Pathology Of The Respiratory System - Dr. Singh Flashcards
(150 cards)
1
Q
Alveoli walls
A
Thin walls + high vascularity
2
Q
Epithelium is respiratory tract
A
Have cilia har sticking up
Mucous Blobs = goblet cells
3
Q
Under respiratory epithelium is what
A
- SM and Submucosal glands
2. Cartilage is under that (chondrocytes)= holds open the trachea ridgedly
4
Q
Type 1 pneumocytes do what
A
Gas exchange (they are very thin and line up with the capillary epithelial cells)
5
Q
Type 2 pneumocytes do what
A
Make surfactant (also develop later in fetus) Replace type 1 pneumocytes (can become stem cells for type 1 cells)
6
Q
Alveolar Pores of Kohn
A
Allow Air, bacteria, fluid, cells or travel between alveoli
7
Q
Pulmonary Hypoplasia is what
A
Lungs dont stretch down to apex of heart
And dont grow as big = should be about x2 size of heart)
8
Q
What can cause pulmonary hypoplasia
A
Diaphragmatic hernia
Low amniotic fluid levels in uterus ——> pulmonary hyperplasia + renal agenesis**
Airway malformation (tracheal stenosis)
Arthrocoposis (strictures preventing baby from expanding chest wall)
9
Q
Immediate death from hypoplasia of lung happen at how many %
A
40 % or less lung weight compared to normal lung weight
10
Q
Foregut cysts are what
A
Outpouching of foregut (respiratory—> ciliated epithelium , esophageal——> squamous epithelium, gastroenteric——> glandular epithelium)
= incidental outpouchings
11
Q
Foregut cysts risks and complications
A
- rupture
- infection
- airway compression
12
Q
Foregut cysts look like what on CT
A
Air-fluid level line inside it (shows there is fluid inside)
13
Q
Congenital Pulmonary Airway Malformation (CPAM) Congenital Cystic Adenomatoid Malformation (CCAM)
What happens and types
A
*Arrested development* of pulmonary tissue + intrapulmonary cysts formation (the stage/type it arrests at is where it keeps cycling and forming a mass of that tissue instead of developing down to distal acinar) Type 0 : Trachebronchial Type 1 : Bronchial Type 2 : Bronchiolar Type 3 : Alveolar duct Type 4 : Distal acinar
14
Q
Congenital Pulmonary Airway Malformation (CPAM) Congenital Cystic Adenomatoid Malformation (CCAM) some deatails about how it can be seen and how it communicates and risks
A
- Communicates with treachebronchal tree
- Fetal US detection
- Hydrops, pulmonary hypoplasia, infection later in life
15
Q
Congenital Pulmonary Airway Malformation (CPAM) Congenital Cystic Adenomatoid Malformation (CCAM) TX
A
Remove before it gets infected of becomes a tumor = lobectomy DX inutero
16
Q
Pulmonary Sequestration is what
A
An extra lobe is formed usually on the left side (non functioning lung tissue “Lung Bud”
= NO COMMUNICATION with treacheobronchial tree + independent arterial supply
17
Q
Intralobar pulmonary sequestration is what
A
Extra lobe formed inside on of the lobes
= has its own blood supply
= not really connected to trachea or bronchus however can have its small own brachial branch however not enough O2 so INFECTIONS + abscess are easily formed
18
Q
Intralobar pulmonary sequestration dx when
A
Usually hides and not until older children or adults
19
Q
Extralobar pulmonary sequestration
A
Extra lobe forms outside the other lobes
= own blood supply and can have a small own airway attached + OWN PLEURA = abscess and infection easily
= you see mass lesion in chest or abd
20
Q
Extralobular pulmonary sequestration dx when
A
Usually after birth with other congenital conditions
21
Q
Other anomaly that can be present with a extralobular pulmonary sequestration
A
Diaphragmatic hernia
22
Q
Atelectasis is what
A
Lung parenchyma cant expand and is acquired
23
Q
Resorption Atelectasis
A
Airway obstruction (tumor, mucous,….) + gradual resorption of air = reducing lung expansion = most common = obstructive
24
Q
Compression Atelectasis
A
Material accumulation in pleural cavity = compression of lung parenchyma
25
Contraction Atelectasis
