Pneumonia

Sources: Ninja Nerd, AMBOSS ( video included), , Master the Board, Step-up to Medicine, ,

Objectives
Knowledge Cognitive skills
1. Choose the appropriate laboratory/imaging tests to
1. Define CAP, HAP, and VAP
evaluate patients with possible pneumonia
2. Outline the pathophysiology of CAP, HAP, and VAP and 2. Interpret the CXR findings suggestive of pneumonia and
Identify the common microbiological organisms distinguish different causes of alveolar pattern
3. Formulate and prioritize a differential diagnosis for
3. List clinical features of pneumonia
patients with cough and fever.
4. Recognize and prioritize patients with CAP who need
4. Utilize the CUREB-65 pneumonia severity scoring system
hospital admissions.
5. Develop an evidence-based management plan for
5. List the causes of non-resolving pneumonia
pneumonia management (CAP, HAP, and VAP).
6. Describe pneumonia complications and their appropriate 6. Formulate a follow up plan for patient with CAP, HAP, and
management VAP
7. Describe the basic pharmacology of different empirical
7. Demonstrate the appropriate skills for patient education.
antimicrobials used in treatment of CAP, HAP, and VAP

High yield information

Organisms and antibiotics
Typical vs atypical pneumonia
Indication for hospitalization

Definitions
Pneumonia: respiratory infection characterized by inflammation of the alveolar space and/or the interstitial
tissue of the lungs, causing consolidation. It can be classified in many ways:
Consolidation: inflammatory exudate and cells fill the alveoli and leave little to no space for air
o According to Location:
Community Acquired Pneumonia (CAP)
Hospital Acquired Pneumonia (HAP): (onset > 48 hours after admission)
Ventilator-associated Pneumonia (VAP): (typically in the ICU, 48-72 hours following intubation)

o According to Clinical features:

Typical: Classic signs and symptoms. Manifests as lobar pneumonia or bronchopneumonia
Atypical: less distinct classical symptoms and signs. Manifests as interstitial pneumonia

Pathophysiology
Pathogenesis:
o Failure of protective pulmonary mechanisms
o Infiltration of the pulmonary parenchyma by the pathogen leading to interstitial and alveolar inflammation
o Ventilation/perfusion (V/Q) mismatch with intrapulmonary shunting (right to left)
o Hypoxia due to increased alveolar-arterial oxygen gradient
Hypoxia is worsened when the affected lung is in the dependent position, as perfusion to the dependent
lung is better compared to the nondependent lung.
In the case of a large unilateral pulmonary abscess, it may be helpful to position the patient so that the
affected lung is in the dependent position to prevent the pus from filling the unaffected lung.
 Causes
Most common pathogens of Community acquired pneumonia:
o Typical pneumonia:
Streptococcus pneumoniae (most common)
Klebsiella pneumoniae: common in diabetic or alcoholic patients
Staphylococcus aureus: commonly post upper respiratory tract infection
Hemophilus influenzae
o Atypical pneumonia
Atypical Bacteria: They do not respond to beta lactam antibiotics (e.g., Amoxicillin)
- Legionella pneumophila: associated with hyponatremia, GI symptoms and CNS symptoms
- Mycoplasma pneumoniae: common in children, spreads among crowds
- Chlamydia pneumoniae: pneumonia associated with sex transmitted disease
Viruses: Respiratory syncytial virus (RSV), Influenza viruses, Parainfluenza viruses, Cytomegalovirus
(CMV), Adenovirus, Corona Virus (e.g., SARS-CoV-2)
Most common pathogens of Hospital and ventilator acquired pneumonia:
o GNRs, Staphylococcus, anaerobes
o Pseudomonas aeruginosa: treat with Tazocin (piperacillin + Tazobactam)

Pathogens with an HIV patient

o CD4>200: Streptococcus pneumoniae is the most common organism
o CD4<200: Pneumocystis jirovecii pneumonia
o CD4 less than 50-100: Mycobacterium avium complex (MAC)

Pathogens with a bronchiectasis patient

o Pseudomonas aeruginosa

Clinical features
- Typical pneumonia:
o Typical pneumonia is characterized by a sudden onset of symptoms caused by lobar infiltration
o Symptoms (the first four are the most important)
1. Fever, might be associated with chills
2. Cough, productive with purulent sputum (yellow greenish)
3. Tachypnea and dyspnea (nasal flaring, thoracic retractions)
4. Pleuritic chest pain when breathing, often accompanying pleural effusion
5. Pain that radiates to the abdomen and epigastric region (particularly in children)
o Signs:
Crackles and bronchial breath sounds on auscultation
Decreased breath sounds
Enhanced bronchophony, egophony, and tactile fremitus
Dullness on percussion

- Atypical pneumonia:
o Atypical pneumonia typically has a slow onset and commonly manifests with extrapulmonary symptoms
o Symptoms include:
Nonproductive, dry cough
Infiltration is often bilateral
Auscultation often unremarkable
Common extrapulmonary features include fatigue, headaches, sore throat, myalgias, and malaise
Diagnosis
Chest X-ray (the most essential investigation, confirmatory test)
o Airspace shadowing and Air bronchograms (black tube going through a consolidated area)
CBC (will show infection)
Urea and electrolytes (Dehydration, used in the CURB-65 explained below)
Liver function test (low function suggests Legionella infection, confirmed with urine antigen)
ESR/CRP (nonspecific, inflammatory marker)
Blood culture (to identify bacteremia)
Serology and Cold agglutinins (for diagnosis of mycoplasma pneumonia)
ABG (hypoxia)
Oropharynx swap and Gram stain (to identify the class of the bacteria)

X-ray of Pneumonia:

Consolidation is unilateral Consolidation is Bilateral

Suggesting typical pneumonia Suggesting atypical pneumonia

Treatment
- Antibiotics:
a. Typical pneumonia: Fluoroquinolone (levofloxacin, moxifloxacin) or Ceftriaxone and Azithromycin
b. Atypical pneumonia: Azithromycin (usually in healthy and young patients)
c. MRSA: Vancomycin
d. Hospital acquired:
- Piperacillin + Tazobactam, Cefepime, Meropenem, or Imipenem
- OR a respiratory fluroquinolone e.g., levofloxacin, ciprofloxacin
- Asses the need of hospitalization:
To measure the severity of the pneumonia and the need of the patient for hospitalization:

CURB-65 Clinical features Points

C Confusion 1
U Urea > 7 mmol/L (19 mg/dL) 1
R Respiratory rate 1
B Systolic BP OR Diastolic BP 1
65 Age > 65 1
 CURB-65 Score Risk group Management
0-1 1 Low risk, consider home treatment
2 2 Probably admission or close outpatient management
3 3 Admission to the medical ward, manage as severe
4-5 4 Admission to the ICU, manage as severe

Other scoring systems (not as important to remember but good to know)

- PSI/PORT score
- SMART-COP score

Causes of non-resolving pneumonia:

1- Complications: empyema, effusion, or abscess
2- 2ry to bronchial obstruction or recurrent aspiration
3- Wrong treatment: resistant organism
4- Wrong diagnosis

Complications:
- Parapneumonic pleural effusion: see the next lecture
- Parapneumonic pleuritis
- Pleural empyema: a chest tube might be needed to drain the collection of pus
- Lung abscess
- Respiratory failure: supportive measurements are necessary
- Acute respiratory distress (ARD): supportive measurements are necessary
- Sepsis: medical emergency, establish IV access and contact ICU

Summary
Pneumonia is a respiratory infection characterized by inflammation of the alveolar space and/or the interstitial
tissue of the lungs. In industrialized nations, it is the leading infectious cause of death. Pneumonia is most
transmitted via aspiration of airborne pathogens (primarily bacteria, but also viruses and fungi) but may also result
from the aspiration of stomach contents. The most likely causal pathogens can be narrowed down based on patient
age, immune status, and where the infection was acquired (community-acquired or hospital-acquired). Pneumonia is
classified based on clinical features as either typical or atypical; each type has its own spectrum of commonly
associated pathogens. Typical pneumonia manifests with sudden onset of malaise, fever, and a productive cough. On
auscultation, crackles and bronchial breath sounds are audible. Atypical pneumonia manifests with gradual onset of
unproductive cough, dyspnea, and extrapulmonary manifestations. Auscultation is usually unremarkable. Some
patients may present with elements of both types. Diagnostics include blood tests for inflammatory parameters and
pathogen detection in blood, urine, or sputum samples. Chest x-ray in cases of typical pneumonia shows opacity
restricted to one lobe, while x-ray in atypical pneumonia may show diffuse, often subtle infiltrates. Together with
the characteristic clinical features, newly developed pulmonary infiltrate on chest x-ray confirms the diagnosis.
Management consists of empiric antibiotic treatment and supportive measures (e.g., oxygen administration,
antipyretics).

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 Last edited: 9/15/2021

1. PNEUMONIA
Pneumonia | Pathophysiology Medical Editor: Maxine Abigale R. Bunao

Location Function Inhibited by:

OUTLINE
Antitussive
I) PATHOPHYSIOLOGY Alcohol seda Klebsie
II) STAGES OF PNEUMONIA Irritant Food/ Fluid Opioid analgesics:
III) CAUSES OF PNEUMONIA receptors in undesirably goes ● Hydrocodone
IV) CLINICAL SETTINGS bronchi down through ● Fentanyl
V) SIGNS AND SYMPTOMS respiratory area ● Morphine
VI) APPENDIX Gagreflex Damaged brainstem
VII) REVIEW QUESTIONS swonawing
VIII) REFRENCES
C
(3) Antibodies
Ab
● Specific: IgA antibodies
I) PATHOPHYSIOLOGY Location Function Damaged by
Mucosal immunity
Definition: also found in GIT,
Mucosa of ● Smoking
o Pneumonia is the infection and inflammation of the GUT
respiratory ● ↑↑ Alcohol
lung parenchyma (lung tissue) itself. Binds onto bacteria/
epithelium
(A) MODE OF TRANSMISSION
pathogen to trigger xna
immune system
Acquired through:
(4) Alveolar macrophage
(1) Inhalation
Location Function
Foreign pathogen Phagocytose foreign matter 
Aspiration means to o 75-80% bacterial influenza legionenacwater Fixed /
● chemotaxis: (+) cytokines, immune cell
4
sources
draw in or out using Permanent
a sucking motion.
Secretion
(2) Aspiration oropharyngeal Gastric
Éffighlamydia ● bacteria digested + inflammatory
response triggered
● Example: Food or fluid goes down the wrong pipe
Normally● Immune system:
o Defense mechanism is to cough  spit out the
offending food / fluid instead of swallowing and going
down the respiratory system
● Situation aspiration is more common:
o Regurgitation due to underlying swallowing issues:
 Achalasia
 Zinger’s diverticulum
Klebsiellaanaerobic E
o Aspiration pneumonia
an
 more common from anaerobic bacterial etiology f
o IV drug users via hematogenous spread:
 Staphylococcus aureus

(B) DEFENSE MECHANISM

● Defense mechanisms:
o Any defect in the following 
 Bacterial colonization
o Bacteria can be dangerous  ↑↑ issue damage 
infection  pneumonia

o
(1) Cilia “muco-ciliary escalator”
Location Function Defect
Pseudo- Smoker: iticataraiese
stratified com
↑ ciliary damage
ciliated Cytoplasmic
extensions to beat ↓ escalator function
columnar ↑ bacterial
epithelial mucus & large
bacteria upwards colonization 
tissue tissue damage,
 spit it out
pace inflammation,
infection Fas
am
t basis mucas pseudomonas Figure 1. Pathophysiology and causes of pneumonia.
C
(2) Cough Reflex
Pathophysiology:
reflexswanning
Gag

o Irritant receptors in bronchi activate afferent fibers via

the vagus nerve  respiratory center in medulla
o Efferent fibers of intercostal & phrenic nerves 
trigger cough reflex.

