2025 USMLE STEP 1 Collection

Pu lm on o lo gy

Designed for you to pass USMLE Step 1

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 Table of Contents

Pulmonology
Lung Embryology 3
Bronchial Tree 4
Alveoli 5
Cystic Fibrosis 6
Lung Anatomy 7
Chest Wall Physiology 8
Respiratory Physiology 9
Obstructive Lung Diseases 10
Asthma Pharmacology 11
Restrictive Lung Diseases 12
Pneumoconioses 13
Pulmonary Blood Flow 14
Ventilation/Perfusion Mismatch 15
Lung Injuries 16
Pleural Effusion 17
Regulation of Breathing 18
Sleep Apnea & Pulmonary Hypertension 19
Oxygen Transport 20
Carbon Dioxide Transport & Pathologies 21
Upper Airway Conditions 22
Upper Airway Malignancies & Infections 23
Pneumonia 24
Pneumonia Organisms 25
Systemic Mycoses 26
Lung Malignancies 27
Mycobacterium 28
Tuberculosis Pharmacology 29
Notes 30
References 31
About the Author 32

LEGEND

Pharmacologic MEMORY TRICKS RISK FACTORS HIGH-YIELD CONCEPTS

2 Management

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 Lung Embrylogy
Every Pulmonologist Can See Alveoli!
Embryonic

E = Embryonic (4-7) weeks

Period

2
Lung buds develop into the Trachea and Bronchi.

Embryonic
Pathological error: Tracheoesophageal fistula
6
8

Pseudoglandular
P= Pseudoglandular (5-17) weeks
10 12 14

Bronchioles begin to develop with capillaries forming around

Respiration not possible (incompatible with life!)
16 18

C = Canalicular phase (16-25) weeks

Canalicular
20 22 24 26 28 30 32 34 36 38 40
Period
Fetal

Pneumocytes begin to form leading to the development of

Alveolar Ducts, Pneumocytes and Alveolar Macrophages.
Synthesis LecithiN & Sphingomyelin begins!

S= Saccular (26 weeks to birth)

Saccular

Alveolar ducts become terminal sacs which are divided by

Surfactant

primary septation.
BIRTH
Weeks

A = Alveolar (Week 36 > 8 years)

Postnatal

Alveolar
Period

Terminal ducts continue to differentiate to adult alveoli

Years
2 4

(secondary septation).
Birth: Rapid decrease in pulmonary resistance as amniotic
6

fluid is expelled.
8

Lecithin : Sphingomyelin Neonatal Respiratory

Helps assess fetal lung maturity.
Distress Syndrome
Surfactant deficiency  Increased surface tension 
L:S > 2 Healthy | L:S < 1.5 Increased Risk of NRDS Alveolar collapse (ground glass appearance on lung fields)

3 Presents as: Respiratory distress (i.e. tachypnea, nasal

Concentration (mg)%

Mature L/S age flaring), decreased breath sounds, Cyanosis (due to

At Risk L/S age pulmonary hypoxic vasoconstriction!)
15
RF: Prematurity, C-section, Gestational Diabetes
L/S Ratio

2
in

Tx: Intrapartum corticosteroids (mum), Exogenous

ith
L ec

10 1.5 surfactant (infant) +/- Therapeutic supplemental O2

tio Sp h 1 Supplemental O2 Complications:

5 L/S ra ingo
m ye
lin
R.I.B.
20 26 30 35 40
R etinopathy of Prematurity
Gestational Age (weeks)
I ntraventricular Hemorrhage
L:S Poem If L over S is 2 or more, your baby’s lungs will soar B ronchopulmonary Dysplasia 1

3
If L over S is less than 1 and a half, they’ll struggle and gasp! Characteristic “Ground-glass” opacities found on CXR!
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 Bronchial Tree
Conducting Zone
Goblet Cell Ciliated Cell Basal Cell
Trachea
Airway resisitance decreases as you go deeper due to increased surface area

Pseudostratified
Warms & humidifies air Ciliated Columnar
Epithelium

Mucocillary escalator Smooth Muscle

comprised of
Pseudostratified
Bronchi columnar epithelium Cartilage
responsible for clearing
debris
Simple
Ciliated
Bronchioles
Anatomical dead Columnar
space: Does not Epithelium
participate in gas
Smooth Muscle Club Cell Ciliated Cell
exchange.
Club Cell Cuboidal Ciliated
Simple Cell
Terminal
Ciliated
Bronchioles
Cuboidal
Epithelium
Smooth Muscle
Respiratory Zone
Cuboidal Club Cell Squamous Cell
Respiratory Bronchioles Simple Cell
Respiratory Cuboidal &
Cilia terminates in Squamous
Bronchioles
Respiratory Bronchioles Epithelium
Smooth Muscle

Alveolar Sacs Alveolar ducts

See Next
Alveoli Page 

Bronchogenic cyst K”A.R”tagener Syndrome

¬ Dilation of large and terminal bronchi due to Autosomal Recessive (AR) dysfunction in Dynein
abnormal foregut development. arm which can lead to ciliary dysmotility in:
¬ Associated with recurrent pulmonary infections.
Lungs Bronchiectasis

Cardiac
Cilia Structure Development
Dextrocardia
9 pairs of microtubules in a
concentric ring with one pair Immotile Sperm
Reproduction
in the center. Ectopic Pregnancies
Axonemal Dynein
ATPase that coordinates
movement by bending cilia.

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 Alveoli

Type 1 Pneumocytes
¬ Made of simple squamous epithelium.
Pulmonary Hypoplasia
¬ Represents 95% of alveoli Underdeveloped bronchial tree
¬ Ideal for gas exchange. resulting in decreased number of
alveoli.
Associated with:
¬ Oligohydramnios
¬ Potter Sequence
¬ Congenital diaphragmatic
hernias

Type 2 Pneumocytes
Alveolar Macrophages Two functions:
¬ Clear debris in the alveoli 1. Stem cell precursor: Becomes type 1/2
¬ Primary residence of pneumocytes in response to alveolor
Tuberculosis (TB) damage.
¬ Produce 1α hydroxylase in
2. Produces Surfactant
Sarcoidosis
¬ Decreases surface tension
Leads to increased levels of ¬ Decreases lung recoil
1,25-dihydroxyvitamin D (calcitriol)
which can cause hypercalcemia and ¬ Increases compliance
hypercalciuria!

Law of LaPlace
Expiration causes decrease in radius
Surface = increased collapsing pressure
Collapsing
Pressure of Tension

P=2xT
Alveoli
Surfactant concentration increases
as alveoli shrink

r Result: Alveoli can remain patent

despite decreasing radius
Radius

r=2
P=2xT r=1
2
P=T P=2xT
1
P = 2T
5
Pierre Simon Laplace
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 Cystic Fibrosis

C stic Fibrosis Normal Role of CFTR genes in:

General Features: Sweat Glands Exocrine Glands
¬ Autosomal recessive mutation of the CFTR Cl -
Na +
Normal Mucus
gene on chromosome 7 CFTR ENaC
¬ 80% is due to the deletion of Phe508 (F508)
¬ CFTR genes express Cl- channels on
Exocrine glands and Sweat glands
Cl- H2O Na+
Presenting Signs:“CF PANCREAS”
Maintains normal viscosity of
C hronic Cough & Wheeze Role of Cl- channels is reversed in sweat
glands  Promotes Cl- to enter secretions by allowing Cl- to enter
extracellular space = less water
F ailure to Thrive intracellular space, driving Na+ to follow.
entering intracellulary.