Fibrotic or other restrictive process in pleura or peripheral lung = restricting lung expansion
= pleural fibrosis most common form
26
Pulmonary edema looks like what on histology
A lot of pink more then white, increase in epithelial cells = Left side HF since more P in the BVs + congestion
27
Pulmonary edema what causes it
1. Left sided HF****, pulmonary V obstruction
2. Hypoalbuminemia , nephrotic syndrome, liver disease = fluid leaks out
3. Bacterial, sepsis, smoke, aspiration = alveolar wall injury
4. high altitude + CNS injury
28
Gas exchange in Pulmonary edema
Alveolar spaces = lower O2 exchange
29
Heart failure cells
After a while of Pulmonary edema , microhemorrhage in alveoli = M accumulate (hemosiderin-laden) ——-> look brown
= in HF and CHF chronic
30
ALI (Acute Lung Injury)
Acute hypoxemia, bilateral infiltrates (PaO2/FiO2 < 300)
| = no cardiac failure
31
ARDS
= acute respiratory distress, bilateral infiltrates
= worsening hypoxia ( PaO2/FiO2 < 200)****
= no cardiac problems
32
DAD (Diffuse Alveolar Damage)
The histologically findings of ARDS
33
What can cause ARDS
1. Sepsis
2. Diffuse pulmonary infections
3. Gastric aspirations
4. Trauma injury (including head)
5. Pancreatitis
6. Toxins (like E cigs)
34
What happens in ARDS from cellular level
Edema in alveoli = from damage at endothelial cells of alveoli + capillaries (from Blood circulation)
= N activation and come inside alveoli = kill type 1 cells
= fluid + hyaline membranes form**** from alveolar damage
= NOT from lung itself
35
Hyaline membrane form as from what
Edema+ Fibrin + cellular debri
= DAD (diffuse Alveolar Damage)
= ventilation - perfusion mismatch
36
ARDS can lead to what
Fibrosis (irreversible) or resolution
37
ARDS death rate
40 % die in exudate stage (edema and hyaline membrane ) before the proliferation stage (fibroblasts and pneumonia, early fibrosis)
= Fibrotic stage is last and if reached can never be reversed
38
Neonatal RDS
= reduced surfactant
= hypoxemia
= pulmonary hypoperfusion —> endothelial damage
= you can see Hyaline membranes *****
39
Restrictive Lung Disease is what and pulmonary function test you see what
Restriction in expanding = V restriction
= FEV1/FVC normal
= FVC reduced
= TLC decreased
40
Obstructive Lung Disease is what and PFT you see what
```
Exhalation problem
= decreased air flow
= Low FEV1/FVC
= TLC increase
= FEV1 decreased
```
41
Restrictive Lung Disease also called
Interstitial lung disease (disease between alveoli)
42
3 common Obstructive Lung Diseases
1. COPD (chronic bronchitis)
2. Emphysema
3. Asthma
43
What happens to cause COPD
1. Toxins causing more mucous to form to protect airway and get rid of it
2. Thickening of the muscle around airway + mucous buildup = narrowing of tract
3. This irritates and damages the airway, inflammation
44
Chronic Bronchitis is defined as what
Cough + sputum production for 3 months in 2 consecutive years
= mucous gland hyperplasia ——> damages the airway
45
Reed index
How hick the submucosal layer is in the respiratory epithelium
= to see if there is chronic bronchitis
46
What neoplasm can form from chronic bronchitis
Squamous metaplasia ——> dysplasia ——> carcinoma
47
Emphysema is what location
Irreversible airspace enlargement distal to terminal bronchiole
48
Centrilubular emphysema is seen when
Smoking
49
Panlobular emphysema is seen in when
A1-antitrypsin deficiency
50
Chronic bronchitis can cause what in smokers
Damages the alveolar walls + alveoli collapse due to contraction upstream = air trapping = centrilobular
= chronic bronchitis traveling down from the bronchus
51
Reason smokers have contrilobular emphysema
Started at terminal bronchus (constricted with mucous)——> dilation starts at respiratory bronchiole and travels down
52
CXR and physical look of emphysema
Black lungs
| = barrel chest ( square like chest)
53
Auscultation of emphysema
Exaltation wheezing
| = flow graph shows (chair looking graph)
