Pseudostratified columnar epithelium
Mucociliary elevator: Ciliated columnar cells (move particular matter upward and out of respiratory tract) & goblet cells (secrete mucus)
• Basal cells (found in the bottom can give rise to columnar cells or...

neuroendocrine cells

capillaries
and connective tissue (interstitial cells; basement membrane),
lined by Type I (98%; functions for gas diffusion)
and Type II cells (secretes surfactant that reduces surface tension and replace type 1 cells

)

Left: centriacinar or centrolobular emphysema

(Distal alveoli are spared until severe; more severe in the upper lobes; associated with heavy smokers)

Right: panacinar or panlobular emphysema

(Associated with alpha-1 antitrypsin deficiency.
• Most severe at the bases and anterior margins ofthe lung.
• First causes enlargement of the alveolar duct andalveolus.
• Later affects the respiratory bronchiole)

Physiological parameters

Patient #1: decresed TLC & RV; reduced VC; decreased the FEV1 , FVC & normal or increased FEV1/FVC ratio

Patient #2: increased TLC & RV; reduced VC; decreased  FEV1/FVC ratio

Patient 1 has restrictive lung disease

Patient 2 has obstructive lung disease

Left: centriacinar or centrolobular emphysema

Center: normal lung

Right: panacinar or panlobular emphysema

A: centriacinar emphysema

B: panacinar emphysema

C: normal

D: distal acinar emphysema

E: irregular emphysema

Distal acinar emphysema; dangerous sequelae?

Answer: bullae formation that pop --> pneumothorax

Which genotype/phenotype is mostly associated with alpha-1 antitrypsin deficiency?

Normally the enzyme (a-1 antitrypsin) performs what function?

pi-zz / Pi-ZZ;

alpha-1 antitrypsin inhibits proteolytic enzymes (trypsin, chymotrypsin, elastase) which are released by neutrophils; in other words, without a-1 antitrypsin, neutrophils cause damage in the lungs esp in the lower lobes where perfusion is more (thus more neutrophils)

hyperexpansion

- after surgery is called?

- due to tumors, foreign bodies & congenital defects

- fractured ribs,chest wounds, severe coughing with bronchial obstruction, artificial ventilation (on ventilators)

Compensatory hyperinflation
Obstructive overinflation

Interstitial emphysema

Left:  chronic bronchitis; submucosal gland hypertrophy (lecture) & hyperplasia (Robbins) aka thickened mucus gland layer

Right: normal lung

Bullous emphysema;

danger: can lead to pneumothorax if bulla pop

Chronic Bronchitis:

increased number of mucus gland cells (many clear spaces - maybe goblet cells too)

thicker basement membrane & smooth muscle cell layer

squamous metaplasia over the BM thickening

chronic inflammatory infiltrate

(neutrophils & macrophages)

Chronic Bronchitis or asthma:

mucus plug (so much & thick --> obstruction)

explains the sputum production with persistent cough (at least 3 months in 2 consecutive years, not caused by tuberculosis or cancer)

Distinguish between bronchitis & emphysema by:

What is a physiological feature of chronic bronchiOLITIS?

What are some dangerous sequela associated with chronic bronchiolitis?

• Ventilation/perfusion mismatch with
arterial oxygen desaturation.

• Results in pulmonary arterial vasospasm
pulmonary hypertension, cor pulmonale

(Small airways disease - affects the bronchioles
• Usu. associated with chronic bronchitis.
• Tobacco smoke and dusts

chlamydia pneumoniae)

A 10-yr old girl is brought into the ER in acute respiratory distress.  The patient is allergic to cats & pollen. Her mom states that she has a recent URI. She also complains of a hx of moderate intermittent dyspnea that is exacerbated by exercise.  VS: no fever; RR 32, BP normal, PE inspiratory & expiratory wheezes; hyperresonant to percussion; enlarged chest AP diameter. CBC eosinophilia (13%); PFT: low FEV1/FVC; CXR: hyperinflation with flattened diaphragm;

gross pathology: hyperinflation with air trapping in alveoli; inspissated mucus plugs; edema of mucosal lining; micro pathology: Charcot-Leyden crystals;  curschmann's spirals (plugging of airways with thickened mucus)

bronchial (extrinsic/atopic) asthma

DD:

bronchiolitis

a1-antitrypsin syndrome

churg-strauss syndrome

foreign body aspiration

GERD

chf (cardiac asthma)

allergic bronchopulmonary aspergillosis

tx according to severity (4 levels):

bronchodilators, steroids & O2

(mast cell stabilizers - cromolyn; leukotriene inhibitors - zafirlukast)

extrinsic or atopic

most common in children

type I hypersensitivity

instrinsic asthmas are triggered most commonly by what?

other less common triggers?

