Introduction to Clinical Medicine

ICM
The primary purpose of this course is to promote a
transition from the principles of basic science to
diagnostic and theraputic medicine.
As such you will be presented with a series of clinical
case histories involving various organ systems and will
be asked to assess the problem, interpret the laboratory
and radiographic data and submit a differential
diagnosis.
During these sessions I expect you will have thoroughly
reviewed the evidence presented in each case, correlate
the history and physical findings, be able to explain the
underlying patho-physiologic mechanisms involved and
be prepared to discuss and justify your differential and
final diagnosis.
Introduction To Clinical Medicine
ICM
Student Case Studies
Pulmonary Diseases

Prepared by:
Robert W. Wilhoite M.D.
 Introduction
The process of physical diagnosis is of prime
importance in the evaluation of any patient.
This process consists of three major modalities
that one should employ.
1.Observation look at the patient
An initial clue to the diagnosis may be observed
2. History
Present and past S & S
3. Physical exam
Positive and negative findings
 Signs and Symptoms
of
Cardiopulmonary disease
Define and explain the patho-physiology of
each of the following:
Fatigue
Due to decreased cardiac output to skeletal muscle

Dyspnea
Secondary to pulmonary congestion resulting in
transudative leakage of fluid into the pulmonary
parenchyma
PND/orthopnea
Due to accumulation of gravity dependent fluid in the
recumbant position secondary to redistribution of
intravascular fluid resulting in increased intracardiac
filling pressure
 Signs and Symptoms
of
Cardiopulmonary disease
Peripheral edema and weight gain
Due to fluid retention because of elevated right sided
cardiac pressure resulting in an accumulation of
interstitial fluid
Abdominal distention
Due to elevated right sided cardiac filling pressure
resulting in hepatic swelling and intestinal edema.
Decreased mental acuity
- Due to diminished blood flow to the brain
 Case # 1
This 58 year old man is 4 days post-op
following a gastric resection for carcinoma.
In the last 24 hours he has noted difficulty in
breathing and now has developed severe chest
pain exacerbated during inspiration. He has
become increasingly tachypneic. An ECG
reveals sinus tachycardia and non specific ST
and T wave changes.
Preliminary laboratory findings are
unremarkable.
 Case # 1
A chest x-ray reveals right lower lobe
atelectasis and questionable pleural
effusion.
 Case # 1
Findings:
Post- operative status
Acute dyspnea !
Chest pain
Atelectasis
? Pleural effusion
 Case # 1
What are the various mechanisms that may
produce dyspnea?
Three different mechanisms may be involved:
Mechanical
COPD, restrictive lung disease,pneumonia,pericarditis,
asthma, pneumothorax, PE.CHF, AMI, , respiratory
muscle weakness
Compensatory
Hypoxemia, acidosis
Psychogenic
 Case # 1
How would you assess a patient who
complains of dyspea?
Acute versus chronic
Position at onset
Relationship to activity
Obtain allergic, occupational and smoking history
grade on a scale of 1-10
 Case # 1
At this time what other information would you
seek in your evaluation of this patient?
Monitor vital signs, pulse oximetry
From the observational standpoint what do the
following findings suggest?
Pursed lips in breathing
Use of extra respiratory muscles
Barrel chest
Asymmetric pulmonary excursions
Kussmal breathing
Increased jugular venous pressure
Peripheral edema
Homans sign
Pericardial friction rub
 Case # 1
At this time what other information would you
seek in your evaluation of this patient?
Monitor vital signs, pulse oximetry
From the observational standpoint what do the
following findings suggest?
Pursed lips in breathing airway obstruction
Use of extra respiratory muscles -airway obstruction
Barrel chest COPD
Asymmetric pulmonary excursions -pneumothorax
Kussmal breathing metabolic acidosis
Increased jugular venous pressure - CHF
Peripheral edema -CHF
Homans sign - thrombophlebitis
Pericardial friction rub r.o pericarditis
 Case # 1
What is your differential diagnosis for
this patient?
ARDS
Pulmonary embolism
Pneumonia
AMI
Pericarditis
Asthma
 Case #1
What initial tests would you order in your evaluation of
this case?
Arterial blood gases (pulse oximetry)
? Hypoxia oxygen saturation values < 94 % strongly suggest hypoxemia
? Respiratory alkalosis due to hyperventilaton
ECG
ST elevation (r.o. AMI)
Venous ultrasound
r.o. Phlebothrombosis/ thrombophlebitis )
D-dimer
Elevated in thromboembolism
<500 ng/ml probably not a thrombus
Troponin
r.o. AMI
BNP-differentiates dyspnea due to heart failure (left ventricular end diastolic
pressure (LVEDP) from non-cardiogenic causes
 Case # 1
What additional procedures would you
consider?
Continue to monitor patients blood pressure
Helical CT scan with contrast media
(replaces ventilation- perfusion scan)
Suggests diminution of blood flow to lungs
If diagnosis is in doubt perform pulmonary angiography
Also detects small infarcts
MRI
Same sensitivity and specificity as CT scan
Ventilation perfusion scan
 Case # 1
What is your principal diagnosis at this
time?