PNEUMONIA RESPIRATORY PATHOLOGY: Note #4. 1 of 5

 (C) PATHOGEN INVASION II) STAGES OF PNEUMONIA
• Bacteria causes release of endotoxins TissueDange
► Tissue damage response (1) First Stage: Congestion (Day 1-2)
o Leukotriene LB4:
■ LB4 can move into the circulatory system
 chemotactic agent which draws WBCs
Due to ↑ vasodilation, ↑ vascular permeability:
o Fluid starts leaking into the alveoli
Fluid
& other immune system structures into the
area of the infection / inflammation
o Other leukotrienes: LTC4, LTD4, & LTE4
■ Binds: different endothelial cells  ↑
capillary permeability
◊ If ↑ intravascular space due to
permeability  ↑ Fluid leaking out
◊ Manifestation: Edema
■ Binds: respiratory smooth muscle 
bronchoconstriction / bronchospasms
◊ Manifestation: Dyspnea, shortness of
breath totissuedam
response
o Mast cell activation:
■ Release of histamine  ↑ vasodilation, ↑
vascular permeability Edema
o Macrophages:
■ Phagocytose bacteria  releases ↑
(2) Second Stage: Red hepatization (Day 3-4)
Accumlation
chemicals (IL-1, -8, TNF-a)  ↑ vascular PusRe
C
permeability
■ Manifestation: Feverpyrexia
Due to ↑chemotactic factors & WBCs into the area: Fibrin're

o Interleukin-1 (IL-1) o Exudative fluid is formed (↑ Specific gravity or

o Interleukin-8 (IL-8): proteins in it)
■ Chemotaxis o When ↑↑↑ damage to pulmonary capillary  RBCs
o Tumor necrotic factor-a (TNF-a)
leak as well
► Amino acid release

f
o Informal methionine which humans do not have Inflammatory exudates which accumulated to form
■ Move into the circulatory system  consolidation:
iww chemotactic agent which draws WBCs & o Alveolar exudates: protein, water, plasma
other immune system structures into the components  Congestion
area of the infection / inflammation o WBC
• Note on importance of ↑ vascular permeability: o RBC
► ↑ WBC, complement proteins to fight off against o Fibrin
bacteria o Manifestation: Hypoxia
► Later on causes pneumonia
• Summary:
(3) Third Stage: Gray hepatization (Day 4-7)
BrokenI
RBCs start getting destroyed and broken down  take on
► Bacterial endotoxins induce inflammatory
response which release: a different appearance
o Leukotrienes
o Histamine
o Prostaglandin
(4) Fourth Stage: Resolution (Day ≥8)
Broken II
Breakdown:
o Platelet activating factor o More RBCs, WBCs, fibrin are starting to be
► Major effect: CLEARED
o Vascular permeability o Some are cleared, some COUGHED UP
o Vasodilate
Relation with lobar pneumonia with consolidation:
Location of Response
Release o During breakdown of consolidated materials 
action
sputum production or productive cough is released
Intravascular Chemotaxis
Leukotriene
(circulatory RECALL:
LB4
system)
Normal V/Q Ratio = 0.8
Intravascular, capillary permeability
endothelial = edema o If ↓ V  0.8 will decrease so in order to be balanced, Q
LTC4, LTD4, cells will have to drop
& LTE4 Respiratory
smooth
Bronchoconstriction =
dyspnea, shortness of
o Poor ventilation  capillary constriction in order to
c
prevent circulation and send them to other parts of the

TT
muscle breath lung where there is adequate ventilation
Mast cell ↑ vasodilation, Clinical manifestation of poor ventilation:
o Hypoxia jam
activation
(histamine)
↑ vascular
permeability
2
o Tachycardia How
Intravascular
(circulatory Phagocytose bacteria
o Tachypnea um in
system) 
Macrophages
↑ vascular
permeability = fever

2 of 5 RESPIRATORY PATHOLOGY: Note #4. PNEUMONIA

 III) CAUSES OF PNEUMONIA (7) Klebsiella
Epidemiology:
75-80% are caused bacteria
o Common in chronic alcoholics
Others: Viruses, fungi
o Common in aspirators
(A) BACTERIAL o Seen in chronic illnesses

(1) Streptococcus pneumoniae ptiseldertsmoner (8) Pseudomonas aeruginosa

Gram positive bacteria Epidemiology:
Epidemiology o Seen in immunocompromised:
communitya cquired
p neumonia
o 65% of CAP are due to this  HIV
 AIDS
(2) Haemophilus influenzae  Structural abnormality of respiratory system:
Gram negative bacteria • Bronchiectasis
Epidemiology: • Cystic fibrosis
o 2nd most common cause of CAP
o Common in those with underlying pulmonary diseases
 COPD (B) VIRAL
 Asthma
7
 Bronchiectasis
Generally, not treated and take their own course over a
couple of weeks
 Cystic fibrosis
o More common in status-post organ transplant patients
(3) Mycoplasma pneumoniae o Immunocompromised
Also known as “walking pneumonia” is
(1) Respiratory Syncytial (Parainfluenza) Virus
Neither a gram negative or positive bacteria
Epidemiology
o NO cell wall
o More common in infants and young children
jumonia o Type of ATYPICAL pneumonia
pharynx
Epidemiology: (2) Influenza Virus
o ↑ risk in school age Epidemiology
o Younger individuals o More common in adults
o Most common cause of ATYPICAL pneumonia (3) Cytomegalovirus (CMV)
ENT Signs: Epidemiology
o Bullous myringitis o More common in status-post organ transplant patients
 Skin lesion o Immunocompromised
 Circumscribed deposit of serous fluid coming from
the tympanic membrane (4) Varicella Zoster
 Inflamed tympanic membrane Can cause serious pneumonia
o Pharyngitis
(C) FUNGAL
(4) Chlamydia pneumonia
Epidemiology:
Intracellular parasite Doxycycline o More common in certain parts of the US or other
(5) Legionella ptiseldertsmoner
world
o More common in immunocompromised:
Gram negative bacteria  HIV
Pathophysiology:  AIDS
o You can develop this  Neutropenic fevers
o MOT:Through  Immunosuppressive drugs
 Contaminated water sources
(1) Pneumocystis jiroveci
• Cooling towers pp
• Air conditioners Also known as pneumocystis pneumonia
 NOT person-to-person transmission Epidemiology
o More common immunocompromised HIvwithCDuc20
Signs & symptoms:
Niv o GIT: nausea, vomiting (2) Histoplasmosis capsulatum