Viral respiratory infections, most common
trigger.

• other triggers: Exercise, cold air, drugs (aspirin,tartrazine dye, bronchodilators??), inhaled irritants or air pollution.

• Usually no allergic or asthma family hx.
• Initiated by non-immune mechanisms that still leads to smooth m contraction, vasodilations & leaks; edema?, activation of eosinophils; mucous secretions

more on aspirin: cox-1&2 inhibitor blocks the production of prostaglandins and leads to excess leukotriene production (LTB4 - strong chemoattractant for neutrophils;  LTB1-3 causes bronchoconstriction, mucus hypersecretion, eosinophil chemotaxis, increase vascular permeability)[image][image][image][image][image][image][image][image]

What is a dangerous sequelae of asthma that can result in death within days?

How do you treat?

status asthmaticus:

serious attack that lasts for days/weeks

tx:

Beta agonists,
methylxanthines,
corticosteroids

Permanent dilation (fusiform/saccular) of
bronchi due to destruction of muscle and elastic tissue
that is due to infection alone or obstruction that can lead to infection

what clinical features of the disease?

Bronchiectasis

signs & symptoms:

Severe persistent cough; Paroxysmal AM cough
• Foul copious sputum (thick mucus plug)
• Bronchopneumonia
• Life threatening hemoptysis (bronchial walls run next to blood vessels; damage can spread to blood vessel)

Prefers lower lobes, especially vertical airways.
• seen in patients with cystic fibrosis (obstruction due to Cl- transport defect:: cftr transporter & thick mucus) and primary ciliary dyskinesia (absent or shortened dynein arms lead to nonfunctioning cilia;

50% get Kartagener syndrome:

bronchiectasis, sinusitis, situs inversus (organs flipped), male infertility)

bronchiectasis

destruction of bronchial wall --> permanent dilation, air space extends to pleural space

cystic fibrosis:

bronchial mucus obstruction

can lead to infection, bronchiectasis, & bronchiolitis obliterans

Name the mold in asthma & cystic fibrosis patients that can lead to bronchiectasis

what are other microbes that can lead to bronchiectasis?

aspergillus fumigatus

TB, Staph aureus, H. flu, Pseudomonas,

adenovirus, flu virus

Neutrophil/ complement defects/ humoral defects leads to infections by pyogenic bacteria.

•
Cell mediated immune defects (T cell deficiencies) lead to infections with mycobacteria, herpes viruses, and organisms with low virulence (pneumocystis carinii).

Aspiration of gastric contents (inadequate cough reflex)
•
Injury to the respiratory mucosal cilia (smoking).
•
Injury to the alveolar macrophages’
phagocytic/bacteriocidal activity (smoking, anoxia).
•
Pulmonary edema from CHF
•
cystic fibrosis or bronchial obstruction --> thick mucus secretions; impaired mucociliary elevator

Streptococcus pneumoniae(most common)

Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus
Legionella pneumophila
Klebsiella pneumoniae
Pseudomonas species

Stages of bacterial pneumonia.

A, Acute pneumonia. The congested septal capillaries and extensive neutrophil exudation into alveoli corresponds to early red hepatization. Fibrin nets have not yet formed.

B, Early organization of intra-alveolar exudate, seen in areas to be streaming through the pores of Kohn (arrow). C, Advanced organizing pneumonia featuring transformation of exudates to fibromyxoid masses richly infiltrated by macrophages and fibroblasts.

1. Congestion-vascular engorgement, leaky capillaries with intra-alveolar fluid and bacteria.

2. Red Hepatization -massive exudate of red cells, neutrophils, and fibrin in the alveolar spaces (grossly like liver).

3. Grey Hepatization -red cells in the alveolar space lyse, but neutrophils and fibrin persist.

4. Resolution or Fibrosis

Lobar pneumonia -

gross: lower lobe pneumonia

CXR: entire right upper lobe radio-opaque ("white out");

no outline of rib over involved lobe

bronchopneumonia:

gross: diffuse patches

CXR -

white, diffuse patches; outline of ribs distinct

Bacterial pneumonia:

cells (bacteria; neutrophils and inflammatory cells) in alveolar space

Viral pneumonia:

interstitial pneumonitis - diffuse alveolar wall damage

no cells in alveolar space but proteinaceous exudate - yes

What principle explains why there's a new flu vaccine each year?