P ancreatic Insufficiency Cystic Fibrosis

A lkalosis & Hypotonic Dehydration Dehydrated Mucus
Cl Na - +

N eonatal Intestinal Obstruction (meconium ileus)

C lubbing of Fingers
R ectal Prolapse Cl H O Na
-
+
2

E lectrolyte Elevation (salty skin)

A tresia (of vas deferens) Diagnostic Criteria

¬ Sweat chloride test: > 60mmol/L
S inopulmonary infections ¬ Decreased Fecal elastase.
¬ Increased Immunoreactive trypsinogen (Newborn screening).

Complications
Gastrointestinal Reproductive
Obstructed pancreatic ducts Males: Obliteration of the vas deferens leads to infertility.
Females: Decreased fertility due to altered cervical secretions.
Early activation of enzymes

Autodigestion of Pancreas Respiratory

Thicker secretions >>> Ciliary dysfunction >>>
Endocrine and Exocrine Insufficiency Increased risk of sinopulmonary infections

¬ Malabsorption Gram + Staphylococcus aureus (common in young patients)

Diabetes
¬ Steatorrhea
Mellitus Gram - Burkholderia cepacia, Pseudomonas aeruginosa (in adults)
¬ Failure to thrive
Fungal: Bronchopulmonary aspergillosis

90% of Meconium Recurrent sinopulmonary infections increase cytokine response (IL-8),

Ileus presentations increasing mucus production and exacerbating symptoms.
are associated with
Cystic Fibrosis Over time: Bronchiectasis Pulmonary HTN Cor Pulmonale
2

Management ALL: IvaCaFToR: CFTR modulator >>> Increase opening of Cl- channels

GI ¬ Pancreatic enzyme supplementation RESP

6 ¬ ADEK supplementation ¬ Pharm: SABA + Dornase Alfa + Guaifenesin
¬ High-calorie diet ¬ Non-Pharm: Chest physiotherapy
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 Lung Anatomy

RALS
RALS
Trachea biFOURcates at T4 Trachea Right Anterior
Left Superior
Other important structures at the 4th vertebra:
Used to relate the pulmonary artery
Common Carotid bifurcates at C4 to the bronchi at each lung hilum.
Abdominal Aorta bifurcates at L4
Superior lobe
Superior lobe
Main (primary) bronchus
Lobar (secondary) bronchus

Middle lobe LEFT

Lung
Segmental (tertiary) bronchus
2 Lobes
Inferior lobe

RIGHT Lung Inferior lobe

3 Lobes
The right mainstem bronchus THINK!
Left has Less Lobes
Foreign Body Aspiration
has a shallower angle, leading
because of the Lingula Erect position
to an increased incidence of Enters the right inferior lobe
right-sided aspiration injuries.
Recombent

Diaphragm Enters the right superior or medial lobe

Important muscle driving inspiration RISK FACTORS for Aspiration

¬ Patients predisposed to loss of
Structures that pass through the diaphragm: consciousness (alcohol overuse, epilepsy)

8
Bronchial obstruction - i.e. cancer
at twelve!”
¬
“I ate ten eggs
Lung Abscesses
Inferior vena cava Pus isolated in the parenchyma of the lungs.
passes through the Associated with aspiration or obstruction.
diaphragm at T8 Esophagus enters the
diaphragm at T10 Treatment: Antibiotics + Drainage
The Vagus nerve is also at T10
REMEMBER!
Organisms:
Vagus nerve = CN 10 Anaerobes or S. Aureus

A T
orta & horacic Duct
enter the diaphragm at T12

Vertebra 3
7
Phrenic nerve: C3, 4, 5 keeps the diaphragm alive! CXR shows air-fluid levels suggestive of cavitation.
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 Chest Wall Physiology
IN (Inhalation) Compliance
Intrathoracic pressure
¬ Ability of the lungs to distend under pressure.
becomes more negative
¬ Inversely proportional to wall stiffness.

Emphysema
⤳ lungs fill
Fibrosis, Pneumonia, ARDS
V
S
Elastic Recoil
Elastic Recoil

External intercostal muscles and diaphragm contract down. Tendency of the lungs to collapse inward and the chest
wall to spring forward.

OUT (Exhalation) Resting expiratory position (at functional residual

capacity):
Intrathoracic pressure ⤳ Airway & alveolar pressure = atmospheric pressure.
becomes positive ⤳ Intrapleural pressure is negative (prevents
atelectasis).
⤳ Pulmonary vascular resistance is lowest.
⤳ lungs expel air
(passive elastic recoil)
Aging: TLC remains the same!

Lung compliance, RV, V/Q mismatch, A-a gradient

Chest wall compliance, FVC & FEV, respiratory

Internal intercostal muscles and diaphragm relax up. muscle strength, ventilatory response

Mediastinal Pathology
Mediastinitis: Pneumomediastinum:
Inflammation of the mediastinal tissues.
Gas in the mediastinum, spontaneous (due to rupture
Most commonly occurs after cardiothoracic
of pulmonary bleb) or secondary to trauma.
procedures, esophageal perforation, or contiguous
infection (e.g. retropharyngeal). Features: Chest pain, Dyspnea, Voice change,
Subcutaneous emphysema, & Crepitus on cardiac
Features: Fever, Tachycardia, Leukocytosis, Chest auscultation
pain, Sternal wound infection

Mediastinal Masses

4T
Anterior (4 T’s)
hyroid (e.g., substernal goiter)
hymic neoplasm
eratoma
errible lymphoma

Middle
Esophageal carcinoma Hiatal hernia
Bronchogenic cysts Metastases

8 Posterior
Neurogenic tumor (e.g., neurofibroma) Multiple myeloma
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 Respiratory Physiology
Lung Volumes Lung Capacities
I: Inspiratory Reserve Volume Lung volumes (LITER) Lung capacities
Inspiratory Capacity:
6.0
Volume that can still be inspired IRV + TV

Volume (L)
after normal inspiration. Volume that can be inspired after
IRV IC VC TLC normal exhalation.
T: Tidal Volume
Volume that moves in or out of Functional Residual Capacity:
the lung with each cycle TV 2.2
RV + ERV
(~500 mL) Volume in lungs after normal
ERV expiration.
E: Expiratory Reserve Volume 1.2 FRC
Volume that can still be expired Vital Capacity:
after normal expiration. RV IRV + TV + ERV
0 Maximum volume that can be
R: Residual Volume expired after maximal inspiration.
IRV = Inspiratory Reserve Volume IC = Inspiratory Capacity
Volume in lung after maximal TV = Tidal Volume FRC = Functional Residual Capacity Total Lung Capacity:
expiration. ERV = Expiratory Reserve Volume VC = Vital Capacity IRV + TV + ERV + RV
RV = Residual Volume TLC = Total Lung Capacity
Volume present in lungs after
CANNOT be measured
maximal inspiration.
with spirometry!

8 Normal
Spirometry
accesses
Expiration
Restrictive
4
FEV1
Flow (L/s) Forced Expiratory Volume
8 6 4 2 0
in 1 second
1 seco
4 nd
Inspiration Obstructive FVC
8 Forced Vital Capacity
in 1 breath
(total volume that can be
maximally exhaled)

FEV1/FVC Ratio
Obstructive Lung Diseases Restrictive Lung Diseases
Normal = 0.7
<0.7 ≥ 0.7
Other parameters
RV
Air Trapping Limited Lung Expansion
(can’t get air out!) FRV (can’t open lungs!)