gg o ↑ Liver function enzymes: ALT, AST, ALP Epidemiology

o Location: Mississippi river valley or Ohio river valleys
o Hyponatremia: ↓ sodium in the blood
 ↑ Bird and bat droppings
(6) Staphylococcus aureus
(3) Coccidioides
Epidemiology:
o Common post-viral upper respiratory tract infections Epidemiology mycosis
o ↑ risk in: o More common in ↑ soil / desert areas
 Immunocompromised PostAflux  Southwestern US
 California
 Elderly
MOT: Blastomycosis
o Hematogenous spread: IV drug users
Methicillin resistant Staphylococcus aureus: especially
East
nasty bacteria
i Ptimmunocompromised
Pseudomonas
Legionella
psp
cmr
PNEUMONIA RESPIRATORY PATHOLOGY: Note #4. 3 of 5
 IV) CLINICAL SETTINGS V) SIGNS AND SYMPTOMS

mostly (A) COMMUNITY-ACQUIRED PNEUMONIA (CAP) (1) Typical

lobar
pneumonia Acquired in community OR if admitted in the hospital for ↑ Consolidation from accumulated RBCs, WBCs, fibrin
<2 days only
 manifestation:
Most common pathogens:
strep o Dyspnea
o S. pneumoniae methicillinsensitive o Hypoxia (later presentation)
o H. influenzas [Link]
o M. pneumoniae g
aureus  ↑ HR (Tachycardia)

I
o Chlamydia  ↑ RR (Tachypnea)
o Legionella
o Moraxella catarrhalis COPD o ↑ CO2 accumulation in the blood
 Common with pulmonary diseases: COPD (most  Stimulate peripheral chemoreceptors
common)  Activates respiratory center in medulla
o Klebsiella: sometimes but more common in HAP • ↑ RR and depth of breathing
Taoism
(1) Ventilator Acquired Pneumonia  Activates cardiac acceleratory center
Subtype of CAP • ↑ HR
Acquired when intubated (endotracheal) > 48-72 hours Resolution of the consolidation
Increased incidence of developing pneumonia because o Fever or pyrexia
they can form these biofilms Gastricaciasuppression o Productive cough with mucopurulent sputum
(2) Healthcare Associated Pneumonia (HCAP) production

Subtype of CAP Extrapulmonary symptoms

Common in: o Fatigue
o residents of a long-term care facility (i.e. nursing o Shortness of breath
homes) (2) Atypical
o receiving home infusion therapy
o Under chronic dialysis treatment within the last 30
days
From the special bacteria:
o Mycoplasma
MI
o Chlamydia

g
o Have a family member with a multidrug resistant
pathogen o Legionella
o Have been in an acute care facility ≥2 days within the o Viruses
past 90 days o Fungi

(B) HOSPITAL-ACQUIRED PNEUMONIA (HAP) ↑ RR, ↑ HR

Extrapulmonary symptoms:
Acquired in the hospital after being admitted for >2 days
o May be associated with healthcare associated 2 o Headache
then
Bronchopneumonia procedures, ventilators

Sequelae:
already
o Nausea & vomiting
o Diarrhea JURTItypes
o Significant fatigue and malaise
o ↑ Virulence or resistance  must be careful o Myalgia
 Resistance: develop enzymes (i.e. B-lactamases) Differentiating signs & symptoms
that breakdown B-lactams (Penicillin, o Low grade fever
cephalosporins, carbapenems, monobactams)  o Dry cough
render them ineffective a
Noaccumlation
o ↑ Chance of developing multidrug resistant
pathogenic bacteria
Most common pathogens:
o MRSA
 Take note that S. aureus is seen in CAP, bust
MRSA is more common for HAP
o Pseudomonas aeruginosa
o Klebsiella
o Enterobacter
o Actinobacteria
isn
o Serratia

4 of 5 RESPIRATORY PATHOLOGY: Note #4. PNEUMONIA

 VI) APPENDIX

Table 1. Abbreviations.
MOT Mode of transmission
MRSA Methicillin resistant Staphylococcus aureus
V (V/Q) Ventilation
Q (V/Q) Perfusion

VII) REVIEW QUESTIONS VIII) REFRENCES

● Boron WF, Boulpaep EL. Medical Physiology.; 2017.
1) What stage in the development of pneumonia is a
● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
patient in when a patient is already coughing up with Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth
concomitant mucopurulent sputum production at Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical; 2018
Day 9? ● Le T. First Aid for the USMLE Step 1 2020. 30th anniversary
edition: McGraw Hill; 2020.
a) Stage 1 ● Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
b) Stage 2 Pearson; 2020.
c) Stage 3 ● Papadakis MA, McPhee SJ, Rabow MW. Current Medical
Diagnosis &amp; Treatment 2018. New York: McGraw-Hill
d) Stage 4 Education; 2017.
2) Select the most appropriate statement in ● Sabatine MS. Pocket Medicine: the Massachusetts General
Hospital Handbook of Internal Medicine. Philadelphia: Wolters
differentiating typical from atypical pneumonia: Kluwer; 2020.
a) The underlying pathophysiology is their differing ● Williams DA. Pance Prep Pearls. Middletown, DE: Kindle Direct
factor. Viruses and fungi which are more common in Publishing Platform; 2020.
atypical pneumonia follow a different
pathophysiology, hence the difference in symptoms.
b) Atypical pneumonia presents with a low-grade fever
and dry cough.
c) Typical pneumonia is due to special bacteria like
Moraxella, Legionella, other viruses, and fungi.
d) B & C
3) Marc is a 24-year-old male patient who had been
admitted to the hospital for the third time within the
past 3 months. This is his 2nd day of admission and
was observed to be in respiratory distress. Each visit
to the hospital, he was admitted for more than 2
days. Past medical history revealed he had an
underlying asthma and frequented the hospital due
to his unmaintained conditions, thus frequent
exacerbations. Where is the most probable clinical
setting from which he got the pneumonia?
a) CAP
b) HAP
c) VAP
d) HCAP
4) Which pneumonia is frequently seen in school-aged
children and which often present with pharyngeal
inflammation and a skin lesion with serous fluid
coming from the tympanic membrane?
a) Mycoplasma pneumonia
b) H. influenzae
c) Moraxella catarrhalis
d) Pseudomonas aeruginosa