What principle explains the H1N1 (swine flu) pandemic?

antigenic drift

antigenic shift

mneumonic: shift is shit, more severe presentation than drift (thank you Christin Barry)

Mainly pregnant women & children <5 years old

others:

>65 years old

asthmatics

diabetics

immunocompromised patients

sickle cell patients

Corona virus causes what aggressive disease?

what is the reservoir?

How is it spread?

SARS

masked palm civit

respiratory secretions & stool

pandemic: airborne (human --> human)

What is COPD?

What must be present in order to use it as a diagnosis?

It's an umbrella clinical term for disease that leads to airway obstruction, which is defined as FEV1/FVC ≤ 70% and
- FEV1 <80% of predicted (may be ≥80% in mild COPD)

Spirometry must indicate obstruction

Pneumonia caused by fungi are determined by where the patient geographically came from or have traveled to. 

What are 3 opportunistic fungal infections that can cause pneumonia? 

What diseases are they associated with, if applicable?

Pneumocystis jiroveci or formerly carinii

Aspergillus - (fungus ball with TB; acute angle branching & true septa)

Candida (pseudohyphae)

Cryptococcus neoformans

mucormycoces/zygomycetes (diabetes, metabolic acidosis, organ transplantation, chronic steroid use, leukemia/lymphoma, tx with desferoxamine & AIDS; broad angle branching; unilateral eye lacrimation & nasal stuffiness in diabetes patients)

How do you treat fungal infections?

what med specifically to tx cryptococcus infx?

what other broad spectrum antifungal?

Amphotericin B ("ampho-terrible": headache, chills, fever immediately - almost all pts, renal toxicity late 80% of pts, phlebitis - hypochromic normocytic anemia 27% of pts)

Nystatin (more toxic than amphotericin, used topically)

Flucytosine (co-admin. w/ amphotericin to tx cryptococcus; granulocytopenia, thrombocytopenia, decreased bone marrow formation, contraindicated for pregnancy)

-azoles:

fluconazole (oral or IV; enters CSF - crosses BBB; GI distress; in HIV pts: Stevens Johnson syndrome, eosinophilia, thrombocytopenia, hepatic fxn changes)

itraconazole (crosses placenta - teratogenic, GI distress

voriconazole)

voriconazole (high bioavailability; visual disturbances)

A) normal bronchiole

B) uninjured bronchiole with mucus plug

C) COPD bronchiolitis with luminal exudate

D) COPD bronchiolitis with surrounding fibrosis

CT scan to visualize vascular deficiency pattern, bullae

(CXR not good enough)

What is the most likely cause of COPD?

This occurs in 80-90% of COPD pts.

Not all smokers develop COPD. What does this elucidate?

tobacco smoking

Other causes:

noxious inhalants - pdts of biomass combustion

(poor & developing countries)

chronic asthma

childhood infections, air pollution, malnutrition, HIV

Only ~20% of smokers develop COPD.  This points to individual genetic susceptibility (e.g. a1 antitrypsin deficiency - normal repair mechanisms impaired)

LRT damage - impaired mucociliary clearance due to hypersecretions: risk of infections (H. influenzae, strep pneumo, Moraxella; severe COPD: H. parapinflu, pseudomonas aeruginosa, staph aureus)

- increased IgA & IgG suggests new infection

hypoxemia (V/Q mismatch) --> Pulmonary hypertension --> cor pulmonale (right heart failure) --> edema --> death

hypercabnia (too much CO2 in blood) when FEV1 drops to 1-1.5L

exertional dyspnea --> inactivity --> exacerbation --> health deteriorates --> death

Sys effx:

Nutritional abnormalities, weight loss: - ↑ metabolic rate, inflammation, drugs

• Skeletal muscle dysfunction: ↓ muscle mass, deconditioning, changes in ultrastructure

• Cardiovascular effects: CV disease is increased 2-3 fold (after adjustment for traditional risk factors)
- systemic inflammation? other interactions?

• Other possible extrapulmonary effects:
- Nervous system: depression, peripheral neuropathy, autonomic dysfunction?
- Hematologic: mild anemia
- Bone: osteoporosis

How do you manage COPD?