TLC
FEV1 decreased FEV1 FEV 1 decreased
more than FVC! proportionally to FVC!
FVC 9

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 Obstructive Lung Diseases

COPD
(Chronic Obstructive Pulmonary Disease)
¬ #1 risk factor = Smoking
¬ Hyperinflated lungs (air trapping) can push

Emphysema
heart to midline
¬ CO2 retainers  Chronic respiratory acidosis

“Pink Puffer”

Chronic Bronchitis
Barrel-shaped chest, prolonged
expiration through pursed lips.
“Blue Bloater”
¬ Loss/destruction of alveolar surface area
Cyanosis, wheezing, crackles, dyspnea, CO2 retention.
 decreased gas exchange.
¬ Hypertrophy/hyperplasia of mucous-secreting glands in
¬Bullous changes on X-ray.
bronchi.
¬Smokers: Get centrilobular emphysema ¬ Productive cough for > 3 months in a year for > 2
(proximal alveoli destroyed, "Smoke consecutive years.
rises"  affects upper lobe).
¬ Diagnosis via Reid index > 0.5 (ratio of mucous-
¬α-1 antitrypsin deficiency: secreting glands to bronchial wall).
Patients get panacinar
¬ Can lead to pulmonary hypertension  right heart
emphysema (entire lung
failure!
destroyed, common
in lower lobe).

α-1 Antitrypsin Deficiency Asthma

⤳ Enzyme produced by the liver that breaks down
neutrophil elastase. Asymptomatic
⤷ Elastase is an enzyme that normally damages baseline with episodes of
the alveoli. coughing, wheezing,
⤳ Lookout for early-onset emphysema & cirrhosis. tachypnea, dyspnea,
and hypoxemia.

Bronchiectasis Reversible
bronchospasm (after
THINK!
methacholine challenge).
BRONCHIOL-EXCESS "Bronchioles are filled with EXCESS!"
¬ Loss of musculature of airways leading to Triggers:
permanent dilation. Viral URIs, allergens, stress.
¬ Copious foul-smelling sputum, recurrent
infections (P. aeruginosa), hemoptysis, and ¬ Smooth muscle hypertrophy & hyperplasia.
clubbing. ¬ Curschmann spirals (mucous plugs) & Charcot-
¬ Associated with poor ciliary motility, bronchial Leyden crystals (eosinophilic).
obstruction, and cystic fibrosis. ¬ Acute respiratory alkalosis (CO2 low as it diffuses
quickly, O2 diffuses slowly).

Cough variant: Dry cough, worse in winter.

Atopy: Seasonal allergies, rhinoconjunctivitis, urticaria.
Aspirin-induced: Inhibition of COX  increased
10 4
leukotrienes  increased bronchoconstriction.
Cystic dilation of airways on CT
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 Asthma Pharmacology
Avoidance Exposure to allergen
(dust, pollen, etc) Allergin specific IgE

FC receptor for IgE

COPD Pharm Corticosteroids Anti-IgE monoclonal therapy
Fluticasone Omalizumab
1st line TX: Budenoside
Long acting muscarinic R antagonist (i.e. Chromones
LAMA - tiotropium) OR Long acting B2 Cromolyn
agonist (i.e. LABA - salmeterol) Degranulation
Anti-IL-5 monoclonal therapy
Proinflammatory mediators Mepolizumab
(leukotrienes, histamine, interleukins, etc) Reslizumab
Benralizumab

ACUTE RESPONSE (bronchoconstriction) CHRONIC RESPONSE (inflammation)

ATP
β2- agonists AMP Muscarinic antagonists
Proinflamatory cytokines
Methylxanthines Tiotropium
AC PDE Theophylline Adenosine Ipratropium
cAMP ACh
PDE-4 inhibitors
Roflumilast (COPD only)

Bronchodilation Bronchial Tone Bronchoconstriction

Mucus secretion Phospholipase A2

Plasma exudation
Corticosteroids
Eosinophil recruitment
Montelukast Arachidonic acid Fluticasone
Budenoside
Antileukotrienes
5-Lipoxygenase COX1/COX2
Zileuton
Prostaglandins
Leukotrienes Prostacyclin
Thromboxane

ACUTE Muscarinic Antagonists (-tropium)

¬ Competitively block muscarinic receptors 
Inhaled B2 Agonists prevent bronchoconstriction.
¬ Relaxes bronchial smooth muscle ¬ Narrow therapeutic index, metabolized by CYP450.
⤷ REMEMBER! β2 for 2 lungs!
¬ Short-acting (e.g., Albuterol) for acute Methylxanthines (e.g., Theophylline)
exacerbations. ¬ Phosphodiesterase (PDE4) inhibitor  increased
¬ Long-acting (e.g., Salmeterol) for prophylaxis. cAMP  bronchodilation.
¬ Adverse Effects: Tremor & arrhythmia.

Anti-LEUkotrienes
CHRONIC ¬ Montelukast: Blocks lipoxygenase receptor (CysLT1).
¬ Zileuton: 5-lipoxygenase inhibitor.

Inhaled Corticosteroids
¬ Inhibit synthesis of proinflammatory cytokines by inactivating NF-κB and PLA2.
¬ First-line for chronic asthma (use a spacer or rinse mouth to prevent oral thrush).

MONOCLONALS ¬ Omalizumab = anti-IgE (blocks binding Monoclon

a ls target
Ig
of FcεRI), used in allergic asthma. REMEMB E and IL-5!
E is the 5t ER!
¬ Mepolizumab & Reslizumab = anti-IL-5 h letter o
f alphabe
¬ Benralizumab = anti-IL-5 receptor, used t!
11
in eosinophilic asthma.
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 Restrictive Lung Diseases

Idiopathic Pulmonary Fibrosis Hypersensitivity Pneumonitis

¬ Progressive fibrotic lung disease of unknown etiology. ¬ Mixed type III/IV hypersensitivity reaction to
¬ Classic restrictive picture with unexplained dry cough. environmental antigens.
¬ Complications: Pulmonary hypertension (loud P2 heart ¬ Bilateral lung involvement + fever in farmer/
sound). bird-fancier with exposure (e.g., hay).
¬ CXR/CT: Reticular or reticulonodular pattern. ¬ Self-limiting.

Also look out

for the classic
“honeycomb”
appearance on
chest CT!

Drugs That Can Cause Pulmonary Fibrosis

CYCLOphosphamide BUSulphan CARmustine methoTRUCKsate AmioDaRONE

Look out for occupational exposure to (See Next Page)

Sarcoidosis
Immune-mediated widespread non-caseating granulomas:
⤷ Consist of activated macrophages (aka epithelioid histiocytes).
⤷ Secrete 1 α-hydroxylase, which converts inactive 25-OH-D3 into active 1,25-(OH)2-D3.
⤷ Increased calcium absorption  hypercalcemia (PTH is suppressed via negative feedback).

Etiology:
μ African american female.
μ Often asymptomatic (with enlarged lymph nodes).
μ Associated with Bell palsy, uveitis, pulmonary fibrosis, erythema
nodosum, rheumatoid arthritis-like arthropathy.

Findings:
μ Bihilar lymphadenopathy seen on CXR.
μ Elevated serum ACE
μ Elevated CD4/8 ratio in bronchoalveolar lavage fluid.

Treatment: 6

Steroids (oral prednisone)

12

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 Pneumoconioses

Silica, Coal & Berries are from the Ground

but affect the ceiling (upper lobe)!

Berylliosis
¬ Associated with beryllium exposure in Coa
aerospace & manufacturing industries lW
¬ ork
¬ Granulomatous (non-caseating)
¬
Pr olo e r ’s
inflammation Mac nged e Pne
F i b r ro p h a x p o s u r umo
ge
osis
( “B s l a d e
e to
coa coni
lac n
k lu with
ng car
l du
st os is
dis b
eas on >>
e”) >

Silicosis
¬ Associated with sandblasting, foundries & mines
¬ Macrophages >>> fibrogenic factors >>> fibrosis
¬ Silica disrupts phagolysosomes >>> increased TB risk
¬ Eggshell calcification of hilar lymph nodes

Asbestosis affects the Base (lower lobe)!