Pulmonary embolism
 Case # 1
What are the classic symptoms of a PE?
Sudden onset of unexplained dyspnea
Pleuritic chest pain
Cough (seen in 1/3 of patients)
Hemoptysis (not common) if present think of pulmonary
infarction
 Case # 1
What are the potential causes of pulmonary
thromboembolism?
Deep vein thrombosis
Amniotic fluid embolism obstetrical accident
Air from central venous catheter
Fat bone fracture
Foreign body talc
Parasitic eggs - Schistosoma
Septic embolus - endocarditis
Tumor e.g. renal Ca
Immobility
Hypercoagulable state e.g. patients on oral contraceptive
Factor V deficiency (Leiden factor)
 Case # 1
How would you treat this patient?
Anticoagulation secondary prevention
Heparin binds to accelerate the ability of anti-thrombin III
to inactivate thrombin and factors IX and X thus retarding
additional thrombus formation.
Note: heparin may cause thrombocytopenia in 39 % of
patients
Therefore: use Low molecular weight heparin (LMW)

Coumadin (Warfarin) Control level - INR 2.5

 Case # 1
Other treatment options:
Thrombolytic therapy
Streptokinase, urokinase, tPA
- accelerates resolution of emboli
- contraindicated in acute bleed or a CVA

Inferior venal caval filter

 Case # 1
Pathophysiology of pulmonary embolism:
Increase in pulmonary pressure
causes
Damage to alveolar walls
with
Influx of fluid into interstitial space
which
Washes away pulomonary surfactant
resulting in
Alveolar collapse
and
Right heart failure
Peripheral pulmonary embolus
 Case # 1

Final diagnosis
Pulmonary embolism
secondary to
deep vein thrombosis
and thrombophlebitis
 Case # 1.5
This 69 year old woman has a past
history of congestive heart failure due to
long standing hypertension. Following
her Thanksgiving dinner she began to
experience shortness of breath, fatigue
and upon laying down her breathing
became more labored. Medcu was called
and she was taken to the emergency
room.
 Case # 1.5
Physical findings revealed a pale, cool,
diaphoretic woman experiencing severe
dyspnea. Her vital signs included a pulse of
100, BP 220/110, respiratory rate of 28 and an
oxygen saturation of 87 %
Her neck veins were distended, her lungs
revealed some crackles. There was 2 +
peripheral edema with good peripheral pulses.
There was also noted a pink frothy sputum.
Mild hepatomegaly
A chest x-ray revealed diffuse interstitial
 Case # 1.5
Findings:
Severe acute dyspnea
Tachypnea
Low O2 saturation
Distended neck veins
Pink frothy sputum
Peripheral edema
Mild hepatomegaly
Interstitial pulmonary edema
 Case # 1.5

What is your differential diagnosis?

Acute pulmonary edema
Congestive heart failure
Hypertensive cardiovascular disease
Acute myocardial infarction
Acute LV valvular overload
( e.g. regurgitation)
 Case # 1.5
What is your principle diagnosis at this time?

Congestive heart failure

with
Acute pulmonary edema
 Case # 1.5
How would you define pulmonary edema:

A disorder of fluid transfer in which there

occurs an increased pulmonary vessel
hydrostatic pressure resulting in the flow of
edema fluid into the alveoli.
 Case # 1.5
How would you treat this patient?
Have patient sit at side of bed with legs dangling over the side
(facilitates respiration and reduces venous return )
High flow O2 via face mask
Nitrates
Diuretics
Morphine
 Case # 1.5
What is the rational for each of these
treatments?
High flow O2 by facemask
Reduce pressure gradient across alveolar membrane
Nitrates
Causes pulmonary vasodilatation that decreases vascular
hydrostatic pressure
Mild sublinqual
Severe I.v. drip
Diuretics
Causes rapid decrease in intravascular volume decreasing
hydrostatic pressure
Morphine
 Case # 1.5
What are the risk factors associated with
the development of pulmonary edema?
Increased pulmonary hydrostatic pressure
Left sided heart failure i.e. AMI
Mitral or aortic valve stenosis or insufficiency
i.e. right heart failure
Medical non-compliance with diuretics, high
sodium diet
Heart failure cells
 Final Diagnosis
Acute pulmonary edema
due to
Hypertensive cardiovascular
disease
and
Left and right sided heart failure
 Case # 2
This 26 year old man has a history of chronic
lung disease (bronchiectasis) characterized by
a chronic cough, productive sputum and
occasional hemoptysis. He also complains of a
purulent nasal discharge with sinus tenderness.
A culture of this revealed Pseudomonas species.
.
A CT scan confirms the diagnosis of
bronchiectasis.
 Case # 2
Findings:
Chronic lung disease (bronchiectasis)
Productive cough
Hemoptysis
Purulent nasal discharge
Positive culture for Pseudomonas
 Case # 2
1.What is your differential diagnosis?
Mucoviscidosis (cystic fibrosis)
Kartageners syndrome
Lung infection ( e.g. TB, fungal)
Alpha-1-antitrypsin deficiency
Immunodeficienty states (IgA, IgM, IgG)
AIDS
Allergic bronchopulmonary mycosis
(e.g. Aspergillus )
 Case # 2
What is your principal diagnosis at this
time?