Pls check Hill's lecture for more details

Smoking cessation

Flu vaccine

Bronchodilators

steroids

Non-med therapy:

exercise training (lack of exercise b/c of exertional dyspnea)

nutrition

psychosocial support

Squamous cell carcinoma is mostly associated with what?

what electrolyte abnormality is it associated with?

site of tumor?

smoking

hypercalcemia (PTH hypersecretion)

central / hilar

small cell (oat cell) carcinoma starts with what cell?

what electrolyte imbalance?

site of tumor?

pleuripotent bronchial precursor cell (normally defense)

Low Na, K (not Ca) but still concentrating urine because of ACTH & ADH hypersecretion

associated with Cushing's syndrome

central (hilar)

many pts with small cell carcinoma are smokers

carcinoid tumor: the syndrome is characterized by what symptoms?  pathogenesis? location?

precursor cell?

gross?

histology?

immunohistochemistry?

carcinoid syndrome:

diarrhea, flushing, wheezing

(oversecretion of serotonin - muscarinic agonist)

may arise centrally or may be peripheral

Kulchitsky cell

 gross: central tumors grow as finger-like or spherical polypoid masses that commonly project into the lumen of the bronchus and are usually covered by an intact mucosa. They rarely exceed 3 to 4 cm in diameter. Most are confined to the main stem bronchi. Others, however, produce little intraluminal mass but instead penetrate the bronchial wall to fan out in the peribronchial tissue, producing the so-called collar-button lesion. Peripheral tumors are solid and nodular. Spread to local lymph nodes at the time of resection is more likely with atypical carcinoid.

Asbestosis

which forms are toxic? which form is still in use today (post '72)?

associated with what malignant lung tumor?

serpentine fibers(chrysotile) - longer - and amphibole fibers(crocidolite, amosite, and anthophylite).
•
Toxicity is linked to amphibole fiber type, (shorter, smaller aerodynamic diameter - look like short nails) and avoid the upper airways defense mechanism and enter lower airways.
•
Over ten years of exposure is required before asbestosis becomes evident.

CXR and CT scans: calcific plaques are found in the lower lobes and (peripheral) pleural surfaces.
•
A restrictive ventilatory defectis usually seen. Obstruction is also seen but this may relate to the patients smoking history.
•
 diminished DLCO- more sensitive test for detecting early asbestosis and occurs before x-ray changes or a change in lung volumes.

Mesothelioma:

site - pleura

psamoma bodies (concentric rings of calcification) - malignant

ferrugous bodies (Iron) (first aid) - benign?

adenocarcinoma:

what site?

histological finding?

peripheral (e.g. upper lobe)

fibrosis (chronic infection or inflammation)

What are the NORMAL VALUES?
PA systolic pressure?
PA diastolic pressure?
Mean PA pressure?

PC wedge pressure?

Extra credit?

Pulm. Vascular resist

NORMAL VALUES
PA systolic pressure 15-30 mm Hg
PA diastolic pressure 4-12
Mean PA pressure 9-16

PC wedge pressure 2-12

Pulm. Vascular resist.:

150-200 dyne sec cm -5

How is Pulmonary hypertension defined?

How is it determined?

Pulmonary hypertension is defined by
mean PA pressure:
a) >25 mm Hg at rest
or
b) >30 mm Hg with exercise

PA pressure is measured by right heart catheterization.

PH will result from either (notes p. )
a) hypoxic vasoconstriction from COPD**  or decreased area of pulmonary vascular bed from vasculitis, extrinsic compression of large vessels, panlobular emphysema --> increased PVR,

**the development of pulmonary htn is an ominous sign: 5 yr survival for these pts <10% compared with COPD pts w/o pul htn

or
b) mitral valve diseases --> pressure overload --> increased CO, or

c) L to R shunt (ASD, VSD) --> volume overload --> increased CO
d) left heart disease --> increased PCWP, or
e) combination of a,b, and c

what are simple vs toxic asphyxiating gases? Name some.

irritant gases? which irritant is potentially more dangerous? why?

fumes?

Gasses generally exert their effect by displacing oxygen in the alveoli.
–
Simple Asphyxiating gases: CO2, CH4

Toxic Asphyxiating gases: CO, cyanide, H2S.