¬ Pulmonary Fibrosis Fibrous
¬ Associated with shipbuilding, roofing, and plumbing. Pleural
Plaque
¬ Ivory white, calcified supradiaphragmatic and pleural plaques.
¬ Risk of bronchogenic carcinoma greater than mesothelioma

Asbestos (ferruginous bodies)

are golden-brown fusiform rods
Mesothelioma
resembling dumbbells, found in
¬ Malignancy of the pleura associated with asbestosis.
alveolar sputum sample, visualized
using Prussian blue stain, often ¬ Can result in pleural effusion & pleural thickening (white
obtained by bronchoalveolar lavage. plaque that encases/wraps around lung tissue).
¬ Positive for calretinin & cytokeratin

Tobacco is NOT a risk factor

13
8

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 Pulmonary Blood Flow

Minute Ventilation (VE ) Alveolar Ventilation (Va ) Perfusion (Q )

Total volume of gas entering lungs Volume of gas that reaches alveoli Flow of blood from alveoli to
per minute per minute alveolar capillaries

VE = VT x RR VA = (VT - VD )x RR
Exercise
⤷ INCREASES cardiac output
Physiologic Dead Space (VD) = alveolar and anatomical
⤷ Vasodilation of apical capillaries
dead space of conducting airways. The volume of inspired ⤷ Reduces dead space
air that does not take part in gas exchange (~150mL/breath) ⤷ V/Q approaches 1

ZONE Mechanism Key Points

Apical Segment O2 partial pressure
1 ¬
¬ High aeration
¬
is higher INC risk
P A>P a>P V ¬ High alveolar pressure of Mycobacterium
& low PBF tuberculosis (TB)
Alveolar
PA
Pa PV 2 ¬ Middle Segment ¬ V/Q = 1
¬ Optimal Gas exchange
Arterial P a>P A>P V
Venous

¬ Basal Segment
V/Q ratio is the lowest
3 ¬ Compression of Alveoli
¬
in basal segments of the
¬ Highest V and even
P a>P V>P A lung
Higher Q

DLCO
VQ : Ratio of air that reaches ¬ Diffusion capacity of lungs for carbon monoxide (reflects extent
the alveoli (V) to alveolar of gas exchange across pulmonary capillaries)
blood supply (Q) per minute ¬ Decreased in most lung diseases (i.e. interstitial lung disease)
Ideal = 1 ¬ Unchanged in diseases due to poor breathing mechanics
¬ Increased in asthma (due to transient INC pulmonary blood flow)

Alveolar-arterial (A-a) gradient

⤳ Difference between Alveolar [O2] compared to Arterial [O2] ⤳ Normally: 5 - 10 mmHg

Alveolar Gas Equation NORMAL

HIGH
PaCO2
PAO2 = PIO2
= Lung Issue R = Not a Lung Issue
√ Impairment of gas exchange PaCO2 √ Hypoventilation (i.e. opioids,
√ Poor lung compliance (i.e. age) 150 mm Hga heroin, benzos & barbiturates)
0.8
√ V/Q mismatch √ High altitude
PAO2 = Alveolar PO2 (mmHg)
PIO2 = PO2 in inspired air (mmHg)
Patient has low arterial O2 despite PaCO2 = arterial PCO2 (mmHg) Patient has low arterial O2 because of
14 sufficient respirations, where alveolar
R = respiratory quotient: insufficient respirations, where alveolar
PO2 is normal in unaffected lung areas! O2 is low throughout the lungs!
CO2 produced/O2 consumed
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 Ventilation/Perfusion Mismatch
SHUNT perfusion Normal dead space ventilation
Perfusion without ventilation Perfusion and ventilation Ventilation without Perfusion

Air Air
Alveolus
CO2 O2

Wasted perfusion (e.g. airway Gas exchange between capillary Wasted ventilation (e.g. pulmonary
obstruction, pneumonia) and alveoli: Blood Oxygenation embolism, cardiogenic shock)
LOW V/Q V/Q = 0.8 high V/Q
ZERO V/Q INFINITY
Airway obstruction (low V) Pathologic dead space pulmonary
low PAO2 hypoxic vasoconstriction Right (deoxygenated) to Left blood flow is compromised (low Q), but
shunts blood to better ventilated alveoli (oxygenated) mixing of blood ventilation is not affected (high V)
O2 admin fails to increase PaO2! DECREASED arterial O2 O2 admin increases PaO2!

Acute Respiratory Distress Syndrome (ARDS) Pulmonary Emboli (PE)

Low V/Q (shunt) High V/Q (Dead space)
Alveolar damage Obstruction of pulmonary artery due to foreign
⤷ Inflammatory mediators material (typically thrombus)
⤷ Endothelial damage & INCREASED permeability
PRESENTATION: sudden onset dyspnea, pleuritic
⤷ Leakage of protein-rich fluid into alveoli
chest pain, tachypnea, tachycardia, hypoxemia
⤷ Intra-alveolar hyaline membranes
⤷ Non-cardiogenic pulmonary edema TX: Anticoagulation (i.e. heparin) OR IVC filter (if
anticoagulation contraindicated)
CAUSES: sepsis, aspiration, pneumonia, trauma,
pancreatitis DX
DX:
ECG = Sinus tachycardia +/-
A bnormal Chest X-ray S1Q3T3 abnormal
CT Pulmonary Angiogram

R espiratory Failure within 1 week of insult

D ecreased PaCO /FiO2 2
Other Types of Emboli:
S ymptoms of respiratory failure are FAT
NOT due to a cardiogenic cause
Associated with long bone fractures (Triad =
⤷ NORMAL PCWP! hypoxemia, neurologic ab, petechial rash)
TX:
¬ Underlying cause AIR
¬ Mechanical Ventilation Nitrogen bubbles in ascending divers
10

⤳ DECREASED Tidal Volume 9 TX: Hyperbaric O2 Large saddle emboli may

⤳ INCREASED PEEP cause sudden death!
Diffuse Bilateral Opacities Amniotic fluid
“ground glass appearance” 15
Labor/postpartum (can lead to DIC!)

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 Lung Injuries
PNEUMOTHORAX AIR IN PLEURAL SPACE BLOOD IN PLEURAL SPACE HEMOTHORAx

11 12

Associated with hypotension,

flattened neck veins, and soft
heart sounds!
THINK!
X Clinical Findings
P-THORA
Primary Spontaneous breath sounds
Clinical Features percussion DULL
Rupture of sub-pleural blebs/
P leuritic pain
¬
io tactile fremitus
n

es cysts
rd sl
a ! Risk factors: Smoking (main),
T racheal deviation tow tall-thin stature & young males
Tension Pneumothorax
H yper-resonance Can
lead Medical Emergency
Secondary Spontaneous
O nset (sudden) ¬ Associated with diseased lung
to: Associated with tracheal deviation
AWAY from lesion which leads to:

R educed breath sounds (i.e. COPD), Marfans, malignancy

Obstruction of IVC 
Dec. venous return 
A bsent fremitus Traumatic Increased JVP 
X -ray shows collapse ¬ Associated with Trauma
CARDIOGENIC SHOCK

ATELECTASIS: Collapse of lung parenchyma (alveoli)

Obstructive Compressive Contraction Adhesive

EXAM I.e. Foreign Body I.e. Pleural Effusion I.e. Sarcoidosis I.e. NRDS
FINDINGS

Tracheal deviation: Towards lesion Percussion: Dull Breath Sounds: Tactile Fremitus:
16

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 Pleural Effusion
Accumulation of fluid in the pleural space

Because fluid is in between the

lungs and not on the lungs (like
pneumonia), sound is insulated and
not amplified resulting in reduced
breath sounds.