Mucoviscidosis
(cystic fibrosis)
 Case # 2
What additional tests would you order?
Culture of sputum (r.o. Pseudomonas infection
Pilocarpine iontophoresis sweat test
Arterial blood gases check degree of hypoxemia
CFTR gene determination
(Cystic fibrosis transmembrane conductance regulator)
?Biopsy for ciliary dyskinesia (r.o. Kartegeners
syndrome)
What is your principal diagnosis at this time?
 Case # 2
What is the underlying mechanism of this
disorder?
An abnormalty in the epithelial membrane chloride
channel protein resulting in altered chloride
transport and water flux across apical surface of
epithelial cells resulting in retention of sodium and
chloride values.
Etiology: CFTR protein gene
(diagnostic values =Na and Cl >60 mEq./l.)
The result is a mucoid obstruction of the exocrine
glands resulting in atrophy.
 Case # 2
What are the systemic manifestations of
this disease process?
 Cystic Fibrosis
(Mucoviscidosis)
Systemic features:
Recurrent pulmonary infections viscid mucoid secretions
Pancreatic insufficiency a result of exocrine atrophy
Steatorrhea lack of enzymes lead to impaired fat absorption
Malnutrition faulty absorption of fat soluble vitamins
e.g.Vitamin A deficiency
Hepatic cirrhosis
Intestinal obstruction meconium ileus (viscid plugs)
Salivary glands duct dilatation, squ. metaplasia, atrophy
Male infertility due to congenital absence of vas deferens
Azospermia and infertility (95%) , congenital absence of vas deferens
Cystic fibrosis - pancreas
Dilatation of ducts with
inspissated material
Exocrine gland atrophy
Cystic fibrosis
lung
Meconium ileus
 Bronchiectasis
Cystic fibrosis Kartageners
Syndrone.
Bronchiectasis Bronchiectasis
Sinusitis Sinusitis
Situs inversus
CFTA gene no CFTA gene
High Na & Cl Normal Na & Cl
Ciliary dyskensia
 Case # 1.5
What is ciliary dyskenesia?
An autosomal recessive syndrome occurs in 1 of 15,000
Results in retention of secretions (mucociliary clearance defect)
resulting in recurrent infections which ultimately leads to
bronchiectasis.
Seen in 50 % of patients with Kartegeners syndrome.
 Case # 2

Final diagnosis

Cystic fibrosis
(Mucoviscidosis )
 Case # 3
This 34 year old man has developed non-
specific respiratory symptoms over the past 3
weeks and more recently has experienced two
separate episodes of hemoptysis, some dyspnea
and mild anemia.
A routine urinalysis revealed hematuria. A
chest x-ray shows diffuse bilateral fluffy
infiltrates.
A bronchoscopic biopsy of the lung was
obtained and the microscopic section is
representative of his underlying condition.
 Case # 3
Findings:
Respiratory symptoms
Hemoptysis
Mild anemia
Hematuria
Fluffy pulmonary infiltrates
 Case # 3
1. What is your interpretation of the lung
biopsy specimen?
Intra-alveolar hemorrrhage
2.What additional tests would order?
Anti-glomerular basement membrane antibody

3. What is your differential diagnosis?

Diffuse pulmonary hemorrhage syndromes:
Goodpasteurs syndrome young males
Idiopathic pulmonary hemosiderosis children
Vasculitis e.g Wegeners, SLE
 Case # 3
What are the typical findings in a patient
with Goodpasteurs syndrome?
Idiopathic, recurrent pulomanary
hemorrhage
Rapidly progressive glomerulonephritis
Occurs in men 30-40s
 Case # 3
What are the typical findings in a patient with
idiopathic pulmonary hemosiderosis:
A disease of children
Recurrent pulmonary hemorrhage
No renal involvement
No anti-glomerular antibodies
Iron deficiency -typical
 Case # 3
1. What is the classic triad of findings seen
in Goodpasteurs syndrome?
Pulmonary hemorrrhage
Focal glomerulonephritis
Cytotoxic antibody to glomerular basement
membrane
 Case # 3

