PREFORMED HOST Abs to donor ABO or HLA

NEUTROPHILIC infiltration with FIBRINOID NECROSIS and THROMBOSIS

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25
Q

Acute Lung Transplant Rejection

onset? etiology? pathophys?

A

up to 6 months after

CELL-MEDIATED response to MISMATCHED DONOR HLA

perivascular (SMALL VESSELS) and submucosal (BRONCHIOLES) infiltrates of LYMPHOCYTES

26
Q

Chronic Lung Transplant Rejection

onset? etiology? pathophys?

A

6 months to years after

chronic, slowly progressive CELL-MEDIATED response to HLA antigens

SUBMUCOSAL inflammation causes GRANULATION, scarring and BRONCHIOLOTIS OBLITERANS

27
Q

Main triggers of COPD exacerbation?

4 things: 2 categories and 2 separate items

A
  1. Viral infections
  2. Bacterial Infections
  3. Air pollution
  4. PE
28
Q

main viral (3) and bacterial (3) exacerbators of COPD

A

Viral - rhino-, influenza (orthomyxo), parainfluenza (paramyxo)

Bacterial - M. catarrhalis, S. pneumo, H. flu

(M S H genuses of bacteria increase mucus production in copd pt…. lungs become “MuSHy” … gross)

29
Q

What are the cellular changes seen in the lung in idiopathic pulmonary fibrosis?

A

type 1 pneumocytes are lost

type 2 pneumocytes undergo hyperplasia but do not differentiate into type 1 as usual

fibroblasts + myofibroblasts migrate + proliferate

30
Q

What is respiratory quotient?

What does it estimate?

What is its normal value?

A

ratio of CO2 to O2 across alveolar membrane

used to estimate metabolic rate

normal value is 0.8

31
Q

How can total blood O2 content be calculated (formula)?

What 3 parameters are used?

A

Blood O2 content = (O2-binding capacity x % saturation) + dissolved O2

32
Q

How does carbon monoxide poisoning affect the Hb-O2 dissociation curve?

A

leftward shift

decreased tendency for O2 to dissociate in tissues

33
Q

Normal “ALVEOLAR-ARTERIAL OXYGEN GRADIENT” values

A

10-15 mmHg in healthy adult (can be as low as 5)

rises some with age

34
Q

If hypoxemia presents with NORMAL alveolar-arterial O2 gradient, what can the 2 causes be?

(2 categories, 3 examples in first cat)

A

indicates that BOTH the alveolar and arterial pO2 are low (either less fresh O2-rich air gets in, or air has lower Po2)

can be due to:

  1. HYPOVENTILATION - acute as in opioids/barbiturates; chronic as in obesity hypoventilation syndrome or neuromuscular disorder
  2. HIGH ALTITUDE - inspired pO2 is low
35
Q

If hypoxemia is present with ELEVATED alveolar-arterial O2 gradient, what can the 3 causes be?

(3 categories + examples)

A

elevated A-a gradient means O2 in alveoli is higher than in arteries; can be due to:

  1. V/Q MISMATCH - pulm. embolism, COPD
  2. R-TO-L SHUNT - septal defect, pulmonary edema
  3. IMPAIRED DIFFUSION - interstitial lung disease
36
Q

What results from OBESITY HYPOVENTILATION SYNDROME?

3 main changes

A
  1. SLEEP-DISORDERED BREATHING - incl. obstructive sleep apnea
  2. INCREASE CO2 PRODUCTION - via increased mass + surface area
  3. REDUCED VOLUMES + COMPLIANCE - compression of lungs by excess abdominal fat

results in fatigue, chronic hypoventilation, dyspnea, difficulty concentrating, increased PaCO2

37
Q

General pathophysiological cause of Kussmaul breathing

Mnemonic for specific causes?

A

Metabolic acidosis

KUSSMAuL

Ketones (DKA)
Uremia
Sepsis
Salicylates
Methanol
Aldehydes
Lactic acidosis
38
Q

Lung Adenocarcinoma

location, clinical associations, who gets it?

A

PERIPHERAL

clubbing + hypertrophic osteoarthropathy

non-smoker women (most common lung cancer)

39
Q

Lung SCC

location, clinical associations, who gets it?

A

CENTRAL (with necrosis + cavitation; in larger bronchi from squamous metaplasia)

hypercalcemia (PTHrP)

smokers

40
Q

SCLC

location, clinical associations, who gets it?

A

CENTRAL (basal cells of bronchial epithelium; neuroendocrine)

Lambert-Eaton
SIADH
Cushing

smokers (almost exclusively)

41
Q

Large Cell Lung Carcinoma

location, clinical associations

A

PERIPHERAL

Gynecomastia + galactorrhea

(undifferentiated; features of both ADC and SCC)

42
Q

How does oxidized “ferric” iron (Fe3+) in hemoglobin affect the Hb-O2 dissociation curve?