Opacification of
lung parenchyma

Clinical Findings
breath sounds I/X Chest X-ray
13

percussion DULL Diagnostic Thoracentesis Blunting of the

costophrenic angle
to determine
tactile fremitus

Light’s Criteria

PRO ve please ... that this is an exudate!

Transudative exudative
PROTEIN LDH Mechanism
INC. Hydrostatic Pressure INC. Capillary
DEC. Oncotic Pressure Permeability
“PRO” = PROtein “please” = 6 Letters
“PRO ve ” = 5 Letters Pleural fluid LDH/
Serum LDH
Pleural Protein
Serum Protein < 0.5 > 0.5
Pleural fluid protein/
Serum protein
> 0.5
> 0.6 Pleural LDH
Serum LDH < 0.6 > 0.6
<2/3 upper limit of > 2/3 upper limit of
LDH
normal serum LDH normal serum LDH
EXUDATIVE

Causes of Transudative Pleural Effusion Causes of exudative Pleural Effusion

√ Infection
√ Congestive Heart Failure
√ Pulmonary Embolism
Increased √ Hepatic Cirrhosis √ Malignancy
hydrostatic √ Nephrotic Kidney Disease √ Autoimmune
pressure

Decreased colloid osmotic pressure Fluid and protein leakage 17

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 Regulation of Breathing
Pneumotaxic
center
Regulates tidal volume by
delaying/limiting inspiration PONTINE
APNEUSTIC
CENTER
Controls intensity of inspiration
center THINK!
Pons = Pulmonary
Dorsal Controls basic rhythm;
Respiratory Group Responsible for inspiration
MEDULLARY
VENTRAL Controls expiration; Mostly inactive, CENTER
Respiratory Group becomes active during exercise

Since Po
ns is abo
ve the m Sends input to respiratory centers to adjust breathing in response to either
edulla,
T H IN K
“Pons o
verseas
! INCREASE CO2 OR DECREASE O2
pneumo medulla
ry
Respiratory -tactica
lly (pneu activity
centers
control
motaxis
)”
CHEMORECEPTORS
Central Peripheral
Inspiration
& Expiration Primarily responds to Responds to decrease
changes in CO2 & H+ in PaO2
PaCO2
CSF Activity signifanctly INC.
h+
h+
when PaO2 < 60mmHg
CO2
Bloo

CO2 Located on the Carotid &

d Br

h+

Aortic bodies
ain B

CO2 CO2
arrie
r

CO2 h+
HCO3-

pH
Factors the affect
CO2

Central Chemoreceptors
Peripheral Chemoreceptors:
¬ Accessory muscle innervation
¬ External & internal intercostal muscles INCReased RR
INC. PaCO2 > INC. H+ >
√ INC. Elevation
DEC. pH in CSF
√ Metabolic acidosis
Unlike Respiratory acidosis which does affect
central chemoreceptors, Metabolic acidosis CO2 crosses BBB
only affects peripheral chemoreceptors. DECreased RR
INC. DRG activation √ INC. PaO2
This is because their metabolites do not
cross the BBB! √ Pulmonary Stretch
INC. RR to breathe CO2 out

Pathological KussmauL Biot’s Cheyne-stokes agonal

Breathing Breathing Breathing Breathing
Breathing Patterns

Irregular breathing with periods Cycles of gradual increase in

Deep and labored Slow, irregular gasping
Pattern of rapid breaths of equal depth
breathing
breathing depth followed by a
breaths with long pauses
followed by periods of apnea decrease, then a period of apnea
18
THINK Ketones THINK Brain insult THINK Cardiac insult Severe hypoxia
Association i.e. DKA i.e. CNS infection i.e. CHF, Stroke (i.e. cardiac arrest)
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 Sleep Apnea & Pulmonary HTN

Sleeping Obstructive Sleep Apnea pnea

z
al
z
A

z z z
ep
z
Risk Factors:

z z
m

Sle
Nor

! Obesity
! Adenotonsillar hypertrophy (children)
! Increased parapharyngeal tissue (adults)

Features:
¬ Loud, irregular snoring, periods of Apnea
¬ Daytime somnolence
¬ PaO2 normal during day
TX: CPAP + Weight loss
DX: Sleep Study

Obesity Hypoventilation Syndrome Central Sleep Apnea

Impaired respiratory effort due to:
Risk Factors:
! Obesity (BMI > 30) ! CNS insult
Thin
Features: ! Congestive Heart Failure k of
the
Persistent hypercapnia
! Cheyne-Stokes C's
!
Sleep Apnea may lead to Opiods

PULMONARY HYPERTENSION
Types of Pulmonary Hypertension (WHO Classification)

Group 1: Pulmonary Arterial Hypertension (PAH) Group 3: Pulmonary Hypertension due to

Lung Diseases and/or Hypoxia
1-A
Group 2: Pulmonary Hypertension due to Left Heart Disease o x i = 3 letters
1 2
Group 4: Chronic Thromboembolic
Pulmonary Hypertension (CTEPH)
Pathophysiology
c l o t = 4 letters
Increased Pulmonary Arterial Pressure (>20mmHg)

Increased Right Ventricular Pressure Group 5: Pulmonary Hypertension with

Increased Right Ventricular Hypertrophy Unclear multifactorial Mechanisms

Right-heart failure m u l t i = 5 letters

Pulmonary Hypertension Pharm

ENdothelin Receptor Analogs: PDE-5 Inhibitors:

Antagonizes endothelin-1 receptors  Decreases breakdown of cGMP  Increased concentration of
Decreases pulmonary vascular resistance cGMP  Sustained vasodilation
Example: BosENtan Example: Sildenafil, Dipyridamole
Contraindication: Concomitant Nitrate Use
Prostacyclin (PGI2) Analogs:
19
PGI2  Vasodilation of vascular beds
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 Oxygen Transport
Hemoglobin Partial pressure of O2
1 Hb can bind 1.34ml O2 Arterial O2 sats
(normally 97%) in arterial blood

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

Amount carried by Hb Amount dissolved in plasma

O2 delivery: O2 content x Cardiac Output

HEMOGLOBIN
O2 O2 β2 β1
SaO2 H b
PaO2 O2 O2 Iron

Dissolved O2 Total O2 Heme

PATHOLOGIES Hb Conc. % O2 Sat Hb
(PaO2) content Group
Anemia Normal Normal

Polycythemia Normal Normal a2 a1

MYOGLOBIN √ 4 peptide subunits (2 alpha, 2 Beta)

√ Single peptide VS √
√
Oxygenated Hb has high affinity for O2
Deoxygenated Hb has low affinity for O2
√ Higher affinity for O2 (hyperbolic O2 curve)

O2 Dissociation Curve
LEFT Shift 100
Right Shift
O2 is Latched on O2 is Released
⤷ HEMOGLOBIN Affinity for O2 80 ⤷ HEMOGLOBIN Affinity for O2

Everything L ower Everything R aised

60 P50
SO2(%)

P50 PCO2
PCO2
40
TEMPERATURE TEMPERATURE
2, 3 DPG 20 2, 3 DPG
High
H+ H+ Altitude