Final diagnosis

Goodpasteurs syndrome
 Case # 4
This 52 year old man, a chronic smoker of long
standing duration has developed hypertension,
low back pain, truncal obesity, ptosis of the left
eye with some miosis.
A chest x-ray shows a three cm. lesion in the
left hilar region of the lung as well as a mass
lesion in the left supraclavicular area.
A trans-bronchial biopsy was taken and the
microscopic slide is representative of his
underlying pathology.
 Case # 4
Findings:
Hypertension
Low back pain
Truncal obesity
Supraclaviclar mass
Ptosis and miosis of the left eye
? Syndrome
 Case # 4
1. What is your histologic diagnosis?
Small cell (oat cell) carcinoma of the lung
2. How do you explain his physical findings?
This patient demonstrates a paraneoplastic
syndrome with a pancoast tumor
Small cell carcinomas may elaborate an ACTH like
polypeptide which in turn stimulates the adrenal
cortex to secrete increased levels of cortisol resulting
in a clinical Cushinoid appearance
3. How would you treat this patient?
Radiation/chemotherapy
Surgical resection ????
 Case # 4
What is a Pancoast tumor and what are
the classic findings?
Metastatic tumor to supraclavicular area with
involvement of sympathetic ganglion
Horners syndrome
Enophthalmus
Ipsilateral ptosis
Miosis
Anhidrosis
Etiology: inferior cervical ganglion and paravertebral
sympathetic chain involvement with tumor
 Case # 4
What methods are available in evaluating a
radiographically demonstrable lung lesion:
Depends on location of the lesion
Central bronchoscopy with biopsy
Peripheral CT guided needle biopsy
Open thoracotomy
Medastinoscopy with biopsy
CT abdomen ? liver and adrenal metastases
 Case # 4
Final diagnosis

Small cell carcinoma of the lung

with
Paraneoplastic syndrome
and Pancoast tumor
 Case # 5
Following a resection for colon cancer this 71 year old
man had his endotracheal tube removed and
subsequently experienced an episode of severe
coughing and one episode of vomiting. Twenty four
hours later he experienced a rapid onset of dyspnea
with accentuated intercostal retraction.
A chest x-ray exhibited bilateral patchy infiltrates
without blunting of the costo-phrenic angles.
He was placed on supplemental oxygen therapy and
failed to respond. Over the next 24 hours his WBC
rose to 25,000, BUN 43. Temperature 39.2 BP 110/60
 Case # 5
Findings:
History of colon cancer
Severe coughing
One episode of vomiting
Increasing dyspnea
Pulmonary infiltrates
No blunting of lung bases
 Case # 5
1. What is your differential diagnosis?
ARDS
Acute pulmonary embolism
Acute pulmonary edema
Sepsis

2. What is your principal diagnosis ?

ARDS
Acute Respiratory Distress Syndrome
(ARDS)
A clinical syndrome caused by diffuse alveolar capillary
damage

Characterized by:
Rapid onset of profound dyspnea and tachycardia
Increased hypoxemia unresponsive to treatment with O2
Cyanosis
Respiratory failure
Intercostal retraction
Bilateral pulmonary infiltrates become confluent

Mortality rate - 60 %
 Case # 5
3. What are the more common risk factors
associated with the development of ARDS?
Sepsis (33 % have sepsis)
Aspiration of gastric contents
Shock
Hemorrhagic pancreatitis
Pulmonary infections
Toxic inhalants
Narcotic overdose
Immunogenic (e.g. Goodpasteurs, SLE)S
 Case # 5
What are the potential causes of
ARDS ?
Systemic insult Pulmonary insult
Trauma Aspiration
Sepsis Embolus\
Shock Tuberculosis
Burns Diffuse pneumonia(SARS)
Drugs Near drowing
TTP Toxic gases (Cl,ammonia)
Head injury
Foreign body giant cell reaction
Due to aspiration of gastric content
 Case # 5
Final diagnosis

Adult respiratory distress syndrome

(ARDS)
 Case # 6
This 46 year old Afro-American man gives a history of
periodic episodes of respiratory insufficiency
characterized by shortness of breath, cough and chest
pain. These symptoms will frequently disappear after a
few weeks only to return three months later. More
recently he now complains of weight loss and night
sweats.
Physical exam reveals some peripheral
lymphadenopathy and mild hepato-splenomegaly.
A chest x-ray was obtained. (see slide)
A bronchoscopic biopsy was obtained and a
microscopic section made.
 Case # 6
Findings:
Afro-American male
Respiratory insufficiency
Lymphadenopathy
Hepato-splenomegaly
 Case # 6
What is your differential diagnosis?
Granulomatous disease process:
Sarcoidosis non-caseating granulomas
Tuberculosis caseating granulomas
Fungus infection no organisms seen
 Case # 6
1. What is your interpretation of the
chest x-ray?
Bilateral hilar lymphadenopathy
(potato nodes)

2. What is your interpretation of the

microscopic section of the lung?
Diffuse non-caseating granulomata
(also look for Schaumann bodies and asteroid bodies)
 Case # 6

What is your working diagnosis?

