Quiz Yourself - Respiratory. The FEV 1 is reduced when: airway obstruction is present as with these diseases: Asthma Emphysema FEV 1 /FVC ratio is reduced when airway obstruction is present. The normal ratio is: 70-75 The FVC is reduced with restrictive lung disease
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What does each of these represent?
What is the standard version (room air/temp)?
Key pt: regions with a high V/Q ratio cannot compensate for regions with a low V/Q ratio b/c the high V/Q is normal!
What’s this? them?
Dilated bronchi them?
Muco-Purulent Debris in Dilated Bronchi
What disease is this?
Charcot-Leyden crystals – eosinophil granule contents
This is ASTHMA!!!!
Curschmann Spirals – mucus casts
Centrilobular them?Emphysema in COPD
Intrinsic Asthma them?-
No allergic or (personal family) history
Usually adult onset
Often follows severe respiratory illness
Symptoms usually perennial
More refractory to treatment, become other diseases, progress to vasculitis
Eosinophils still impt
Strong family history of allergies
Usually onset at a young age
Other allergic manifestations in patients
History of specific allergic association triggers (e.g. pollen, animal dander)
Correlation with skin and inhalation responses to specific antigens
Type I hypersensitivity rxn
IgE mast cell and eosinophilsClassification of Asthma
Increase lung volumes (TLC, FRC, RV)
Decreased peak flow, FVC, FEV1, FEV1/FVC
Increased - useful in establishing dx
Reversible airflow obstruction when treated; albuterol
Increased in blood and found in sputum
Low PO2, low PCO2
2 second line pharamcotherapies for smoking:
Peribronchovascular space smoking?
Coal dust macules smoking?
Patchy Sub-Pleural Fibrosis smoking?
Fibrotic Nodules smoking?
Fibroblasts in the interstitium smoking?
Proliferative phase DAD
Identify which is interstitial lung disease, obesity,
and inspiratory & expiratory muscle weakness.
A. Pleural Disease
1. Pleural Effusion
2. Diffuse Pleural Thickening
3. Localized Pleural Thickening (Plaques)
B. Diffuse Pulmonary Fibrosis (asbestosis)
A. Malignant Mesothelioma
- bad stuff
- cigarette smoking is NOT related
- latency is 30-40 years
B. Bronchogenic Carcinoma
C. Possibly Laryngeal Carcinoma
One of these things is not like the others.
One of these things just doesn’t belong…
Small cell is treated differently and has a much more severe progression!
Squamous Cell Carcinoma
Mucin production (red on PASd stain)
- Note the mucin in the alveoli. Gas exchange is gonna suck in this patient!
Response to therapy
Small Cell Carcinoma
Loss of C-P Angle
= Pleural effusion or mass
Normal thickness pleura
Thin delicate microvilli
Associated w/ ferruginous bodies
IIIA, IIIB = locally advanced
IIIB, IV = advanced, effusion
Got Your Sound On? here…
Is it close to midnight?
And that exam is lurking in the morn
Neutrophils filling alveolar space in acute pneumonia likely disease process
Interstitial likely disease process lymphocytes in viral pneumonia
Giant Celll likely disease process
Histiocytes and multinucleated giant cells (granulomatous inflammation)
in mycobacterial pneumonia
What does this it? Sxs? Pathology?
Center of pulmonary abscess showing acute
inflammation with destruction of
Normal pulmonary architecture (no alveolar walls)
Alcoholics on the right
lung b/c that’s where
Who’s likely to get it and where?
necrotizing granulomatous inflammation it? Sxs? Pathology?
Peripheral focus of granulomatous
Inflammation (Ghon focus)
In hilar lymph node
Beaded look to the bact
Initial tuberculous infection: Ghon complex
(Ghon focus + involved hilar nodes)
Cryptococcus: mucicarmine positive capsule
Cryptococcus on GMS stain showing narrow based budding
Blastomycosis: Large yeast with broad based budding
Aspergilloma (fungus ball) within pre-existing cavity
Aspergillus: septate hyphae with 45 degree branching tissue lined
Aspergillus within tissue lined
blood vessel wall
Mucomycosis tissue lined
Pneumocystis on GMS stain: cup shaped organisms within alveolar spaces
Cytomegalovirus pneumonia inclusions
Viral inclusion inclusions
Herpes virus on cytology specimen
Mycoplasm pneumonia: sparse lymphocytic interstitial inflammation
Typical Pneumonia inflammation
High fever, rigors (shaking chills), chest pain, purulent sputum
Consolidation, rales on exam
Airspace filling/lobar infiltrate on CXR with air bronchograms
Meant to describe: S. pneumo, S. aureus, GN bacilli like Klebsiella
Indolent onset (7-10days)
Less ill appearing
Low-grade fever, malaise, headache, dry cough
Rales without consolidation
Mild/no leukocytosis; negative cultures
Patchy/interstitial infiltrates on CXR
Meant to describe: Mycoplasma, or ChlamydiaTypical vs Atypical Pneumonia
NOT HIGHLY PREDICTIVE OF SPECIFIC PATHOGENS!!!