(poisoning & entry into circulation & cells --> irreversible damage --> kill)
–

Irritants react with water in the mucus membranes and cause irritation of the nose and eyes, vocal cord dysfunction, dyspnea, cough and wheeze:

ammonia (highly soluble; URT closure above vocal cords, immediate response), chlorine (less soluble - drops down into the lower resp tract --> big problem; min - hours), nitric oxide.
–
Fumes: products of combustion with complex composition. Example: volatile organic products (VOP) or hydrocarbons generated by fire.

a compatible hx

physical exam and

*elevated carboxyhemoglobin level:

carboxy-hemoglobin up to 15 % can be seen in active cigarette smokers. (no symptoms) if there are symptoms is due to some other cause like cyanide poisoning

>25% Sx:
carboxy-hemoglobin ~ 30% altered mental status.
–
carboxy-hemoglobin ~ 45 % coma
–
carboxy-hemoglobin > 50% death

What diseases leads to increased PVR (and if it progresses later pulmonary htn)?

directly

indirectly (lung disease)

Increased PVR
Diseases Directly Involving the Pulmonary Vasculature

 primary pulmonary HTN
 thromboembolic disease
 pulmonary vasculitis
 toxin-induced vascular disease
 congenital heart disease
 chronic portal HTN
 high altitude-induced hypoxia
Sickle-cell disease

Parenchymal Lung Disease
 chronic obstructive lung disease
 cystic fibrosis
 infiltrative or granulomatous diseases
* sarcoidosis
* idiopathic pulmonary fibrosis
* connective tissue diseases
* pneumoconiosis
* radiation pneumonitis

Hypoventilation Syndromes
 kyphoscoliosis
 sleep apnea syndromes
 idiopathic hypoventilation
 pleural fibrosis
 neuromuscular disorders

Extrinsic Compression of the Pulmonary Vasculature (decreased area of pulmonary vascular bed)
 mediastinal tumors
 aneurysms
 granulomatous adenopathy
 mediastinal fibrosis

Increased PCWP (L heart disease)

 Left ventricular systolic dysfunction
 Left ventricular diastolic dysfunction
 MV stenosis
 Severe MV insufficiency
 Constrictive pericarditis
 Pulmonary veno-occlusive disease

Increased RV cardiac output

Atrial septal defect
Ventricular septal defect
Large peripheral shunts
AV malformations
Artificial shunts
Hyperthyroidism

What are the symptoms of pulmonary htn?

signs?

SYMPTOMS
 exertional dyspnea
 fatigue
 chest pain
 syncope
angina
 leg swelling & increasing abdominal girth
 hoarseness of voice (Ortner’s syndrome)

signs

PHYSICAL EXAMINATION:
 Jugular vein distention.
Prominent right ventricular impulse along the parasternal border.
Elevated pulmonic component of the second heart sound.
Tricuspid valve insufficiency.
Fixed splitting of the second heart sound.
Hepatosplenomegaly, ascites, or edema.

Chest-x-ray
dilatation of the pulmonary arteries
obliteration of retrosternal space
secondary to right ventricular hypertrophy
possible parenchymal lung disease (fibrosis, COPD)

ECG
* right axis deviation
* tall R wave in V1
* large S waves in V5 & V6
* peaked P waves in leads I & II
* inverted T waves and ST depression in V1 to V3 consistent with right ventricular strain

ECHOCARDIOGRAPHY
* right ventricular dilatation
* paradoxical motion of the inter-ventricular septum
* tricuspid valve insufficiency
* estimation of PA pressure by Doppler

What is the mPAP-PCWP gradient for

pre-capillary pulmonary htn?

post-cap?

Pre-Capillary >10 mm Hg

Post-Capillary 3 – 5 mm Hg

OA is caused by agents found in the work place that are
either irritants and cause the reaction directly, or
sensitizing agents which cause a heightened sensitivity to irritants and other agents

Low-molecular-weight (LMW) chemicals (eg, isocyanates, trimellitic anhydride, formaldehyde) are incomplete antigens (ie, haptens) that combine with a protein to produce a sensitizing neoantigen
•
High-molecular-weight(HMW)organic materials (eg, flour, laboratory animal proteins) are complete sensitizing antigens.

***(see below)

WEA is seen in persons that have preexisting asthma and after exposure to the sensitizer or agent have a heightened reaction.
– This reaction may include reactive airways dysfunction syndrome (RADS)

Both:  cough, chest tightness and wheeze

possible normal spirometry but positive bronchial provocation test
• Symptoms abate when the stimulus is removed.
• A dual response (early within 1 hr and late response within 3-5 hrs) with
symptoms that appear within hours of the
beginning of the work day, abate then recur several hours later.