Sarcoidosis
 Case # 6
Are there any specific laboratory tests or
microscopic findings that would aid you in
making a diagnosis?
Elevated angiotensin converting enzyme (ACE)
(positive in 40-80 % of cases)
Elevated serum (5%)/urinary calcium (20%)
Macrophages are present in granulomatous diseases and
synthesize 1,25(OH)2 D3 resulting in serum and urine calcium
Schauman and asteroid bodies in lymph node
Sputum for culture and acid fast stain
CBC -Anemia with leukopenia

 Case # 6
What other tissues may be involved in this
condition?
Lymph nodes particulary hilar and mediastinal
Spleen 75 %
Liver
Bone marrow 20 % - especially in phalanges
Skin 33-50 % (subcutaneous nodules)
Erythema nodosum
Eye Mikulicz syndome lacrimal, uveal and
parotid gland involvement
Salivary glands 50 %
 Case # 6
What are causes of Mickulicz syndrome?
Sarcoidosis
Lymphoma
Leukemia
 Case # 6
1. What is the underlying pathogenesis of
this lesion?
Primarily an immunologic reaction due to a
development of a cell mediated (CD-4 helper
T cells) response to an unidentified antigen
 Case # 6

Final diagnosis

Sarcoidosis
 Case # 7
This 38 year old man, a known i..v. drug
abuser, has developed progressive respiratory
problems over the past six weeks associated
with fever, weight loss, dyspnea and the
production of a frothy white sputum.
Physical exam reveals generalized
lymphadenopathy.
A culture of his sputum was positive for
Mycobacterium avium-intracellare.
A chest x-ray was taken (slide #1) and a lung
biopsy was performed . (slide # 2)
Slide # 1
Slide # 2
 Case # 7

Findings
i.v. drug abuser
Respiratory problems
Generalized lymphadenopathy
Positive sputum culture
M. avium intracellulare
 Case # 7
1. What is your interpretation of the x-ray?
Diffuse patchy infiltrates
2. What is your interpretation of the lung biopsy
3. Do you attach any significance to a positive culture of
M. avium- intracellulari
2. What is your differential diagnosis?
Pneumocystis pneumonia (P.jiroveci)
Opportunistic infections
Tuberculosis
Non-tuberculous mycobacteria (MAC) infection
Granulomatous disease (e.g. fungal disease)
3. What additional laboratory tests would you order?
CD-4 T lymphocyte count
 Case # 7
What is your final diagnosis?
 Case # 7

Final diagnosis
HIV infection
Pneumocystis pneumonia
Atypical mycobacterial
infection
 Case # 8
This 52 year old long time tobacco smoker gives a history of
insidious and progressive dyspnea. Associated with this is some
whezzing and minimal cough. More recently he has developed
orthopnea. He also has experienced a 15 pound weight loss over
the past six months.
Physical exam reveals a barrel-chested man who is chronically
dyspneic and states that if he sits forward in a hunched-over
position his breathing is easier.
With inspiration there is retraction of the intercostal muscles
Pulmonary ventilation studies suggest pulmonary hypertension.
A chest x-ray was taken.
The slide is a gross specimen of the lung.
 Case # 8
Findings:
Tobacco abuser
Progressive dyspnea
Orthopnea - ? Indication
Barrel chest with intercostal retraction
 Case # 8
1. What is your interpretation of the
x-ray and gross lung findings.
Increased lucency of the lung fields
Dilated air spaces (lobules) with over inflation
2. What would you expect to see in a
microscopic section of this lung?
Dilatation and rupture of alveolar walls
 Case # 8
What is your differential diagnosis?
COPD
Chronic bronchitis
Emphysema
Bronchial asthma
Bronchiectasis
Cystic fibrosis
Bronchopulmonary mycosis
Alpha-1-antitrypsin deficiency
 Case # 8
How would you define emphysema?
A pathologic diagnosis that denots an abnormal
permanent enlargement of the air spaces distal to
the terminal bronchioles with destruction of their
walls without obvious fibrosis
How would you define chronic bronchitis
A clinical diagnosis characterized by excessive
secretion of bronchial mucus and cough for 3
months in two consecutive years
 Case # 8
4. What would you expect to hear with
ascultation of the lungs?
Nothing!
5. What is the significance of the barrel-
chest in this patient?
Hyperinflation of the lungs
 Case # 8
What is the pathology of pulmonary
hypertension?
Pressure within the pulmonary circulation is due to low resistance.
Normally pulmonary blood pressure is 1/8 that of systemic blood
pressure
A definition of pulmonary hypertension is when the pulmonary
pressure reaches of the systemic pressure
Pulmonary hypertension is due to an alteration in cardio-pulmonary
function which results in increased pulmonry blood flow.
e,g. COPD, Cardiac disease ( mitral stenosis with increased left atrial
pressure )
 Case # 8
What does the recent development of his
orthopnea suggest?
Progression of his COPD with left
ventricular heart failure
 Case # 8
How would you proceed in your evaluation of
this case?
CBC rule out anemia
Sputum culture
Pulmonary function tests
Spirometry:
Forced vital capacity (FVC)
Forced expiratory volume/1 second (FEV1)