0
20 40 60 80 100
Affinity for O2:
PO2(mmHg)
Atmospheric O2 (PiO2)  PaO2
Fetal Hb (2α, 2γ) > Adult Hb
Ventilation  PaCO2  Respiratory alkalosis 
due to decreased affinity for 2,3-BPG Altitude sickness (headache, nausea, lightheaded)
(left shift) diffusion of O2 across placenta.
Chronic INC. Ventilation:
Sigmoidal shape due to positive Erythropoietin2,3-BPG (right shift)

20 cooperativity (tetrameric Hb has higher

Cellular changes:
affinity for each subsequent O2 molecule!) Renal excretion of HCO3- (compensate for respiratory alkalosis)
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 Carbon Dioxide Transport & Pathologies
CO2 is transported from the tissues to lungs in 3 forms:
Cl-
Plasma
all
1 HCO3- (70%)
RBC
Capillary w

HCO3-/Cl- cotransporter
CO2 enters RBC and is
converted to HCO3-
on RBC membrane allows
Carbonic HCO3- to diffuse out to
Anhydrase plasma and Cl- into RBC
CO2 CO2 + H2O H2CO3 H+ + HCO3-

HHb H+ + Hb-

CO2 + Hb 2 HbCO2 (25%)

Tissue CO2 is bound to Hb
at N-terminus of
globin (CO2 favors
3 Dissolved CO2 (5%) deoxygenated form)

Methemoglobinemia Cyanide Poisoning Carbon Poisoning

Causes
“Don’t Let Fe3 RIse!” +

¬ Product combustion
Dapsone ¬ Suicidal attempt
¬ Motor exhaust
Local anesthetics ¬ Amygdalin (in apricots)
¬ Gas heaters
Fire victims
Fe3+ (prevent formation) ¬ Fire victims
¬

NitRItes

Pathophysiology
CO inhibits complex IV:
MetHb (Fe2+) MetHb (Fe3+) ¬ Inhibit ETC  no ATP
CN binds Fe3 in complex IV
+

Iron in Hb is normally in: ¬ Anaerobic glycolysis

¬ Inhibits ETC  no ATP
⤷ Reduced state (Fe2+) ¬ Anaerobic glycolysis Forms dyshemoglobin (COHb):
Oxidized state (Fe3 ): Cannot carry O2
+ No change to O2 curve ¬ Left shift  Increased affinity for O2 
 Decreased SaO2  Tissue hypoxia  ¬ O2 saturations may be normal Decreased O2 unloading
Increased EPO  2o Polycythemia initially! Binds competitively with Hb > 200x than
O2 for carboxyhemoglobin!

Presentation
√ Headache √ Headache
√ Cyanosis √ Dyspnea √ Vomiting
√ Chocolate colored blood √ Drowsiness +/- coma √ Confusion +/- coma
√ +/- Bitter almond breath √ +/- Cherry red skin

Labs
Hb Normal Normal Normal
SaO2 (Fe3+ poor binding at O2) Normal (CO competes with O2)
PaO2 Normal Normal Normal
Total O2 Normal

Treatment
Methylene blue & Vitamin C:
¬ Hydroxocobalamin (B12)
100% O2
Oxidize Hb  methemoglobin  Binds
¬ Nitrites (via methemoglobin)
Cyanide  Cyanmethemoglobin 
¬ Sodium thiosulfate
Decreased Toxicity 21

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 Upper Airway Conditions
Rhinosinusitis Complications: sinus infection
¬ Obstruction of sinuses, commonly Maxillary can extend to:
¬ Commonly caused by viruses ¬ Orbit (orbital cellulitis)
i.e. Rhinovirus ¬ Cavernous sinus (cavernous
⤳ Cause of common cold sinus syndrome
⤳ Acid-labile: Destroyed by HCI in the ¬ Brain (meningitis)
stomach and unable to infect GIT
⤳ (+) SS RNA binds to I-CAM-1 on Pseudoephedrine
14 respiratory epithelial cells
Local vasoconstriction via activation
"I-CAM e to see the Rhino" Muc of α-adrenergic receptors
u sP Watch out for rebound congestion
lu upon cessation and CNS stimulation
Epistaxis gg
"Kiesselbach drives his

ed
¬ Nose bleeds

M
Lexus with his L.E.G.S." ¬ Most commonly occurs in the

ax
ill
Most common causes of Kiesselbach plexus

ar
Epistaxis:

yS
L = Labial Artery
• Foreign body

inu
E = Ethmoidal Artery (anterior & posterior) bach
• Trauma el

s
• Allergic rhinitis
G = Greater Palatine Artery

's
Kie ss
S = Sphenopalatine Artery

plex
• Nasal angiofibromas
us
Life-threatening Epistaxis occurs in the Sphenopalatine Artery

Swollen
Epiglottitis epiglottis
A irway inflammation THINK!
I ncreased pulse "AIR RAID"
R estlessness
R etractions (increased work of breathing)
A nxiety
I nspiratory stridor haemoP hilus causes:
D rooling Etiology: epiglottitis
Vaccinated: meningitis
Streptococcus pneumoniae/pyogenes otitis media
Pneumoniae Croup affects
Unvaccinated: the trachea
Haemophilus influenzae type B
¬ Gram (-) rod
¬ Produces IgA protease  Colonizes mucosal "HI 5 and $10 to enter the Chocolate Factory!"
surfaces HI = Haemophilus Influenzae
¬ Transmitted via aerosolized droplets 5 = Factor V (NAD+)
¬ Cultured on chocolate agar containing 10 = Factor X (hematin)
16 factors V (NAD+) and X (hematin) for growth Chocolate Factory = Cultured on chocolate agar

Thumb-print Treatment: MEDICAL EMERGENCY!

sign on X-ray Management: Airway Management + Empiric Antibiotics

Croup
¬ Caused by Parainfluenza virus
¬ Associated with barking cough and inspiratory stridor
Management: Supportive care + Dexamethasone
22 X-ray shows Steeple sign 15
(narrowing of trachea + subglottis)
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 Upper Airway Malignancies & Infections

head & neck cancers Look out for

keratin pearls
Generally on histology!
RISK FACTORS: type of cancer: squamous
HPV-16 Oropharyngeal carcinoma cell
EBV Nasopharyngeal carcinoma carcinomas
Smoking & Alcohol Laryngeal cancer

CORYNEBACTERIUM Diphtheria This is a toxoid

vaccine
¬ Release ¬ Inhibits EF-2 via. CLINICALLY INVESTIGATIONS: TREATMENT:
Exotoxin ADP ribosylation PRESENTS WITH: • Elek (+) • Diphtheriae
encoded by • Pharyngitis • Culture reveals gram (+) anti-toxin +/-
β- Prophage rods w/ metachromatic erythromycin or
• Lymphadenopathy
granules penicillin

Pseudomembranous ADP-ribsoylation/
pharyngitis Antibiotics/Antitoxins
appears as a
greyish white
β = β Prophage Gram (+) Rods
membrane with “ABCDEFG“ Corynebacterium
Spread via
droplets
lymphadenopathy! of Diptheria! Diphtheriae
"Bull's neck Elongation-Factor 2
appearance"
Granules REMEMBER!
Pseudomonas

PERTUSSIS exotoxin A has the

same mechanism
(inactivates
pertussis toxin elongation factor 2)
¬ Secretes ¬ Activates ¬ Increases ¬ Decreases
exotoxins that Adenylyl cAMP WBC’s
inhibit G(i) cyclase phagocytic
activity Pertussis is associated
with significant increase
INVESTIGATIONS TREATMENT in WCC count -
• Bordet-Gengou Agar • Macrolides specifically Lymphocytes!
• Prevented by Tdap & DTaP
gram - aerobic Think! Bordet = Bordetella
coccobacillus
1-2 WEEKS 2-4 WEEKS WEEKS - MONTHS

CATARRHAL STAGE PAROXYSMAL STAGE CONVALESCENT STAGE

• Cough • Paroxysmal intense cough • Reduction of symptoms
• Rhinorrhea (Coryza) w/ subsequent inspiration
• Febrile (high-pitched whoop)
• Posttussive vomiting

DEXTROMTHORPHAN Mechanism of action: adverse events:

Antagonizes NMDA glutamate receptors Avoid MIXing
Dex the NMDA Blocker (+ mild opioid effect). Can be reversed with naloxone! with serotonergic
keeps the cough AWAY, but agents or you'll PAY
don't MIX it or you'll PAY! uses: Cough suppressant (keeps cough away!) (serotonin syndrome). 23

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 Pneumonia
LOBAR PNEUMONIA Bronchopneumonia Interstitial Pneumonia

Multifocal and bilateral—generally involving Infiltration between alveolar spaces. Diffuse

Involves entire lobes of the lungs. Infection more than 1 lobe. and multifocal—often referred to as “walking
centers around intra-alveolar infiltration.
Infection descends from bronchioles to alveoli. pneumonia.”