***OA symptoms may be accompanied or preceded by rhinitis and conjunctivitis

Absence of hyperresponsiveness on methacholine challenge (bronchial provocation test) indicates what?

if positive test?

rule out asthma

if positive, rule in hyperresponsiveness & asthma

Methacholine Challenge test (from occupational & env lung disease)
A test used to detect occult airway disease and establish a diagnosis of hyper-responsiveness.
•
Also known as bronchial provocation.
•
A known concentration of methacholine or histamine is used to produce a 20% decline in the FEV1
•
A dose of less than 8 mg/ml (4 μmol) resulting in the decline of FEV1 by 20% defines hyper-responsiveness.

A form of occupational asthma which occurs
after a single exposure to a high concentrations of irritants.

no delay in sx and dual response; SOB immediately from exposure

• RADS is an asthma-like syndrome distinct in its genesis from typical occupational asthma, and the triggering exposure need not be occupational.

• Clinical presentation may be different in that there is no latent period as with hypersensitivity pneumonitis and a dual response is usually not present as in occupational asthma. Symptoms occur within minutes of the exposure.

positive challenge test finding (signifying hyperactivity) following the exposure.

• There may (or may not) be chronic airflow obstruction confirmed on PFT.
• Other pulmonary disorders are excluded.

Persons with preexisting asthma are more
likely to develop RADS when exposed to
irritants.

silicosis

Chest x-ray show upper lobe opacities which
consolidate over time to become large nodules
progressive massive fibrosis (PMF).
• A classic x-ray pattern seen in silicosis is “egg shell calcification”.
• Silica is toxic to lung macrophages. This can result in susceptibility to infections.
• Pulmonary T.B. is the most important of these infections

-increases risk of getting lung cancer

- associated with autoimmune connective tissue diseases

silicosis

CXR finding?

Chest x-ray show upper lobe opacities which consolidate over time to become large nodules progressive massive fibrosis (PMF); eggshell calcification (depicts silica-macrophage deposits in hilar lymph nodes)
•
Silica is toxic to lung macrophages. This can result in susceptibility to infections, e.g. TB (impt)

also increases risk of lung cancer

associated with autoimmune connective tissue diseases

(e.g. scleroderma and rheumatoid arthritis, lupus, systemic vasculitis, end-stage kidney disease)

What aerosol particle can lead to Hypersensitivity Pneumonitis (HP) or extrinsic alveolitis?

symptoms?

diagnostic criteria?

mold spores leads to HP (prototype: farmer's lung)

Symptoms occurs hours after the exposure (latency) and present as a flue-like illness.  delayed immune response
•
Symptoms usually abate when the stimulus is removed, however recurrent exposure may lead to chronic symptoms and irreversible lung impairment.

sob & flu sx (febrile)

(diff from OA: sob only)

diagnostic criteria:

history.
•
Compatible clinical, radiographic, or physiologic findings:
–
Respiratory (±constitutional) symptoms such as crackles on chest exam, weight loss, cough, breathlessness, febrile episodes, and wheezing, especially suggestive if worsening several hours after antigen exposure.
–
Reticular, nodular, or ground glass opacity on CXR or HR CT
–
Altered spirometry and/or lung volumes (may be restrictive, obstructive, or mixed pattern), reduced DLCO.

BAL with lymphocytosis Usu with low CD4 to CD8 ratio.
•
Inhalation challenge to the suspected antigen in a hospital setting.
•
Histopathology showing compatible changes.
–
Poorly formed, noncaseating granulomas or mononuclear cell infiltrate

Coal Worker's Pneumoconiosis

distinguish btw simple and complex

is coal pmf distinguishable from silicosis pmf?

coal deposits in lung in 2 forms: simple (lil pathologic consequence) and complex.

most miners smoke
Simple pneumoconiosisis a collection of dust laden macrophages (black deposits) that collect around bronchioles around lymphatics. 

PFT are generally normal and patients are asymptomatic.

Deposits may coalesce and form cavities (progressive massive fibrosis PMF similar in silicosis PMF) - complex penumoconiosis
•
CXR upper lobe nodules.
•
Spirometry abnormalities show restriction. There is evidence that reduction in PFT’s is proportionally related to dust exposure.
•
Reduced TLC and DLCO occur.
•
Disability occurs with this type of disease.

what is the #1 cause of lung cancer in US?