CHECK YOUR ANSWERS

PNEUMONIA RESPIRATORY PATHOLOGY: Note #4. 5 of 5

 Last edited: 9/10/2021

1. PNEUMONIA | CLINICAL FEATURES

Pneumonia | Clinical Features Medical Editor: Maxine Abigale R. Bunao

• consolidation, fluid, proteins

OUTLINE
• ↑ lung density
I) DIAGNOSTIC WORKUP • ↑ air travels faster in water / fluid THAN
II) APPENDIX
III) REVIEW QUESTIONS sound ↑ vibrations against the palms
IV) REFRENCES
(3) Percussion

I) DIAGNOSTIC WORKUP ● General rule: compare bilaterally

● Penetrates about 5-7 cm beneath the chest or posterior
(A) PHYSICAL EXAMINATION back surface
• Not as sensitive and specific a compared to other ● May miss deeper lesions
diagnostic tests: i.e. chest x-ray ● Steps:
o Use two fingers, plexor (2 fingers) to tap onto the
(1) Inspection pleximeter (third digit)
fever
Highgrad o Start at a higher area
Chest examinations:
o Anterior-posterior (AP) diameter  2-4 cm above the inner third of the clavicle
 Position onto specific areas of anterior and
 ↑ AP diameter or Barrel chest: COPD posterior chest wall  tap plexor onto pleximeter
o Thoracic kyphoscoliosis  May use the ladder technique
o Pectus excavatum o Listen for sounds:
o Pectus carinatum  Resonance
 Hyperresonance
↑ RR
• COPD
o Use of accessory muscles: • Asthma
 sternocleidomastoid, pectoralis major and minor,
scalenestrapizusexternal
o Intercostal retractions:
intercostal
onsoft Dullness: ↑fluid within the actual lung tissue

tissue • sounds like the liver

 muscles get pulled inwhileinspartion • Pneumonia will present with dullness
o Observe depth of breathing
 Heavy, rapid
p Tympanic: hollow, drum like
filed• sounds like the percussion from the stomach
cavity
withaeve at the left upper quadrant
● Pleuritic chest pain retonans• Pneumothorax: if heard in the thorax
o Inflammation of visceral and parietal pleura  rubs
against each other  friction  Flatness
o Pain upon inspiration
onsoldBone• Pleural effusion
muscle
shorttone
(4) Auscultation
(2) Palpation
● General rule: compare bilaterally ● General rule: compare bilaterally comparetoliverto the
cheek
sounde
dilness
● Respiratory expansion Listen for normal breath sounds and depends on where
o Steps: you listen to them and hear them:
 Position hands on the back of the patient o Location of inspection:
 Upon deep inspiration and expiration, observe if  Anterior: hands on the hips
the hands are moving:  Posterior: have the patient cross arms and hug
• symmetrically themselves
• delay  May use the ladder technique
• little movement o Use diaphragm
o Example: Lobar pneumonia  Deep breath in  listen to inspiration
 Unilateral decrease / delay in chest expansion in  Deep breath out  listen to expiration
lobar pneumonia  Listen for pitch, intensity Duration
Location Normal Abnormal
● ↑ Tactile fremitus
Manubrium Bronchial Adventitious: superimposed
o Function: to determine lung tissue density
Trachea Tracheal to normal breath sounds
o Steps:
 Hypothenar aspect of palm Entire lung Crackles/rales: ripping velcro
Vesicular
 Location of inspection: tissue apart
• Anterior: hands on the hips
● Due to fluid in the alveoli &
• Posterior: have the patient cross arms and bronchial tissue
hug themselves ● Inspiration: sound of
1st – 2nd
 Radially deviate wrist and put against the chest bronchus popping open
intercostal
OR back Broncho-
space
 Have the patient say “99” vesicular Types
anteriorly and
 Cover the entire lung field interscapularly ● Fine: shorter duration,
• Midline softer
• Lateral side ● Coarse: longer duration,
o Pneumonia: louder
 Pathophysiology: o Examples:

PNEUMONIA | CLINICAL FEATURES RESPIRATORY PATHOLOGY: Note #5. 1 of 3

  Pneumonia: Lobar pneumonia
• Bronchial breath sounds o Pointed triangular structure is a classic presentation
• Harsh, hard, tubular high-pitched sound of consolidation
• Adventitious sounds: ↑ Crackles / Rales
 Atypical pneumonia:
• ↑ Rhonchi
● Transmitted voice sounds
o Hands across the chest
o Only done on the POSTERIOR aspect
o May use the ladder technique
Types Steps Interpretation
(-): muffled, indistinct
Broncho- (+): clear & distinct  sound
Say “99”
phony is transmitted better due to
fluid or consolidation
(-): soft, muffled
(+): “Ae/Aaah” 
Egophony Say “ee”
consolidation, ↑ lung tissue
density
Whisper (-): soft, indistinct
Whisper
slowly (+): Clear, distinct  ↑ lung Figure 2. Bronchopneumonia chest x-ray, posteroanterior (PA)
pectoriloquy view.
“1, 2, 3” tissue density
o If all of these are positive  signs of ↑ lung tissue ● Bronchopneumonia
density OR consolidation o Patchy and diffuse scattered pattern
o Reticular pattern / opacities  Squiggly lines
(B) RADIOGRAPHY o Nodular opacities
o Most of the time bilateral in presentation
(1) Chest X-ray o Location: base of the lung
● Types of Pneumonia:
Types Results
Lobar (most common) ● Alveolar exudate: WBC,
cap proteins, fibers
spneumonia ●● RML, LUL, LLL
Consolidation of ● Damage to pulmonary
alveoli and associated capillaries: RBC
bronchi
Hap Bronchopneumonia ● Diffuse, patchy, reticular (lines
do
Psu as
mon Present at the base of & nodes)
misa the lungs ● White opacities
Apspneumonia
nie
Hunt bsia
Interstitial Pneumonia ● Diffuse, patchy
(Atypical) ● Primarily reticular
I ● Location: Perihilar
Present at the o Pulmonary artery, vein,
interstitial space root
(between: pulmonary o Primary bronchi
capillaries, alveoli, & o Nerves
surrounding o Lymphatic vessels
bronchioles) Figure 3. Interstitial pneumonia chest x-ray, posteroanterior
(PA) view.
● If (+) Klebsiella spp.
o Bulging lobe ● Interstitial (Atypical) pneumonia
o Cavitation o Organisms:
o Abscesses  Mycoplasma
 Chlamydia
 Legionella
o Similarly patchy and reticulonodular opacities
o Difference: reticulonodular pattern concentrated on
the PERIHILAR region, near the heart borders
(2) CT Scan
May also be requested

Figure 1. Lobar pneumonia chest X-ray, posteroanterior (PA)

view.

