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Pulmonary Pathology Flashcards

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1
Q

3 factors involved in adequate respiration?

A
  • Adequate intake of air
  • Rapid diffusion
  • Adequate perfusion of pulmonary vasculature
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2
Q

Hyaline Membrane

A

Pathological finding second to some other disease. Not a disease itself.

The respiratory lining is covered with protein-rich fluid and dead alveolar epithelial cells.

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3
Q

Acinus

A

Function unit of the lung consisting of the respiratory bronchiole and associated alveolar ducts and alveoli

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4
Q

Type -1 pneumocytes

A

Structural

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5
Q

Type-2 pneumocytes

A

Produce surfactant

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6
Q

Which view of x-rays is an exact 1:1 ratio of the persons body

A

Posterior - Anterior

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7
Q

What is the purposed of the lateral view x-ray?

A

To differentiate the R middle and lower lobes

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8
Q

Why is it important to see the costophrenic angles in an x-ray?

A
  • Because if there is any fluid present, we know that there is up to 500ml of fluid in the lungs already.
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9
Q

Classical classifications of pulmonary pathology

A

Degenerative
Inflammatory
Neoplastic
Pleural

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10
Q

What is the most common type of TE Fistula

A

Type C

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11
Q

Neonatal Respiratory Distress Syndrom (NRDS)

A
  • Lack of surfactant, so lungs won’t open to become filled with fluid
  • Incidence is dependent of gestational disease
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12
Q

Surfactant Deficiency Disease

A

AKA: Hyaline membrane disease of the newborn

- Have this because they were delivered early and they were delivered early because of the NRDS

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13
Q

60% of children born at what age are likely to get NRDS

A

28 weeks

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14
Q

Causes of NRDS

A
  • Over-sedation of mother
  • Head injury during delivery
  • Aspiration of blood or amniotic fluid
  • Intra-uterine hypoxemia
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15
Q

Treatment of NRDS

A

Surfactant delivery or corticosteroids of mom

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16
Q

Atalectasis

A

Reabsorption, compression and/or contraction of the lung

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17
Q

Is Atalectasis a disease?

A

NO, it is an anatomic feature seen in many diseases.

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18
Q

Lesion of R upper lobe indicates what?

A

TB

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19
Q

What is pulmonary edema?

A

Accumulation of fluid in the lungs, leading to impaired gas exchange and possible respiratory failure

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20
Q

Cardiogenic pulmonary edema

A

Failure of the heart to remove fluid from lung circulation

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21
Q

Noncardiogenic pulmonary edema

A

Direct injury to lung parenchyma

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22
Q

Rales

A

Sounds like Rice Krispies in the lung of a pt with pulmonary edema

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23
Q

Causes of Pulmonary Edema

A
  • Fluid overload
  • Hypoalbulminemia
  • Lymph obstruction
  • Injury to capillaries of Alveolar septa
  • Infection
  • Liquid aspiration
  • Gas inhalation
  • Chemo
  • High altitude sickness
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24
Q