#2?

other causes?

1. smoking

2. radon (non-smokers; radon geographic belts, like in NJ)

others:

vinyl chloride, nickel chromates, asbestos and coal products.
Radioactive elements: uranium

High altitude hypoxia may lead to what condition in the lungs?

lung disorders associated with diving?

Disorders at high altitude occurs as a result of decreases atmospheric pressure  -->  high altitude sickness and pulmonary edema

increased atmospheric pressure leading to diffusion of nitrogen into the blood stream. The gas expands as the pressure decreases causing cellular damage.

bleomycin can lead to what condition in the lungs?

other drugs that leads to similar condition?

drugs that lead to bronchospasm & cough?

Bleomycin is a cancer drug that increases radicals and is toxic to cells that can lead to interstitial pneumonitis leading to fibrosis.
–
Surveillance and early monitoring for toxicity of this agent is the DLCO.

Amiodarone an anti-arrhythmic drug,
•
Antirheumatic drugs e.g. methotrexate, penicillamine, gold salts.
•
Non-steroidal anti-inflammatory agents.
•
Oxygen toxicity.

drugs that induce bronchospasm & cough:

Beta blocker drugs.
•
ACE inhibitors.
•
NSAID agents including aspirin.
•
Contrast media, and neuromuscular blocking agents.
–
Most result in increased obstruction to air flow and a reduced FEV1.

What is Popcorn workers lung disease?

WTC cough?

A 30 -year-old white male is brought to the emergency room of your hospital unconscious after being extracted from a burning building. He has no history of chronic illness and has never been hospitalized.

On exam he has a temperature of 99 F a pulse of 118, and BP 120/68. His chest exam reveals faint wheezes. Except for the soot on his face his lips and face are pink, and the rest of the physical exam is normal.

Selected labs: ABG pH 7.28 pCo2 30, po2 79 SAO2 96%. COHgb (carboxy-Hgb) 15%.

What treatment would most benefit this patient?

The most likely cause of this patients unconscious state?

supportive therapy, supplemental oxygen, and treatment for cyanide poisoning.

Inhalation of complex products of combustion (like in a fire) including cyanide.

Penicillin (10d) is drug of choice


Alternatives in allergic patients:
 Cephalexin
 Clindamycin

 Macrolides (resistance!)

not good for group A strep  Co-trimoxazole

How do you tx bordetella pertussis?

which phase is infectious?

vesicles in the pharynx indicates what kind of infection?

erythromycin

(vaccine is available; DPT)

catarrhal phase

coxsackievirus group A type 16 (hand foot mouth disease)

give normal values for:

Pa02= partial pressure of 02 in arterial blood
PaC02=paarrttiiaall prreessssurree off C02 iin aarrtteerriiaall bllood
PA02= partial pressure of 02 iin aallveeollaarr gaass
PvO2= partial pressure of 02 iin veenouss bllood
Sa02=saturation of hemoglobin with 02 in
aarrtteerriiaall bllood
Sp02= ssaatturraattiion off heemogllobiin wiitth 02
bypullssee oxiimeettrry
Ca02=ccontteentt off 02 iin aarrtteerriiaall bllood

PPaa002 = 95--100 mmHg (sea level, decreases with age)
 PPaaC002= 38-42 mmHg
 PPA002= 110 mmHg
 PPvvO2= 40 mmHg
 SSaa002== 9966--110000% ((sseeaa lleevveell,, ddeeccrreeaasseess wiitthh aaggee))
 SSpp002= 96-100% (sea level, decreases with age)
 Caa002= 20 ml/100ml blood (assumes Hgb = 15 gm)

How do you calculate PaO2 and account for age?

Pa02 / FI02 <200  indicates what?

Pa02 = 100 - age/4

ARDS due to RL shunt

What is the clinical significance of Alveolar-arterial Oxygen Difference (AaD02)?

How do you calculate it?

AaDO2 == PA02 – Pa02

Normal 5 -- 15mmHg. on room air

PPrroovviiddeess aann aasssseessssmeenntt ooff iinnttrraa-pulmonary gas eexxcchhaannggee

increase indicates lung pathology not diagnostic of any specific lung disease

PA02 = 150 - 1.2 (PaC02)