2 of 3 RESPIRATORY PATHOLOGY: Note #5. PNEUMONIA | CLINICAL FEATURES

 (C) SPUTUM CYTOLOGY III) REVIEW QUESTIONS
(1) Gram stain/ Culture 1) A new infiltrate that forms a bulging lobe and over
May send to the laboratory pre-existing chest lucencies over the right
paracardiac area is suggestive of pneumonia from:
a) K. pneumoniae
(2) Macroscopic appearance of sputum b) S. aureus
Gain idea as to what kind of bacteria might be associated c) P. aeruginosa
with this infection d) Acinetobacter
o Rusty + blood-tinged sputum: Streptococcus 2) Left lower lobe crackles, fever, abscess without
pneumoniae pedal edema in a patient with hypoxemia is most
o Currant jelly sputum: Klebsiella likely due to
as É o Foul smelling sputum: Anaerobes, sometimes from
aspiration from GIT contents
a) Congestive Heart Failure
b) Pneumonia
o Green sputum: Pseudomonas aeruginosa, c) ARDS
Haemophilus influenza d) Emphysema
(D) BLOOD WORK-UP 3) Select from the following the correct sputum
characteristic : organism pairing:
↑ WBC a) Rusty + blood-tinged sputum: Streptococcus
o Leukocytosis can be indicative of infection pneumoniae
b) Foul smelling sputum: Pseudomonas aeruginosa,
● ↑ Erythrocyte sedimentation rate (ESR) Haemophilus influenza
o Sign of non-specific inflammation c) Yellowish sputum: Anaerobes
ammation
o RBC move to the bottom of the test tube at a faster d) Green sputum: Klebsiella
rate because of some condition with increased
4) How do you differentiate the radiologic findings of
fibrinogen production
bronchopneumonia and atypical pneumonia in a
● ↑ C-reactive peptide (CRP) chest x-ray?
o Produced by the liver as an acute phase response a) They are the same hence the need to order a
protein sputum cytology to differentiate the offending
o Sign of inflammation organisms
b) White opacities are only found in bronchopneumonia
● ↓ O2 saturation c) Atypical pneumonia’s reticulonodular pattern is more
o Hard time breathing and to saturate the hemoglobin concentrated on the perihilar region
with inside the RBCs d) Bronchopneumonia’s reticulonodular pattern is
unilateral in presentation
● Serum cold agglutinins
o Not routinely done 5) What other ancillary test can you order for a
o RBCs can be attacked by antibodies  clumping / confirmed pneumonia patient presenting with bullous
“agglutinate” at cold temperatures myringitis?
a) Erythrocyte sedimentation rate
o Mycoplasma ↑ agglutination of RBCs at cold
b) CRP
temperatures c) Serum cold agglutinins test
 Presents with d) Electrolyte panel
• Bullous myringitis
• Pharyngitis CHECK YOUR ANSWERS

● ↑ LFTs + Hyponatremia + Urinalysis with Legionella IV) REFRENCES

antigens ● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
o Present in pneumonia caused by Legionella Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth
Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical; 2018
 Recall: other symptoms from this are GIT upset, ● Le T. First Aid for the USMLE Step 1 2020. 30th anniversary
nausea, vomiting, diarrhea edition: McGraw Hill; 2020. Williams DA. Pance Prep Pearls.
● Middletown, DE: Kindle Direct Publishing Platform; 2020.
● IgG & IgM titer ● Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
o For pneumonia caused by Chlamydia Pearson; 2020. Boron WF, Boulpaep EL. Medical Physiology.;
2017.
II) APPENDIX ● Papadakis MA, McPhee SJ, Rabow MW. Current Medical
Diagnosis &amp; Treatment 2018. New York: McGraw-Hill
Education; 2017.
Table 1. Abbreviations. ● Sabatine MS. Pocket Medicine: the Massachusetts General
Hospital Handbook of Internal Medicine. Philadelphia: Wolters
LFT Liver function test Kluwer; 2020.
LLL Left lower lobe of the lung
LUL Left upper lobe of the lung
RML Right middle lobe of the lung
RR Respiratory rate

PNEUMONIA | CLINICAL FEATURES RESPIRATORY PATHOLOGY: Note #5. 3 of 3

 Last edited: 9/11/2021

1. PNEUMONIA
Pneumonia | Treatment and Prevention Medical Editor: Maxine Abigale R. Bunao

OUTLINE

I) MAIN HEADING IN
II) CONTENT FORMATTING
III) APPENDIX
IV) REVIEW QUESTIONS
V) REFRENCES

I) COMMUNITY ACQUIRED PNEUMONIA MANAGEMENT

● Duration of therapy:
o At least 5 days
o Have to be afebrile for at least 48-72 hours
o <1 symptom of clinical instability based on CURB 65 score
● If duration of therapy is not completed, pathogen might not be eliminated
o May need to change up the antibiotic

(A) ANTIBIOTICS
RECALL: 2nd
Table 1. MOA. (2) Outpatient setting: CAP + Underlying comorbidities
+ Recent antibiotic therapy (past 90 days)
Drug Group MOA
Inhibit bacterial cell wall formation Underlying comorbidities:
by binding to penicillin-binding o COPD
B-lactam proteins (which aid in peptidoglycan o Asthma
cross-linking in both Gram (-) and o Heart failure
Gram (+) bacteria) o Chronic kidney disease
Inhibit B-lactamase enzyme which o Diabetes mellitus
B-lactamase inactivate B-lactam ring found o Cancer
inhibitors commonly in beta-lactam o Immunosuppressive disease or therapy
antimicrobials o Asplenia
Inhibit bacterial cell wall formation  Prevents the body to be able to fight off
Carbapenem by binding to penicillin-binding encapsulated bacteria
proteins • S. pneumoniae
Inhibit bacterial cell wall through ↓ • H. influenza
Cephalosporin synthesis of peptidoglycan layer • Klebsiella
(component) • N. meningitidis
Macrolide Inhibit protein synthesis Table 3. DOC for CAP + Underlying comorbidities + Recent
antibiotic therapy (past 90 days).
Tetracycline
Drug Group Drug of Choices
Inhibit the peptidoglycan-synthesis
Respiratory Levofloxacin >
process of bacteria
Monobactam fluoroquinolone Moxifloxacin
Only activity for gram-negative
Gemifloxacin
bacteria
Macrolide/ Azithromycin/ Doxycycline
Respiratory Inhibit DNA synthesis
Tetracycline + A/B
fluoroquinolone
Penicillin/ B- ↑ dose Amoxicillin / Augmentin (↑
(1) 1st
Outpatient setting: CAP + No comorbidities + No A lactamase coverage for resistant bacteria)
recent antibiotic therapy (past 90 days) inhibitor
Table 2. DOC for CAP + No comorbidities + No recent antibiotic B 3rd Gen. Cephalosporin
therapy (past 90 days).
Drug Group Drug of Choices
Macrolide Azithromycin (broad coverage)
Tetracycline or Doxycycline