Pathological mechanisms of pulmonary edema

A
  • Inc. venous pressure
  • Inc. oncotic pressure
  • Lymphatic obstruction
  • Alveolar injury
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25
Prophylaxis for HAPE
...
26
Pathophysiology of Pulmonary Edema
1. Capacity of the lymph to absorb and drain fluid is exceeded 2. Alveolar epithelial cells break down 3. Fluid in alveolar spaces halts gas exchange
27
Acute Pulmonary Edema - What is it? What causes it?
Rapid development, leading to pain Life threatening Usu due to left ventricular failure
28
Symptoms of Acute Pulmonary Edema
Tachypnea Extreme dyspnea Restlessness/Anxiety Cardia Asthma
29
Chronic Pulmonary Edema symptoms
- Possibly no pain or other symptoms - Usu secondary to another disease - Fluid = bacterial growth - Micro-hemorrhages - Macrophages phagocytize Fe from micro-hemorrhages = heart failure cells
30
Acute Respiratory Distress Syndrome
Fluid rushes into the lungs High mortality rate Adult version of NRDS
31
What causes ARDS
Sepsis Widespread lung infection Mechanical Trauma Also: Multi-organ failure, burns, inhaled gases, chemicals,
32
How many people get ARDS with no identified risk factors?
20%
33
Pathophysiology of ARDS
``` Damage to capillary endothelium Damage to epithelium Damage to both Microscopic clots Hyalin Membranes Neutrophils ```
34
What happens when Type1 capillary endothelium is damaged?
Increased permeability to capillary (Flash Pulmonary Edema) Flooding of fluid into the alveolus Loss of gas exchange function
35
What happens when Type2 capillary endothelium is damaged?
Decrease production of surface surfactant
36
What does the formation of microscopic clots in the lungs result in?
Decreased blood flow and oxygen levels
37
What inflammatory products do neutrophils produce?
Oxidants Proteases Platelet activating factor Leukotrienes
38
How does the body combat the damage produced by neutrophils?
Antioxidants Anti-proteases Anti-inflammatory cytokines
39
Symptoms of ARDS?
``` Dyspenea Tachypenea Cyanosis Respiratory failure/acidosis Bilateral fluid seen of chest x-ray ```
40
Mortality of ARDS?
30-70% mortality rate mostly due to sepsis mortality increases with age
41
How is the damage from ARDS resolved?
Reabsorption of fluids and removal of debris Replacement of epithelial cells Restoration of capillary endothelial cells
42
What is Acute Interstitial Pneumonia?
Cliniopathological term that is used to describe widespread acute lung injury. Think: ARDS with NO known etiology and progressive clinical course
43
Can ARDS and Acute Interstitial Pneumonia be differentiated histologically?
NO
44
Obstruction Airway Disease
Small airway expiration, air trapping, wheezing
45
Restrictive Airway Disease
Reduced lung volume, normal flow rate, reduced gas transfer, lungs loose elasticity from scaring
46
X-Ray appearance of Obstructive Airway Disease
Hyperextension of lungs, diaphragm is flattened, lucency and less dense
47
X-Ray appearance of Restrictive Airway Disease
Ground glass, opacity, more dense
48
Two major types of Restrictive Airway Disease
Chest wall disorders (normal lungs) | Interstitial and Infiltrative diseases
49
Forced Expansion Curve for Restrictive Airway Disease
Dec. total lung capacity = dec. FVC
50
Forced Expansion Curve for Obstructive Airway Disease
Dec. flow rate = FEV1 usually decreased
51
COPD
- Irreversible enlargement of the airspaces distal to the terminal bronchiole - Destruction of alveolar walls = Loss of elasticity - No obvious fibrosis
52
COPD includes?
Emphysema Chronic Bronchitis (Asthma, Bronchiectasis, Cystic Fibrosis)
53
4th most common cause of mortality and morbidity in US?
COPD
54
Population most susceptible to COPD?
women African Americans smokers
55
Forms of Emphysema?
Centrilobular | Panacinar
56
Centrilobular Emphysema
Central acini affected Upper Lobes In heavy smokers
57
Panacinar Emphysema
Uniformly enlarged acinai Lower, anterior lobes Occurs in alpha 1 antitrypsin deficiency
58
Alpha 1-Antitrypsin
Destroys elastases to eat everything in the lungs, present in serum tissue fluids and macrophages
59
Pathophysiology Emphysema
Mild chronic inflammation Inc. macrophages, T lymphocytes, Neutrophils Release of leukotrienes, IL-8, TNF