A

first, ferric iron can not bind O2

also, any residual ferrous (Fe2+) iron left in the Hb molecule has INCREASED AFFINITY (left shift of curve) for O2

43
Q

what does one of the common mutations to alpha1-antitrypsin cause?

A

the “Z mutation” causes improper folding

44
Q

specific auscultatory sign of pulmonary arterial hypertension

A

P2 louder than A2

indicates high pulmonary P closing pulmonary valve strongly

45
Q

What is FiO2? What is the FiO2 of normal inspired air?

A

Fraction of inspired oxygen - the fraction of oxygen in the volume being measured

normally 0.21 (21%)

46
Q

Equation for physiologic dead space

mnemonic

A

Taco Paco Peco Paco

VD = VT x (PaCO2 - PeCO2)/PaCO2

normally equal to anatomical dead space; increases in V/Q mismatch

Vt normally 500 mL and VD normally 150 mL

47
Q

How are MINUTE VENTILATION and ALVEOLAR VENTILATION different?

equations

A

minute ventilation includes entire tidal volume; alveolar ventilation removes the dead space

VE = VT x RR

VA = (VT - VD) x RR

48
Q

Equation for total oxygen content of blood

A

O2 content = (1.34 x Hb x SaO2) + (0.003 x PaO2)

49
Q

Aspiration usually occurs in what lobe / segment?

What if supine?

A

apical/posterior segments of LOWER LOBE OF RIGHT LUNG

if supine, may also enter posterior segment of UPPER LOBE R LUNG

50
Q

Airway resistance

how much of total R do upper airways account for? (nasal passages, mouth, larynx + pharynx)

A

about 50%

51
Q

Airway resistance

how does airway resistance compare between TRACHEA, BRONCHI, BRONCHIOLES and TERMINAL BRONCHIOLES?

how does the graph look?

A

in order of most resistant to least (numbers not important but relative relationships are; unit is cm-h20/L/sec) :

  1. MEDIUM BRONCHI - 0.085; most resistant due to turbulent flow
  2. TRACHEA + mainstem bronchi - 0.07; small total cross sectional area, but less turbulence
  3. BRONCHIOLES - 0.02; total cross-sectional area is increasing
  4. TERMINAL BRONCHIOLES - near zero; large total CSA causes slow, laminar flow in airways < 2 mm diameter
52
Q

3 forms of CO2 in blood

A
  1. HCO3- makes up 70%
  2. Carbaminohemoglobin (21-25%)
  3. Dissolved CO2 (5-9%)
53
Q

Where does CO2 bind hemoglobin?

A

N-terminus of globin protein

NOT on the heme… so O2 and CO2 do NOT compete for binding sites, but CO2 favors the deoxygenated form of Hb

54
Q

Why does CO2 bind Hb better in deoxygenated blood?

A

HIGH H+ IONS in deoxygenated blood BIND HEMOGLOBIN and cause a “rightward shift” > O2 unloading …

and an Hb conformation that favors CO2 binding (Bohr effect)

(nbme question phrased this as “because Deoxy-Hb is a better buffer of hydrogen ions than Oxy-Hb”)

55
Q

What is most likely to slow the rate of pulmonary function decline in a COPD patient?

A

smoking cessation

56
Q

PROPHYLAXIS vs. TREATMENT of deep vein thrombosis / pulmonary embolism

A

prophylaxis - LMWH (eg, enoxaparin)

treatment - tPA

(streptokinase and all the “-plase” drugs: alteplase, reteplase and tenecteplase)

57
Q

1 lung cancer in US

location?
growth and spread pattern?

A

adenocarcinoma in situ (aka bronchioloalveolar carcinoma)

in PERIPHERY

grows along INTACT ALVEOLAR SEPTA (no vascular/stromal invasion) and undergoes AEROGENOUS SPREAD

58
Q

lung adenocarcinoma in situ

histo?

A

WELL-DIFF but DYSPLASTIC COLUMNAR cells in the alveoli

+/- intracellular MUCIN

59
Q

lung adenocarcinoma in situ

presentation (3 basic, 1 special sign)

imaging (2 possibilities)

A
  1. cough
  2. SOB
  3. hemoptysis
  4. BRONCHORRHEA - copious watery tan-colored sputum from variants with high mucin production
  5. discrete mass, or…
  6. pneumonia-like consolidation
60
Q

Measurement that can differentiate between cardiogenic and noncardiogenic pulmonary edema

Values

A

Cardiogenic would have increased PULMONARY CAPILLARY WEDGE PRESSURE (more than 6-12 mmHg)

Noncardiogenic (ARDS, high altitude) has normal PCWP (but lowered lung compliance, capillary permeability, V/Q ratio and increased work of breathing)

*USMLE* (28 decks)

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