Arterial blood gases

Hyperinlation of the lung
Rupture of the alveolar walls
 Case # 8
The basic problem in this patient is
Chronic Obstructive Pulmonary Disease
(COPD)
Emphysema Chr.Bronchitis
Destruction of alveolar walls Response to inhaled toxins
by chronic airway inflammation Mucous gland
proliferation
Dilated air spaces Destruction of cilia with
Frequent in smokers inability to clear secretions
Activation of protease system Chronic cough with
mucus plug
X-ray hyperinflation Bronchial inflammation
Bronchospasm noisy chest
 Chronic bronchitis
The result of excessive mucus production from
the epithelial goblet cells and mucous glands
with a concomitant decrease in the ciliated
epithelial cells resulting in an inability to clear
the excess mucus and cough
Airway obstruction is primarily due to
bronchiolar inflammation and bronchospasm
Bronchial mucus plug seen in chronic bronchitis
 Case # 8
What does the recent development of
orthopnea suggest?
Progression of his COPD with left
ventricular heart failure
 What are the classic findings in a
patient with emphysema ?
Dyspnea on exertion e,g, climbing stairs
Inc. cough without sputum
No fever or chills
Swelling of feet - complication of CHF
Past history: HTN, hyperlipidemia , Hx of asthma, smoking
Px : inc. resp. rate, diminshed lung sounds, expiratory wheezing
Distended jugular veins; inc. AP diameter of chest
Mild peripheral cyanosis (check finger nail beds)]
Peripheral edema - CHF
Dec. O2 sat (88%)
Anti-alpha-1- trypsin deficiency ?genetic basis
 Case # 8
What is the patho-physiology of emphysema?
The basic defect is a destruction of the alveolar walls.
Inhaled toxins (e.g. smoking ) destroys normal alpha-1-
antitrypsin resulting in increased alveolar macrophages and
neutrophils
These activated PMNs release protease (which is normally
destroyed by alpha-1-antitrypsin) and free oxygen radicals.
The inc. protease activity destroys elastin and cleaves type IV
collagen
The collapse of broncho-alveolar walls leads to a loss of
pulmonary capillaries, a reduction of O2 diffusing capacity
and obstruction of normal air flow
This also results in an increased pulmonary arterial pressure
and subsequent right heart failure.
Hyperinflation of the lungs
 Bullous emphysema
Paraseptal emphysema
 Other types of emphysema
Compensatory emphysema:
Post surgical resection of lung tissue
Obstructive overinflation:
Expansion due to trapped air
Bullous emphysema:
Large sub-pleural blebs
Spontaneous pneumothorax
Interstitial emphysema:
Entrance of air into connective tissue of lung,
mediastinum or subcutaneous tissues
 Case # 8
Clinical patterns of advanced COPD:
Pink Puffer Blue Bloater
(emphysema) (chr. bronchitis)
Severe dyspnea mild dyspnea
rare cough chronic cough
Clear sputum productive sputum

thin over weight

weight loss cyanotic
quiet chest rhonchi, wheezes
 Case # 8

Final diagnosis

Panacinar Emphysema
 Case # 9
This 61 year old woman has suffered from chronic bronchitis over
the past several years. She has a long standing history of cigarette
abuse.
Twenty four hours ago she experienced a shaking chill with right
chest pain. Her temperature at that time was 102. Within the next
12 hours she developed a cough with the production of some grey
green sputa. Her temperature has risen to 103.4.
Physical exam : BP 115/65, pulse 120 respiratory rate 32.
On admission to the hospital she was found to have rhonchi in the
right upper lobe of the lung and now has developed some slight
dyspnea.
A chest x-ray was taken.
From the clinical standpoint what is your assessment of this
patient?
 Case # 9
Findings:
Chromic bronchitis
Cigarette abuse
Shaking chill
Right chest pain
Fever
Cough with productive sputum
 Case # 9
1. What is your interpretation of the x-ray?
Right upper lobe consolidation with mediastinal and
right heart borders obscured.