60
What inhibits Alpha 1 Antitrypsin?
oxidants and free radicals in smoke
61
What is the major source of cellular proteases?
Neutrophils
62
At what age does an Alpha 1-Antitrypsin deficiency typically cause emphysema?
teens and twenties
63
What does nicotine and ROS in smoke activate?
NF-k8 that activates TNF and IL-8 which attracts neutrophils that release granules rich in elastase that damage lung tissue Also enhances elastase in macrophages.
64
What do free radicles in tobacco deplete?
Antioxidants: SOD Glutathione
65
Emphysema manifests when how much functioning lung has been lost?
1/3
66
What happens when a bullea ruptures?
Pneumothorax
67
Pink Puffer
``` Weight loss Barrel-chest Pursed-lip breathing Expiratory airflow is limited Normal Pulse Ox Pt over ventilates ``` Develop cor pulmonale or CHF Death: Respiratory acidosis or coma, Rt. sided HF
68
Chronic Bronchitis
Persistent cough with sputum production for at least three months in at least two consecutive years, in the absence of any other identifiable cause
69
Morphology of Chronic Bronchitis - Similar to? - What predisposes a pt to CB
- Hyper-secretion of mucus in lg. airways - Similar to Emphysema - Cigarette smoking predisposes to infection
70
Histology of Chronic Bronchitis
Inc. thickness of mucous gland layer Inc. number of goblet cells Red. number of ciliated cells Infiltrate of lymphocytes
71
Blue Bloater
``` Persisten cough w/ sputum Dyspenea on exertion Cyanotic Respiration driven by O2 levels Hypoxemis Hypercapnia ```
72
What is asthma?
Chronic inflammatory disorder of the airways
73
Sx of asthma
Wheezing breathlessness chest tightness cough
74
What are the 4 histological findings in bronchial asthma? (5 if allergy related)
1. inflammation 2. bronchial narrowing 3. increased mucous 4. smooth muscle hyperplasia (5. ) increased eosinophils
75
Atopic vs. non-atopic asthma
``` Atopic= allergic non-atopic= infection ```
76
What are the hallmarks of asthma?
increased airway responsiveness to a variety of stimuli resulting in: 1. bronchoconstriction/spasm 2. inflammation of bronchial walls 3. increased mucus secretion
77
When time of day is asthma most common?
At night or early morning
78
Diagnosis of asthma
1. increased airflow obstruction 2. difficult prolonged expiration/wheezing 3. elevated eosinophil count in peripheral blood
79
What is status asthmaticus?
Rare condition, when there are unremitting attacks
80
What is the asthma hygiene theory?
Eradication of infections may promote allergic and other harmful immune responses.
81
Classification/Causes of asthma
1. atopic (seasonal) 2. non atopic 3. drug-induced 4. occupational asthma 5. exercise induced 6. asthmatic bronchitis (smokers) 7. respiratory infections 8. environmental exposure (irritants, cold air, stress, exercise)
82
Atopic asthma - When does it start? - What is it triggered by? - Prevalence? - Positive tests - What type of immune response?
- Often begins in childhood - Triggered by dust, mold, pollens, animal dander, foods - most common type - positive family history, skin testing, and RAST - Type I IgE mediated hypersensitivity
83
Non-atopic/Drug induced asthma - Allergic reaction? - Positive tests? - Triggers?
- No allergic reaction - skin test negative, gen. no family history - viral respiratory infections, air pollutants (SO2, ozone, NO2) are triggers
84
What is the Sampter's triad (aspirin)?
Asthma Rhinitis and nasal polyps Hives
85
What is the supposed mechanism of Sampter's triad?
Inhibition of COX but NOT LOX. | Favors bronchoconstriction.
86
What are causes of Occupational Asthma?
Fumes (plastics) Organic & chemical dusts (wood, cotton) Gases/Chemicals (formaldehyde, grains, yeasts, mold)
87
What is exercise induced asthma?
People who do not experience asthma under other circumstances
88
What is the cause of exercise induced asthma?
Extreme sensitivity to changes in temperature and humidity of air entering lungs
89
What are the two phases of Asthma?
Early & Late Phase
90
Early phase of asthma
Bronchoconstriction Increased mucus production Vasodilation/increased vascular permeability
91
Late phase of asthma