17 18 19

Infiltration in a whole lobe Patchy, multifocal infiltrates Diffuse, reticular interstitial infiltrates

COURSE OF LOBAR PNEUMONIAE

Congestion RED Hepatization Grey Hepatization Resolution

Day 1–2: Day 3–4: Day 5–7: Day 8+:

Bacterial infiltration leads to Alveolar spaces filled with Alveoli filled with lysed RBCs, Digestion of inflammatory by-
vascular congestion and edema. bacteria, leukocytes, exudate, exudate, and white blood cells products by macrophages.
and red blood cells (RBCs). (WBCs).

Common organisms causing pneumonia by age

Neonates Children Adults Adults ELDERLY
(<4 weeks) (4 weeks–18 years) (18–40 years) (40-65 years) (65+ years)
√ Group B Strep √ RSV √ Viruses √ Mycoplasma √ Viruses
√ E. coli √ Mycoplasma √ C. pneumoniae √ Viruses √ S. pneumoniae
√ Chlamydia √ S. pneumoniae √ S. pneumoniae √ Anaerobes
trachomatis √ Mycoplasma √ Anaerobes √ H. influenzae
√ C. pneumoniae √ Influenza virus
√ S. pneumoniae
24

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 Pneumonia Organisms
Typical Organisms
Gram (-): Manifestation: Gram (+):
Moraxella catarrhalis Lobar OR Bronchopneumonia Streptococcus pneumoniae
Haemophilus influenzae Staphylococcus aureus
Associated with IV drug use

Atypical Organisms
Mycoplasma pneumoniae High-Yield Pneumoniae Associations
¬ Most common cause of atypical pneumonia aka
"Walking Pneumonia"
Legionella:
⤷ insidious onset, headache, non-productive Found in residential/office buildings
cough, patchy or diffuse interstitial infiltrates with air conditioning
THI
¬ No cell wall: Does not appear on gram stain! "Myco NK!
p
COLD lasma gets Chlamydia trachomatis:
¬ Treatment: Macrolides (e.g., Azithromycin) withou
(no cell t a coat Neonate with resolving conjunctivitis
¬ Associated with: (+) Coombs test with high well)!"
titers of cold agglutinins (IgM) against RBC cells
Klebsiella & Anaerobes:
Alcohol & Aspiration
HemagglutinIN (HA): !
Involved in attachment THINK
lc o h ol in
(entry coming IN) "Drink a "!"
th e " K lu b

NeuRAminidase (NA):
Involved in the RAlease of new
viruses out of cells
Coxiella burnetii
Orthomyxoviruses (Influenza Virus) Morphologically similar to Rickettsia
but differs in that:
Symptoms: 1. Not spread via arthropods
μ Respiratory distress (transmitted via barn animals)
μ Fevers + Myalgias 2. Causes pneumonia
μ Can cause bacteria-superimposed pneumonia 3. No rash
Cause of Q-fever: Headache, Cough,
Treatment: Influenza-like SX, Pneumonia
+ Supportive therapy Treatment: Doxycycline
+ Neuraminidase inhibitors (e.g., Oseltamivir—must be
taken within 24 hours of symptom onset to be effective)
Beca u s e o
f. .
Why is it difficult to eradicate Influenza? .

Antigenic Shift:
RNA reassortment of two different viruses
New subtype introduced
Virus B Host cell Antigenic shift Associated with major pandemics

New strain

Antigenic Drift:
¬ Random point mutations resulting in
continual viral change
Antigenic drift ¬ Requires vaccines to be updated annually
¬ Associated with epidemics
25
Virus A Virus A
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 Systemic Mycoses

Paracoccidioidomycosis Blastomycosis
Presents similarly to Blastomycosis Inflammatory lung disease
Disseminates to bone & skin

“Paracoccidio
parasails with the Blasto
captain’s wheel to Buds
Latin America!”
Broadly!
20

21
Budding Yeast with "CAPTAIN WHEEL" Formation
Broad-based budding!

Eastern & Cent s

r a l U S , G r e a t L a ke
SYSTEMIC
MYCOSEs
Cause of Pneumoniae
& can disseminate to
other organs!

Tx
So

th
we
u

All Are dimorphic fungi ste

rn U Local:
COLD (20 degrees) = MOLD S, C fluconazole
ali
f or
ni a issippi &
Miss er Valleys
HEAT (37 degrees) = Yeast
Systemic:
v
io Ri
EXCEPT amphotericin B
Oh

Coccidioidomycosis Histoplasmosis
Disseminates to bone & skin Mouth ulcers, splenomegaly,
Erythema nodosum or multiforme pancytopenia, erythema nodosum
Arthralgias Associated with bird/bat droppings
(caves)

“Coccidio c
rowds in Histo Hides
preads in
spheres & s
in
f o u n d wit h
dust!” m ac r o p h ag
es
22

23
Spherule filled with endospores
DX: Urine/serum antigen
Associated with dust exposure
(i.e. evacuations, earthquakes)
26

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 Lung Malignancies
General Features
Presentation: Cough, hemoptysis, bronchial obstruction, wheeze
Risk Factors
¬ "Coin" lesion on CXR or nodule on CT ! Tobacco smoking
! Radiation
¬ Lung metastases: "L ove A ffective B oneheads & B rainiacs" ! Environmental exposure (e.g., asbestos)
⤷ Spreads to: L iver, A drenals, B one, & B rain ! Pulmonary fibrosis
¬ Metastases to lung (multiple lesions) are more common than ! Family history (FHx)
1° tumors. Commonly from: breast, colon, prostate, or bladder.

Complications
Pancoast Tumor ¬ Superior vena cava syndrome
¬ Endocrine (paraneoplastic)
Carcinoma at the apex of the lung, leading to compression of:
¬ Recurrent laryngeal nerve = Hoarseness ¬ Pancoast tumor +/- Horner's syndrome
¬ Stellate ganglion (Horner syndrome) = Ptosis, miosis, anhidrosis ¬ Recurrent laryngeal nerve compression
¬ Brachial plexus = Shoulder pain, muscle atrophy ¬ Effusions
¬ Phrenic nerve = Hemidiaphragm paralysis = Elevation on CXR!