PNEUMONIA RESPIRATORY PATHOLOGY: Note #6. 1 of 4

(3) CAP + Serious illness graded with CURB 65 (4) Pseudomonas suspect
Curb 65 score: Table 6. DOC for CAP - Pseudomonas suspect.
o Criteria: Drug Group Drug of Choices
 Confusion Ams sepsis B-lactamase inhibitor – Tazobactam (Zosyn) –
no ↑urea levels in the blood
 Uremia: B-lactam Piperacillin
to
perfusionk idney
+ +
 Respiratory rate
30 4th Gen Cephalosporin Cefepime
 Blood pressure: low diastolic BP sBpao
 >65 years old DB Poo +
Carbapenem (broad
+
Imipenem, Meropenem
o Scoring: spectrum) + A/B/C
 0-1 of these factors  antibiotics + send patient
A Respiratory Levofloxacin/ Ciprofloxacin
home fluoroquinolone
non
 2 of these factors  admit into the icu for
hospital
observation B Aminoglycoside + Gentamicin + Azithromycin
Macrolide
 ≥3 of these factors  admit into the ICU
C Aminoglycoside + Gentamicin +
● CURB 65: Fluoroquinolone Levofloxacin
o 2 of these factors  admit into the hospital for
observation (5) CAP MRSA suspect
Table 4. DOC for CAP + Serious illness graded with 2 factors Table 7. DOC for CAP MRSA suspect.
from CURB 65.
Drug Group Drug of Choices
Drug Group Drug of Choices
Glycopeptide antibiotics Vancomycin
2nd
Respiratory fluoroquinolone Levofloxacin >
Moxifloxacin Oxazolidinone Linezolid OR
Gemifloxacin

1stMacrolide/ A/B
Tetracycline + Azithromycin/ Doxycycline

A Penicillin Ampicillin
rd
B 3 Gen. Cephalosporin Ceftriaxone
● CURB 65:
o ≥3 of these factors  admit into the ICU
Table 5. DOC for DOC for CAP + Serious illness graded with 3
or more factors from CURB 65.
Drug Group Drug of Choices
rd
3 Gen. Cephalosporin + Ceftriaxone/ Cefotaxime
A/B
A Macrolide Azithromycin
B Respiratory
fluoroquinolone
OR Levofloxacin

Penicillin-B-lactamase Ampicillin-Sulbactam
(Unasyn)
A
Macrolide
Azithromycin
B Respiratory Levofloxacin
fluoroquinolone
● Penicillin or B-lactamase allergy:
o Have to be careful in giving other Penicillin or B-
lactam antibiotics (Penicillin, Cephalosporin,
Carbapenems, Monobactam)
o Penicillin allergy 
 cross reactivity with other B-lactams
 3-10% chance of developing reaction to
cephalosporin
 1% chance of developing reaction to carbapenems
 <1% chance of developing reaction to
monobactam
 Give a broad-spectrum antibiotic Monobactam
(Aztreonam) instead