Secretion of mast cells, epithelial cells, and T-cells recruit: eosinophils, neutrophils, & T-cells Which causes INFLAMMATION
92
What does eotaxin do during the late phase?
Made from airway epithelium Chemo-attractant and activator of eosinohils
93
What does major basic protein do?
Causes epithelial damage and airway constriction.
94
What is airway remodeling?
Overtime, asthma changes the structure of the bronchial wall causing: - Hypertrophy & hyperplasia of mm. layer - Deposition of subepithelial collagen
95
What happens in the morphology of the lungs during asthma?
- Over distention | - Occlusion of bronchi and bronchioles by thick mucus plugs
96
What type of crystals are present in the mucus plugs in asthma morphology?
- Curschmann spirals | - Charcot-Leyden cystals
97
What is bronchiectasis?
- Dilation of the bronchus | - Not a specific disease, but a condition in which LARGE bronchi are damaged and DILATED due to variety of causes.
98
What is bronchiectasis associated with?
Necrotizing inflammation: - congenital - TB (other bact. or viruses) - BRONCHIAL OBSTRUCTION - RA, SLE, IBD, cystic fibrosis
99
What is bronchiectasis characterized by?
Chronic necrotizing infection/mucus hypersecretion/obstruction which leads to: - destruction of muscle and elastic tissue - permanent dilation of bronchi and bronchioles
100
SSx of bronchiectasis?
Cough Fever Copious expectoration of purulent sputum
101
What is the most common lethal genetic disease in Caucasians?
Cystic Fibrosis
102
What gene is mutated in cystic fibrosis?
CFTR (cystic fibrosis transmembrane conductance regulator gene) Which disrupts chloride ion transport of epithelial cells
103
Mutations in CFTR: | I, II, III, IV, V, VI
I: defective synthesis II: abnormal folding, process, trafficking III: defective regulation IV: defective conductance V: reduced abundance VI: altered regulation of separate ion channels
104
What happens in the sweat gland duct of CF patients?
Loss of CFTR decreases Cl- and Na+ ion resorption across epithelium of gland duct, producing hypertonic sweat. "Salty Sweat"
105
What happens in the airways of CF patients?
Loss of CFTR decreases Cl- movement into the lumen and increases Na+ and H20 absorption in lumen. - isotonic but dehydrated/over viscous surface - impairment of mucocillary clearance
106
Clinical manifestations of CF meconium ileus vs. pancreatic insufficiency
-varies in presentation, and age of onset. 5-10% meconium ileus: seen at birth or soon after. Small bowel obstruction due to mucus plug 85-90% pancreatic insufficiency: fat, protein, fat soluble vit. deficiency.
107
What is the most common cause of death in CF pt's?
persistent lung infections and cor pulmonale (80%)
108
What do recurrent sinonasal polyps indicate in children?
Happens in 25% of CF pt's. | -any children with polyps should be tested for CF.
109
What are some pulmonary manifestations in those with CF?
-thick mucous and repeated infections that lead to chronic bronchitis and bronchiectasis
110
Why has the life-expectancy over the last decades increased for CF pt's?
- Increased potency of antimicrobial therapy - Pancreatic enzyme supplementation - Availability of bilateral lung transplantation
111
What is the biggest category of restrictive lung diseases?
"Fibrosing" Follows inflammation but there's an absence of infectious organisms.
112
What are some examples of fibrosing pathologies?
- Idiopathic pulmonary fibrosis (IPF) - Nonspecific interstitial fibrosis - Cryptogenic organizing pneumonia - Collagen vascular disease - Pneumoconiosis - Drug reactions
113
What does reduced compliance mean in the lung?
The lung has lost some of it's elasticity and does not "comply" when moved by respiratory motions.
114
What is the problem with gas exchange in restrictive lung disease?
There are anatomic/functional barriers to gas exchange between endothelial cells and Type-1 pneumocytes.
115
What is IPF (idiopathic pulmonary fibrosis)?
chronic idiopathic inflammation of the alveolar walls with progressive fibrosis
116
What is the pathophysiology of IPF? (What's happening to the cells)
- Alveolar macrophages malfunction - Lung epithelial cells produce abnormal amount of PDFG - Alveolar glutathione levels reduced