Small Cell Lung Cancer

SCLC (15%)
¬ Undifferentiated mass in the hilar region
¬ Paraneoplastic syndromes = Small-LAA
(Sounds like "Smaller")
S "'s are "S "entral and L ambert-Eaton syndrome = L
associated with S moking!
A CTH-producing (Cushing syndrome) = A
A DH-producing (SIADH) = A 26

¬ Neoplasm of neuroendocrine Kulchitsky cells

¬ Chromogranin A (+)

NON-SMALL CELL LUNG CANCERS (85%)

Adenocarcinoma
¬ Most common lung cancer (Females > Males)
¬ Most common in non-smokers
¬ Mutations: Activating mutations in KRAS, EGFR, ALK
¬ Associated with hypertrophic osteoarthropathy (clubbing)
¬ Histology: Glandular pattern, commonly stains mucin (+)

Squamous Cell Carcinoma

¬ Hilar mass arising from bronchus
¬ C avitation, C igarettes, Hyper C alcemia
¬ Paraneoplastic production of PTHrP
⤷ Look for features of hypercalcemia
(i.e. nephrolithiasis, bone pain) 27

¬ Keratin pearls & intercellular bridges

Large Cell Carcinoma

¬ Highly anaplastic undifferentiated neoplasm
¬ Pleomorphic giant cells: REMEMBER! Large

Bronchial Carcinoid
¬ Sx due to mass effect or carcinoid syndrome (5-HIAA)
¬ Good prognosis, neuroendocrine nests & chromogranin-A (+) 27

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 Mycobacterium

O B AC T E
YC R
M. avium-intracellulare
Associated with disseminated non-TB

IA
pathologies in immunocompromised
individuals (i.e. HIV/AIDS)
Gram (+)
Highly resistant to treatment Acid-fast bacilli
Treatment: Prophylactic Azithromycin

24

Reservoir: Armadillo
M. Leprae
Infects skin and superficial nerves
Subtypes: M. marinum
L arge Th2 response Associated with handling
A. Lepromatous :
L ethal fish (i.e. Aquarium workers)
"The L 's of L epromatous"
L ion face appearance
B. Tuberculoid: Hairless skin plaques

TX for both Subtypes of Leprae:

M. scrofulaceum
"R eally D umb C owboys Eat Armadillos" Associated with cervical
lymphadenitis in children
R ifampin, D apsone + C lofazimine

M. TUBERCULOSIS
General Features Virulence Factors
¬ Mycolic acid cell wall is difficult to gram Cord factor: Increases TNFα
stain therefore use Ziehl-Neelsen stain from activated macrophages TB reactivation
(via Th1 pathway) is highest in
¬ Greatest Risk Factor: Immigrants to
immunocompromised
the USA from endemic areas Infiltration of macrophages leads to the patients (i.e. HIV,
¬ Presents as: Fever, night sweats, weight formation of caseating granulomas organ transplant)
loss, cough, hemoptysis 25

Ghon complex 1o TB < 10%

(hilar nodes + ghon focus in Investigations
mid-lower lobes) Miliary TB ¬ CXR
¬ In pts with AIDS, ¬ PPD (Purified Protein Derivative):
malnutrition ⤷ Type 4 hypersensitivity reaction (positive test
¬ Bacteremia depends on risk factors)
> 90%

2o TB
¬ Cavitating lesions ≥ 15mm ≥ 10mm ≥ 5mm
usually seen in the
Low Risk Medium Risk High Risk
upper lobes
! General ! Health care workers ! Immunocompromised
⤷ Localized destruction
population ! Endemic migrants individuals
of tissue
! Children < 4 years ! Close contact with
¬ Healing via Fibrosis active TB patients
28
¬ (+) PPD
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 Tuberculosis Pharmacology

R I P E ¬ Combination therapy used to treat patients with active TB

¬ RIPE used for first 2 months followed by R.I. for following 4
months. 6 months of total therapy.
R I P E R I

MONTH “4 R’s of Rifampin”

1 2 3 4 5 6
R apid resistance - when used alone
R amps up CYP450
R Prevents transcription of Mycoplasma
proteins via. inhibition of DNA R ed/orange urine
dependant - RNA polymerase R NA polymerase inhibitor
RIFAMPIN

Inhibits synthesis of mycolic acid >>> disrupts cell wall synthesis. I soniazid I nhibits CYP450
REMEMBER the I's
I ⤷ Requires catalase peroxidase (KatG-gene) to activate
Needs to be supplemented with B6 (Pyridoxine) or can lead to neuropathy!

ISONIAZID “Don’t use Isoniazid in ISO-lation or you will B-sick (six)

MOA unknown >>> activated in the acidic environment of Phagolysosomes

P

P
ADVERSE EVENTS: Hyperuricemia >>> Gout (commonly found on toes!)

PYRAZINAMIDE “Sideways P looks like a Foot”

Optic
E Inhibits Arabinosyltransferase
neuropathy
is a reported
⤷ Decreases carbohydrate synthesis adverse effect
⤷ Decreases cell wall synthesis “Eye-thanbutol”
Ethambutol
Plasma
Cell wall membrane Interior of cell
MYCOBACTERIAL CELL
ids

mRNA
e lip
comple l lipids

id
ic ac

Mycolic Acid
x f re

mRNA Synthesis
ctin
Acy

Synthesis
Mycol

(DNA-dependent
n
g l yc a
ogala

RNA polymerase)
o

ISONIAZID
A ra b i n

Peptid

RNA Rifampin
polymerase
ARABINOGALACTAN
Synthesis
(arabinosyl transferase)
Intracellular
DNA (unclear mechanism)
Ethambutol 29
Pyrazinamide
Prepared exclusively for Carlos Ruiz valeruizpuyo@gmail.com Transaction: 26357
 Notes

30

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31

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 About the Author
Jacob Portnoff is a passionate medical student (MS4) and social media
influencer, known as “MedSchoolBro,” who has established himself as a
growing presence in the medical community. Combining his knowledge
of medical topics and his ability to communicate complex medical
concepts, Jacob has developed a unique approach to medical education
that has garnered a large following.

As a student preparing for his USMLE licensing exams (Step 1 & Step 2CK)
and Shelf exams, Jacob recognized the need for a comprehensive guide
that encompasses all the essential aspects of Pulmonology. Inspired by
his own successful learning techniques and visual approach to learning,
he created this Pulmonology Review Guide, a 30-page resource that
integrates the various disciplines of medicine to enhance understanding
and retention.

ACKNOWLEDGEMENTS
Jacob would like to extend his gratitude to his colleague Raghavan Vijayakumar for his work assisting with
the content of this study guide. He also thanks Dr. Fahad Ahmed & Dr. Khalid El-Jack for their careful review
of the guide. Finally, he extends his thanks to Amir Ebadi for the beautiful editorial design which helped bring
this guide to life.

Dr. Fahad Ahmed , MD, is a dermatology resident physician at the University

of Miami. He received Alpha Omega Alpha distinction and graduated with his
Medical Doctorate (MD) degree from the University of Pennsylvania’s Perelman
School of Medicine. Additionally, he graduated Summa Cum Laude from the
University of Pennsylvania with a bachelor’s degree in health communication.
He has always been passionate about helping other students reach their full
potential through education and has extensive experience advising/tutoring
medical students along their journey to becoming a doctor.

Dr. Khalid El-Jack, MD, is an ophthalmology resident physician at the University

of Miami’s Bascom Palmer Eye Institute. He graduated with his medical doctorate
(MD) from the University of Pennsylvania’s Perelman School of Medicine. He
graduated Magna Cum Laude with his bachelor’s in human physiology from
Boston University. He has extensive experience tutoring both medical and
premedical students with their application processes and standardized exams.

Raghavan Vijayakumar is an MD3 studying at the University

of Queensland he is passionate about teaching, developing, and
delivering medical education to a global audience to help the next
generation of medical students pass their board exams.

32

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 IMPORTANT INFORMATION AND DISCLAIMERS

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