2. What additional tests would you order ?

CBC, Sputum for culture, blood culture
 Case # 9
3. What is your differential diagnosis?
A pneumonic process:
Acute bacterial pneumonia -
Atypical pneumonia mycoplasma, viral
Nosocomial pneumonia gram negative rods
Aspiration pneumonia anaerobic oral flora
Chronic pneumonia granulomatous disease
Pneumonia in the immunocompromised host
CMV, pneumocystis, M. avium-intracellulari
Lobar pneumonia
Bronchopenumonia
Bronchopneumonia
Alveolus filled with inflammatory cells
 Case # 9
What are the complications of
pneumonia
Organization
Pleuritis
Empyema
Abscess formation
Bacterial dissemination due to embolization
Empyema
Empyema of the lung
 Risk factors for pneumonia
Muco-ciliary dysfunction
E.g. smoking, chr. asthma, bronchitis, cystic
fibrosis, bronchiectasis
Co-morbid diseases
Heart disease, renal failure, COPD, diabetes
Immunocompromised patients
Ca, HIV, chemoRx, chronic. steroid use
 Classic findings in pneumonia
Bacterial :
Rapid onset, fever, chlls, cough, pl. pain
Atypical or viral:
Gradual onset, indolent, low grade fever,
myalgias, arthralgias, fatique headache
 Case # 9

Final diagnosis

Lobar pneumonia
 Case # 10
This 31 year old male with a long standing
history of smoking had a pre-employment chest
x-ray at which time a small (1.0 cm) coin
lesion was found. It was described as a solitary
nodule, opaque, densely calcified nodule with
smooth, well defined margins. There was no
infiltration, atelectasis or adenopathy.
He has no other subjective symptoms.
 Case # 10
How would you define a coin lesion:
A < 3cm. Isolated, rounded opacity on a
chest radiograph and not associated with an
infiltrate, atelectasis or adenopathy
 Case # 10
1. How would you proceed your evaluation of
this lesion?
Evaluate old x-rays
If present estimate doubling time marker for Ca
Sputum cytology
Bronchoscopy
Trans-thoracic needle biopsy
CT scan pick up multiple lesions, lymph nodes
PET scan ( positron emission tomography)
Theory: detects glucose metabolism within malignant lesions
Sensitive 85-97% for Ca. Negative scan >90% -no tumor
! Expensive; ? availability
 Case # 10
2. What is your differential diagnosis of a
solitary pulmonary nodule?
Benign hamartoma (chondroma)
Malignant neoplasm
Carcinoid tumor
Squamous cell carcinoma
Adenocarcinoma
Small cell carcinoma
Bronchoalveolar carcinoma
Infectious granuloma
Tuberculosis
Fungal infection
Pulmonary
hamartoma
Large cell anaplastic carcinoma
 Case # 10

Final diagnosis

Pulmonary hamartoma
(chondroma)
 Case # 11
This 35 year old man was first diagnosed with
an HIV infection eight years ago. He has
remained asymptomatic until three years ago
when he developed periodic episodes of mild
fever and night sweats. In the past two months
he has lost 20 pounds. His most recent lab tests
revealed a LDH of 600 and a CD4 count 100.
A chest x-ray revealed diffuse, bilateral
pulmonary infiltrates.
 Case # 11
Findings
HIV positive
Mild fever with night sweats
Weight loss
Elevated LDH
Decreased CD4 count
Pulmonary infiltrates
 Case # 11
How would you describe the evolution of
this mans condition?
HIV positive eight years ago
Asymptomatic until three years ago when he develops mild
fever and night sweats
Now loses 20 pounds
Exhibits falling CD4 couunt
Develops pulmonary infiltrates
 Case #11
1. What is your differential diagnosis?
Pneumocystis pnemonia
Tuberuclosis
Non-tuberculous mycobacterial infection
Opportunistic infections
Non-specific interstitial pneumonitis
Tumor
 Case # 11
What additional tests would you order?
Sputum culture
Direct flourescent antibody (DEA)
50-80% pos. in pneumocystis infection
TB skin test
Bronchoalveolar lavage
R.o. neoplasm
CT pulmonary scan
 Case # 11
What is your principal diagnosis at this
time?