(yes I know I’m a dork, but you’re laughing – admit it.
And I have to entertain myself SOMEHOW!)
This is a sputum sample and it tells us? patient has pneumonia, do you even care what the causative microbe is?
That it was probably an incompetent med student who this specimen, b/c it SUCKS. Look at all the squamous epithelial cells and where are the inflammatory cells?!?!?
So after you fix that previous person’s mistake, you see this. What are you thinking?
Besides thinking “damn, I’m good”
you should be thinking STREP!!!
Pathogens ~ Modifying Risk Factors You’ll assess the severity looking at what? And
No underlying. disease or modifying factors
Underlying comorbidities or modifying factors (COPD, CHF, alcoholism,…)
Inpatients not needing ICU care
Severe pneumonia requiring ICU care
Low risk for pseudomonas
Risk for pseudomonas
“Irreversible dilation of airways caused by inflammatory destruction of airway walls”
What is suggestive history of bronchiectasis?
How do we diagnose bronchiectasis?
HRCT – procedure of choice to demonstrate presence, location, and extent of disease
What is the Cascade to Lung Disease in CF? specific immune deficit?
CFTR Gene Mutation
Altered Ion Transport
Abnormal airway surface liquid (volume depletion)
Impaired airway defenses (reduced mucociliary clearance)
Chronic airway infection/inflammation
Sodium is reabsorbed WAY too much from the airways. Water follow inwards. This leads to the collapse of mucociliary clearance.
Occluded artery specific immune deficit?
Plexiform lesion specific immune deficit?
Medial and intimal hypertrophy
Necrotizing specific immune deficit?
Elastica disruption = vascular injury
Hemosiderin-laden macrophages = prior hemorrhage
Fibrin-rich “hyaline membranes” increased blood flow through the lungs?
Alveolar filling pattern
with air bronchograms
RBCs filling increased blood flow through the lungs?
Alveolar Hemorrhage Syndrome
Lipid increased blood flow through the lungs?
Aspiration of cooked fat
Foamy increased blood flow through the lungs?
Endogenous (Post-Obstructive) Lipid Pneumonia
Transudate in interstitium and alveolar airspaces increased blood flow through the lungs?
Severe Pulmonary Edema
Indirect Lung Injury
Direct Lung Injury
Nitric Oxide from Vasc. Endothelium
Low Systemic Vascular Resistance
High Cardiac Output Hypotension
Wide pulse pressure ex: (90/30)
Brisk capillary refill
Decreased urine output
Decreased mental status
Lactic Acidosis –
b/c all these tissues are underperfused
Exposure to a Risk Factor
Alveolar Capillary Injury
Epithelial Cell Injury
Leak of Protein Rich Fluid into Interstitium and Alveolus
Arterial hypoxemia refractory to oxygen = SHUNT!
Bilateral patchy infiltrates
VERY Decreased lung compliance (need PEEP)
Rapid onset respiratory failure
2 General Classes of increased blood flow through the lungs?
Hypoxemic - inadequate O2 delivery
Hypercapnic - respiratory acidosis (high PCO2)
secondary to failure to adequately ventilate
Hypoxemic Failure increased blood flow through the lungs?
1. Respiratory drive (e.g., narcotic overdose)
2. Nerve conduction (e.g., cervical cord trauma, Guillain-Barre syndrome)
3. Neuromuscular (e.g., myasthenia gravis, muscle atrophy)
4. Chest wall (e.g., flail chest, kyphoscoliosis)
5. Lung disease (e.g., asthma, COPD)
6. Upper airway obstruction
Arterial blood gases and diagnosis increased blood flow through the lungs?
pH pCO2 HCO3-
7.40 40 24 Normal
7.30 55 26 Acute Failure
7.37 55 31 Compensated Failure
7.25 85 36 Acute and Chronic Failure
Clinical signs of increased blood flow through the lungs?
respiratory muscle weakness
How do you TREAT Hypercapnic Failure? increased blood flow through the lungs?
Gas Exchange Failure
Low Inspired O2
-HCO3 rise by 1 mEq/L for each 10 mmHg PCO2
-HCO3 rise by 4 mEq/L for each 10 mmHg PCO2
If given these Sxs in the history, what diseases Chronic Respiratory Acidosis?
should you be thinking about?
If given these diagnostic results, Chronic Respiratory Acidosis?
what diseases should you be thinking about?
What are these diagnostic tests useful for Chronic Respiratory Acidosis?
in making diagnoses?
Good luck on the exam