117
What does the clinical picture look like for IPF?
-Progressive DOE -Non-productive cough -Crackles -Late: cor pulmonale, clubbing of nails Lung biopsy is usually required for a Dx.
118
What are the results of a CXR (chest xray) for IPF?
Diffuse, bilateral, fine linear opacities, mainly in the lower lungs
119
What does a CT show for IPF?
shows "honey-comb" like appearance due to small cystic lesions in the bases and periphery
120
What does the clinical course and Tx look like for IPF?
- course is progressive, survival of 4-6 ys after dx. | - steroids, cytotoxic drugs, supplemental O2
121
What is non-specific interstitial pneumonia?
It's a wastebasket diagnosis of ANY pneumonia of any known or unknown etiology.
122
What is cryptogenic organizing pneumonia (COP)?
- idiopathic - often occurs in transplanted lung - bronchiolitis obliterans
123
What is bronchiolitis obliterans?
is an inflammatory obstruction of the lung's tiniest airways, called bronchioles.
124
What are 3 examples of collagen vascular disease?
1. RA 2. SLE 3. Scleroderma
125
Pneumoconioses
Occupational lung disease - caused by the inhalation of particulate matter, chemical fumes, and vapors
126
Development of Pneumoconiosis is dependent on which 4 factors?
1. Amount of dust 2. Size and shape of particulate 3. Solubility and Reactivity of particulate 4. Effects of other irritants (tobacco)
127
The most dangerous particles are what size?
between 1 and 5 micro m
128
What happens to particles > 5 micro m
They are trapped in the upper airway and removed by ciliary action and expectoration
129
What happens to particles
Removed by macrophages, neutrophils and lymphatics
130
Restrictive Lung Disease
Inhalation -> Inflammatory response -> fibrosis
131
What is the most common chronic occupational disease in the world?
Silicosis
132
What causes Silicosis
Inhalation of silicon dioxide crystals (sand blasters, foundry workers, stone cutters, etc.)
133
How do the tetrahedral silica crystals damage the epithelial cells?
- Chemical reactivity leads to lipid oxidation, free radicle generation and protein denaturation. - Macrophages induce inflammations - Fibroblasts proliferate and produce collagen around particles
134
What is the pathognomonic sign for Silicosis?
Egg shell calcifications of the hillier lymph nodes
135
SSx of Silicosis
- Develops slowly (can have acute or accelerated ) - Asymptomatic with cough - SOB in late stages - Can worsen without continued exposure
136
Caplan's Syndrome
Pneumoconiosis coexists with rheumatoid arthritis (from asbestos, silicosis, coal worker's pneumonia)
137
What develops with Caplan's Syndrome?
Large pulmonary nodules with centers that crack open
138
Asbestos
Hydrated crystalline silicate fibers (exposure in mining, ship yard work, insulation workers, brake line workers)
139
How do asbestos fibers cause damage in the lungs?
Needle shaped crystals traverse the lung, enter the interstitial and impale the pleural lining
140
What are Ferruginous bodies?
Asbestos fibers in the lungs that are coated with proteins and appear red in color.
141
Pleural Plaques
Large, dense plaques that form on both sides of the pleural surface, found in pts with asbestos.
142
Asbestos workers are at 5x greater risk for what?
Bronchogenic Carcinoma If they also smoke, 55x greater risk
143
Mesothelioma
Rare tumor of the pleura almost always associated with asbestos exposure Smoking does not appear to raise the risk.
144
Berylliosis
Exposure to beryllium in the aerospace, nuclear and defense industries. Not as common today, due to lack of mines.
145
Acute Berylliosis
Rare
146
Chronic Berylliosis
- Due to cell mediated immune response | - Genetic susceptibility (only 2% of exposed workers develop disease)
147
Coal Workers Pneumoconiosis
Coal deposition in the lung parenchyma. | Rarely serious unless additional pathology is present (TB)
148
Anthracosis
Milder form of CWP found in urban populations and smokers.
149
Black Lung Disease
When CWP progressed to more severe diffuse pulmonary fibrosis
150
Siderosis
From inhalation of iron oxide.
151
What are the 3 types of Granulomatous?