AIDS
 Case # 11
What are some of the complications that
an AIDS patient may develop?
 Case # 11
Oppontunistic infections:
Candida esophagitis
CMV
Histoplasmosis
Coccidiodomycosis pulmonary involvement
Toxoplasmosis CNS involvement
Cryptococcosis meningitis -CRAG test
Cryptosporidiosis - enterocolitis
 Case # 11
What neoplasms are associated with an
AIDS patient?
Kaposis sarcoma
Non-Hodgkin,s lymphoma (brain)
Hodgkins disease
Anal dysplasia and SCC
Cervical dysplasia (40 %) ; carcinoma
 Case # 11
Does the CD4 lymphocyte count have any
relationship to the type of opportunistic
infection that may develop?

YES!
 Case # 11
CD4 lymphocyte count > 500
Bacterial infections
Tuberculosis
Vaginal candidias
Hairy leukoplakia
Kaposis sarcoma
 Case # 11
CD4 lymphocyte count <250
Pneumocystis
Toxoplasmosis
Cryptococcosis
Coccidiodomycosis
Cryptosporidiosis
 Case # 11
CD4 lymphocyte count < 100
Dessiminated mycobactium avium complex
Histoplasmosis
CMV
Lymphoma
 Case # 11
Final test results on this patient:
Positive ELISA
Positive Western Blot Test
Negative culture for M. tuberculosis
Positive bronchoalveolar lavage for
M. kansaii
Negative direct fluorescence test for pneumocystis
(DFA)
Negative serologic test for toxoplasmosis
Negative CRAG test
(latex agglutination test for cryptococcal antigen
 Case # 11
With these test results what is your final
diagnosis:

AIDS with non-tuberculous (atypical

mycobacterium) pulmonary infection
Infiltrates of pneumocystis
Pneumocystis jerovici
 Case # 11
Final diagnosis

AIDS
With
Atypical mycobacteria pneumonia
(M. kansaii)
 Case # 12
This 69 year old man with a long standing
history of cigarette smoking consults with his
PCP because of progressive exertional dyspnea
and excretory wheezing. He currently requires
two pillows in order to fall sleep. Physical
exam:pulse 80, temp 98.8, BP 105/70. His
extremities feel cold. Percussion of the chest
suggests some dullness. Liver is slightly
enlarged

A chest x-ray was obtained.

 Case # 12
Findings:
Cigarette abuse
Exertional dyspnea
Orthopnea
Chest radiograph
Dullness over left chest
 Case # 12
What is your interpretation of the chest
film?
 Case # 11
What diagnoses would you consider at
this time?
Pleural effusion
Congestive heart failure
Coronary artery disease
COPD
 Case # 12
With a diagnosis of pleural effusion, what
procedure would you consider?
Thoracentesis
What examinations of the fluid would you
request?
What other judgemental decisions would you
make at this time?
Is this fluid a transudate or exudate?
Does this patient have acute or chronic dyspnea?
Is this patient in congestive heart failure?
 Case # 12
Diagnostic thoracentesis:
Determine if effusion is a transudate or exudate:
Gross appearance
Gram stain
Culture
Pleural fluid glocose <50
Pleural fluid pH <7.0
Pleural fluid to serum protein ratio (>0.5
Pleural LDH > 200 IU
Pleural fluid to serum LDH ratio >0.6
Cytology
 Case # 12
What are the two major types of pleural
effusions?
Transudate:
CHF
Cirrhosis
Nephrotic syndrome
PE
 Case # 12
Types of pleural effusion:
Exudate:
Bacterial pneumonia
Metastatic disease (lung,breast, lymphoma)
Tuberculosis
Collagen vascular disease
Mesothelioma
Viral infection
 Case # 12
Judgemental decision regarding this patients
dyspnea:
Is this a case of acute or chronic dyspnea!
.
Clues acute dyspnea
Wheezing (asthma, heart failre)
Stridor (upper airway obstruction)
Consolidation (pneumonia)
Rales, jugular venous distention )
Cardiac murmurs
Tracheal shift (pneumothorax)
Swelling of legs (DVT)
 Case # 12
Clues: chronic dyspnea
Hyperexpansion (COPD)
Rales (coarse in heart failure)
Evidence of CHF/valvular disease
Pulmonary hypertension
 Case # 12

Final diagnosis

Pleural effusion
Due to
Congestive heart failure
End of presentation
 Pulmonary physiology
Atmospheric pressure at sea level is 760 mmHg
At 11,000 feet it falls to 500 mmHg
At 29,000 feet it falls to 250 mmHg

With decreasing pressure the result is

hypoxemia which leads to hyperventilation and
erythrocytosis
 Pulmonary Disease
Cystic fibrosis Kartageners
Syn.
Bronchiectasis Bronchiectasis
Sinusitis Sinusitis
Situs inversus

CFTA gene Ciliary dyskensia

High Na & Cl Normal Na & Cl