2 of 4 RESPIRATORY PATHOLOGY: Note #6. PNEUMONIA

 II) HOSPITAL ACQUIRED PNEUMONIA MANAGEMENT III) GENERAL MANAGEMENT

(1) General considerations (1) General considerations

Criteria MRSA
o >2 days stay in the hospital RECALL:
● Antibiotic therapy: MRSA or Methicillin-resistant Staphylococcus aureus has
o Minimum of 7 days antibiotic therapy beta-lactamases that break down a lot of different types of
o Pseudomonas: minimum of 14 days antibiotic therapy penicillin antibiotics or beta-lactams.
o Signs of clinical improvement in the first 2-3 days  Patients susceptible to MRSA (↑risk):
can change regimen o Recently admitted to the hospital
o Recent antibiotic therapy
(2) HAP Early Onset o History of colonization OR infections
Table 8. DOC for HAP Early Onset. o Healthcare device invasively presented into the body
Drug Group Drug of Choices
Aminoglycoside + Gentamicin + Azithromycin ● Considerations for shifting IV therapy  PO therapy
Macrolide o Hemodynamically stable patient
Respiratory Levofloxacin o Signs of clinical improvement
fluoroquinolone o Able to tolerate oral medications or food
Carbapenem Ertapenem: weaker ones but ● CURB 65
good for early onset HAP o Confusion, Uremia, ↑ RR, ↓ diastolic BP, >65 years old
Penicillin-B-lactamase Ampicillin-Sulbactam
(2) Other medications
(Unasyn)
Analgesics
Duration of stay:
o Lessen the pain
o >2 days BUT <5 days OR
o No MDR pathogen Antitussives or cough suppressants
o Prevent pain from coughing
(3) HAP Late Onset
Table 9. DOC for HAP Late Onset. IV) PREVENTION AND COMPLICATIONS
Drug Group Drug of Choices
(A) PREVENTION
Aminoglycoside OR
Respiratory fluoroquinolone Levofloxacin (1) Pneumococcal Polysaccharide Vaccine (PPSV23)
A B-lactamase inhibitor – Tazobactam (Zosyn) – PPSV23
B-lactam Piperacillin
o 23 stands for the 23 polysaccharide antigens present
B Carbapenem NOT Ertapenem on streptococcal pneumonia bacteria
Choices: Imipenem, o Importance of antigens:
Doripenem,  Account for 85-90% of the invasive S. pneumonia species
Meropenem
Indications:
C 3rd Gen Cephalosporin Ceftazidime
4th Gen Cephalosporin Cefepime o ≥65 years old
o 2-64 years old + immunocompromised state:
Duration of stay:  HIV
o <5 days OR  DM
o With MDR pathogen  Malignancy
Resistant pathogens  hemolytic disorder like sickle cell disease
o Pseudomonas aeruginosa o 19 years old + history of asthma / smoking
o MRSA If administered first before PCV13  wait at least a year
o Enterobacteria before giving PCV13
o Actinobacteria
(2) Pneumococcal Conjugate Vaccine (PCV13)
(4) HAP Pseudomonas positive
PCV13
Table 10. DOC for HAP Pseudomonas positive. o 13 stands for the 13 polysaccharide antigens present
Drug Group Drug of Choices on streptococcal pneumonia bacteria
B-lactamase inhibitor – Tazobactam (Zosyn) – o Important: All of these antigens are the same as
B-lactam Piperacillin the 23 EXCEPT 1
+ +
Respiratory fluoroquinolone/ Levofloxacin/ Indications
Aminoglycoside/ Gentamicin/ o <2 years old: administer during 2, 4, 6, 12-15 months old
Monobactam/ Aztreonam/ Administer first  8 weeks later administer PPSV23
Carbapenem (broad spectrum) Meropenem
Carbapenem (broad spectrum) Imipenem, Meropenem (A) COMPLICATIONS
+ + Septic shock: Extremely dangerous and fatal
Respiratory fluoroquinolone/ Levofloxacin/ Pleural Effusion:
Monobactam Aztreonam o As pneumonia progresses and chronic, this develops
o Can be deadly
(5) HAP MRSA suspect
Table 11. DOC for HAP MRSA suspect. Meningitis
Drug Group Drug of Choices Abscesses
Hypoxia  problems arise from:
Glycopeptide antibiotics Vancomycin o Shortness of breath
Oxazolidinone Linezolid o Improper ventilation
o Improper perfusion

PNEUMONIA RESPIRATORY PATHOLOGY: Note #6. 3 of 4

 V) APPENDIX

Table 12. Abbreviations.

CAP Community acquired pneumonia
DOC Drug of choice
HAP Hospital acquired pneumonia
MOA Mechanism of action

VI) REVIEW QUESTIONS VII) REFRENCES

● Bui, T., & Preuss, C. V. (2020). Cephalosporins. StatPearls
1) Patient Niko, 66/M, with known Type 2 DM diabetes, [Internet].
presented to the emergency room with low diastolic ● Bush, K., & Bradford, P. A. (2016). β-Lactams and β-Lactamase
BP and confusion. Past medical history revealed that Inhibitors: An Overview. Cold Spring Harbor perspectives in
medicine, 6(8), a025247.
she was recently diagnosed with left lower lung [Link]
pneumonia. Temperate = 41 degrees Celsius, RR=32, ● Butler, M. S., Hansford, K. A., Blaskovich, M. A., Halai, R., &
BP=100/70, HR=130/min. Laboratory results showed Cooper, M. A. (2014). Glycopeptide antibiotics: back to the future.
The Journal of Antibiotics, 67(9), 631-644.
random blood sugar of 320 mg/dL. What is the ● Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL,
appropriate management? Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth
a) Admit into the hospital and administer Ceftriaxone + Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical; 2018
● Khanna, N. R., & Gerriets, V. (2021). Beta Lactamase Inhibitors.
Levofloxacin / Azithromycin StatPearls [Internet].
b) Admit into the ICU and administer Ceftriaxone + ● Le T. First Aid for the USMLE Step 1 2020. 30th anniversary
Levofloxacin / Azithromycin edition: McGraw Hill; 2020. Williams DA. Pance Prep Pearls.
c) Admit into the ICU and administer Levofloxacin only ● Middletown, DE: Kindle Direct Publishing Platform; 2020.
● Marieb EN, Hoehn K. Anatomy & Physiology. Hoboken, NJ:
d) B & C Pearson; 2020. Boron WF, Boulpaep EL. Medical Physiology.;
2017.
2) After undergoing the regimen selected above for 7 ● Pandey, N., & Cascella, M. (2020). Beta lactam antibiotics.
days, patient Niko showed no signs of clinical StatPearls [Internet].
improvement. When further probed, the patient ● Papadakis MA, McPhee SJ, Rabow MW. Current Medical
Diagnosis &amp; Treatment 2018. New York: McGraw-Hill
revealed multiple trips to the hospital due to his
Education; 2017.
pneumonia and was prescribed with antibiotics of ● Sabatine MS. Pocket Medicine: the Massachusetts General
unrecalled drug class, name, and frequency. What Hospital Handbook of Internal Medicine. Philadelphia: Wolters
resistant pathogen should you consider? Kluwer; 2020.
a) MRSA
b) Pseudomonas aeruginosa
c) Enterobacter
d) All of the above
3) 38 y/o laborer develops cough and a fever. One week
earlier, history revealed he was stabbed on the left
chest that was managed with wound sutures and Co-
Amoxiclav. He is currently in distress, highly febrile,
hypotensive with CXR results showing left lower lung
consolidation/lucencies. You are considering CAP
and suspecting pseudomonas as the inciting
pathogen. What is your management?
a) Tazobactam – Piperacillin + Cefepime + Imipenem +
Ampicillin-Sulbactam
b) Tazobactam – Piperacillin + Cefepime + Imipenem +
Gentamicin
c) Tazobactam – Piperacillin + Cefepime + Imipenem +
Azithromycin
d) Tazobactam – Piperacillin + Cefepime + Imipenem +
Levofloxacin
4) Who should be given a PPSV23 vaccination?
a) 60/M with known HIV
b) 19/F with asplenia
c) 40/M with a 10-pack year smoking history
d) All of the above
5) What complications should you look out for a patient
with pneumonia?
a) Pneumothorax
b) Pleural effusion
c) Septic shock
d) A & C
e) B & C

CHECK YOUR ANSWERS

4 of 4 RESPIRATORY PATHOLOGY: Note #6. PNEUMONIA