1. Sarcoidosis 2. Non-Caseating Granulomas 3. Hypersensitivity
152
Sarcoidosis
Granulomatous disorder that affects the lungs, eye (25%), skin (25%), liver (70%), heart, lymph nodes (25-50%) or anywhere
153
What are the characteristic lung findings of Sarcoidosis?
- Non-caseating granulomas with Asteroid Bodies | - Bilateral hilar lymph node enlargement
154
Who is most likely to get Sarcoidosis?
20-40 yo Females African Americans Northern European descent
155
What common skin lesion is found on pts. with Sarcoidosis?
Erythema nodosum
156
If the heart is affected in pts with Sarcoidosis what do they dies from?
Cardiac complications
157
What abnormal labs are found in pts with Sarcoidosis?
Elevated Vit D Hypercalcemia Elevated angiotensin converting enzyme
158
How does Organic pneumoconiosis develop?
As an allergic rxn to inhaled organic dusts that may contain spores, fungi, animal proteins or bacterial products
159
What types of rxns are Organic Pneumoconiosis?
Type 1: IgE Type 3: IgG Type 4: cell mediated
160
Is Organic Pneumoconiosis a more acute to chronic response, compared to other pneumoconiosis?
Acute
161
Actinomycetes Spores
Found in damp harvested hay | Farm workers lung
162
Bagassosis
Hypersensitivity RXN to mold found in sugar cane
163
Byssinosis
Allergic response to airborne fibers of cotton, linen, flax and hemp
164
What do the acute sx of Organic Pneumoconiosis resemble?
Bronchial asthma with wheezing and cough
165
Pulmonary Alveolar Proteinosis
Like pulmonary edema, with a lot of protein, Very rare Minimal cellular inflammatory infiltrate
166
PE's are usually secondary to what two disease states?
1. debilitated states with immobilization | 2. following surgery
167
What veins do PE's generally arise from?
deep leg and deep pelvic veins.
168
Do PE's generally infarct?
No, they generally ventilate
169
What type of infarction will a PE be?
Hemmorrhagic
170
98-99% of emboli are due to what?
dislodged thrombus
171
Is it a perfusion or diffusion problem with PE's?
Perfusion
172
Causes of PE's
- deep vein thrombosis - long standing IV line catheters - pro-thrombogenic blood diseases
173
Do thrombi lyse in the lung?
Immediate lysis occurs and is complete within days to weeks
174
What is PE cardiogenic shock?
emboli occludes >50% of arterial supply to lung. | Death occurs in hours
175
What is a saddle emboli?
emboli blocks the bronchial tree, death can occur in minutes
176
What influences the probability of death in PE's?
emboli size | location and pt's preexisting cardiopulmonary status
177
What is the % of reoccurrence when treated with anticoagulants?
5-20% fatality
178
What do fat and amniotic fluid emboli obstruct?
microcirculation (arterioles and capillaries)
179
Can an emboli induce ARDS?
An emboli in the microcirculation can induce ARDS
180
What % of cases are clinically silent in fat emboli?
90%
181
How many days does it take for symptoms to appear from fat emboli after surgery?
1-3 days
182
What are symptoms of a fat emboli?
Tachypnea, dyspnea, tachycardia
183
What is the problem with obstructive lung issues?
INCREASE in density.
184
What % of emboli actually cause infarction?
185
Morphology of pulmonary infarction
- hemorrhagic consolidation - necrosis of lung tissue - wedge/pie shape infarct - tissue fibroids
186
Sx of PI
- cough - hemoptysis - pleuritic chest pain - fever * severe hypotension occurs with cardiogenic shock*
187
Are routine CXR helpful in diagnosis a PE?
NO. Least helpful.
188
Pulmonary Hypertension
- arterial system in lungs becomes resistant to blood flow - increasing pressure within pulmonary circulation - limited blood flow
189
What is the etiology of primary pulmonary hypertension?
arterial wall thickening and obliteration of lumen of medium and small pulmonary arteries
190
Etiology of secondary PH
- thickening of entire arteriole system | - other cardiac/pulmonary conditions
191
What is the pathophysiology of PH?
- damaged endothelial cells release cytokines & GF - decrease in NO production - hypoxic vascular response
192
What is the hypoxic vascular response?
Diminished oxygenation can cause further vasoconstriction
193
What is cor pulmonale?
Rt. ventricle failure secondary to lung pathology
194
Risks for PH?
- ARDS - sleep apnea - high altitudes - Crotalaria - emphysema
195
Tx for PH?
- supplemental oxygen and vasodilator drugs - iloprost - lung transplant
196
What is the disease prognosis?
1-5 years from time of diagnosis
197
Goodpasture Syndrome?
- multi-system disease that involves lungs and kidneys | - Ab to alveolar and glomerular basement membrane (leads to hemoptysis and hematuria)
198
Tx of goodpasture syndrome
- steroids, cyclophosphosphamide, and plasma phoresis | - renal transplantation if disease is just in kidneys
199
Prognosis of goodpasture syndrome
days to weeks if resistant to tx.
200
What is Wegener granulomatosis?
-form of vasculitis that affects lungs, kidneys, other organs
201
What is the most common cause of a hemorrhagic part of the lung?
Infarct
202
Does pneumonia occur in otherwise healthy people?
No. Suggest underlying issue.
203
Classifications of Pneumonias
- community acquired - nosocomial - aspiration - chronic
204
Risk factors for pneumonia
1. condition leading to diminished cough/gag reflex 2. mucociliary elevator dysfunction/damage 3. accumulation of secretions 4. decrease in phagocytic/bactericidal actions of alveolar macrophages
205
Sx. of Pneumonia
- URI sx. may procede - cough - fever - fatigue/myalgia
206
PE of pneumonia
fever, tachycardia, tachypnea, signs of lung consolidation
207
What is the most common lethal nosocomial infection?
Pneumonia
208
What is the major cause of death in developing countries (2nd to diarrhea)? Of children?
Pneumonia
209
Community acquired pneumonia pathogens
- strep. pneumoniae - H. influenza - M. catarrhalis - S. aureus
210
What is the most common community acquired pneumonia pathogen?
S. pneumoniae
211
Congestion in bacterial pneumonia
- protein leaks into interstitium | - intra-alveolar fluid
212
Consolidation in bact. pneumonia
Exudative reaction and subsequent solidification
213
What are the 3 patterns of gross anatomic distribution
- lobar (entire lobe) - lobular (part of lobe) - bronchopneumonia (patchy)
214
4 stages of inflammatory response in lobar pneumonia
1. congestion 2. red hepatization 3. grey hepatization 4. resolution
215
What is red hepatization?
- RBC, exudate, neutrophils, fibrin fill alveolar spaces | - looks red, firm, airless
216
What is hepatization?
consistency resembles liver tissue
217
What is grey hepatization?
- RBC disintegration, increased fibrinization - persistent neutrophils, fibrin, suppurative exudate - alveoli consolidated - appears greyish, brown,and dry.
218
Streptococcus
classic LOBAR pneumonia
219
Haemophilus pneumonia
most common pneumonia from COPD in adults
220
Moraxella catarrhalis
2nd most common COPD pneumonia after haemophilus
221
Staph areus
most common pneumonia following viral pneumonias
222
Klebsiella pneumoniae
Alcoholics with pneumonia are thought of having Kleb. until proven otherwise
223
Pseudomonas aeruginosa
CF pts are presumed to have this pneumonia until proven otherwise
224
Legionella
- often in outbreaks - spread by water droplets - common on cruise ships
225
Are cultures helpful in community acquired pneumonia?
No.
226
What is community acquired atypical pneumonias? Examples.
caused by less typical pathogens | -mycoplasm pneumoniae is most common
227
Are viral pneumonias interstitial or alveolar?
interstitial
228
What is the most common viral pneumonia in children?
RSV
229
Most common viral pneumonia in adults?
Influenza A or varicella-zoster
230
RSV pneumonia causes formation of what unique cell type?
Giant cells
231
SARS
- corona virus | - 2002 China outbreak
232
In order to have an MRI, what conditions do you need to meet?
2/3 1. Sx of chest pain 2. elevated cardiac enzymes 3. abnormal EKG
233
What type of pneumonias typically lead to abscesses?
Aspiration pneumonias
234
Who are most susceptible to aspiration pneumonias?
- unconscious pts - prolonged bed rest - inability to swallow/gag
235
What is a pulmonary abscess?
localized infectious process characterized by necrosis
236
Histopathology of pulmonary abcesses
-suppurative destruction of lung parenchyma with central cavitation

Pathology 2 (1 decks)

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