54
Blue Bloaters
CHRONIC BRONCHITIS
1. Productive cough
2. Elevated Hb (from CO in smoke causing less O2 delivery)
3. Peripheral edema and higher BMI
4. Rhonchi + wheezing
5. Cyanotic
55
Pink Puffers
EMPHYSEMA
1. Older, thin
2. Severe dyspnea
3. Quite chest (not as much wheezing due to expanded air spaces)
4. Air hunger. Pursed lips, tripod posture
56
A1- antirtypsin deficiency what happens
1. Liver making A1- AT does not make or transport out it right = lever damage
2. Also A1-AT needed in lungs to protect it from Neutrophilic Elastase (during infection or when N are needed they secrete Elastase that damage the respiratory tract walls, only A1-AT can protect the walls from this)
57
A1-AT deficiency what do you see in location
Emphysema is panlobar (starting at the alveoli level), moving up to respiratory bronchus eventually
= also more in the lower lobes
(Where more BF is)
58
Spontaneous Pneumothorax location
Distal acinar (only Alvoli)
59
A1- AT deficiency hesitance and gene
Chr 14 Pi gene = normal
Pizz (homozygous for it)
Autosomal Recessive
60
Asthma what happens
Reversible with bronchodilator
Inflammation + hyper-responsiveness
= muscle constriction
= mucous hypersecreation
61
Atopic Asthma is from what
Extrinsic
1. 2/3 pts
2. Childhood + any age
3. high IgE (type 1 hypersensitivity)
- E, Mast cells, Lymphocytes
4. Allergens cause this
5. FH link
62
non-Atopic Asthma
Intrinsic
1/3 pts
= older pts
= normal IgE levels so not allergy induced
= cold and exercise and infection can cause it
63
Steps of how Asthma comes on
1. Allergen = exaggerated Th2 cells response
2. IL4 and IL5 secreted and tells B cells to make IgE
3. Mast cells secrete IL5
4. Eosinophils come —> release granules (on second exposure)
64
Leukotrines do what
1. Bronchoconstrict (also uses PGE, Ach, Histamine)
2. Mucous secretion
3. Increase vascular permeability
65
Interleukins do what
Recruit inflammatory cells
66
When you go to doctor and the pt has asthma what do they need to do
Take asthma control test
= to see if asthma is controlled or not
= important because if not controlled then there are many long term effects
67
Asthma uncontrolled effects
1. Airway remodeling (fibrosis, SM hyperplasia, increased goblet cells + submucosal glands)
= bronchodilators and corticosteroids stop working on these pts
68
Status Asthmaticus what is it and what do you see
1. Asthma attack that does not stop, mucous completely obstruction airway,
= fatal asthma attack
2. Curschmann spirals (coiled thick mucous plugs), Charcot Leyden crystals (E granules and breakdown products)
69
Genetics + environment associated with atopic Asthma
- seasonal allergies
- eczema
= pollution
= X allergen exposure at early age
= early infections
70
Aspirin Sensitive Asthma
BLOCKED COX 1 + 2 = Arachidonic Acid goes towards 5-Lipoxygenase pathway which increases leukotreins
= increased bronchospasm
= increased chemotaxis
= SAMTERS TRIAD
71
SAMTERS Triad
1. Nasal polyps
2. Recurrent rhinitis
3. Aspirin sensitive Asthma
72
Bronchiectasis
Chronic inflammation causing destruction of proximal bronchi = permanently dilated airways
1. Dilated diameter
2. More mucous
3. Destroyed airway wall
4. Loss of cilia
73
What can cause Bronchiectasis
1. Allergic Bronchopulmonary Aspergillosis (ABPA)
2. CF
3. TB
4. Primary Ciliary dyskinesia
74
CF in lung
CL- not leaving
= Na and H2O goes into cells
= mucous is dehydrated and thick and bacteria easily infects it, sticks to everything, cant be cleared
75
Bronchiectasis what do you see on the lung
The bronchioles are so dilated they go all the way to the periphery of the lungs
76
Kartageners Syndrome
Primary Ciliary Dyskinesia
| = dynein arm not working (in microtubules ——> X flagella and cilia) = X cilia in respiratory tract
77
Kartageners Syndrome TRIAD
1. Sinusitis
2. Bronchiectasis
3. Situs inversus (heart is on right side , gastric bubble on right side = which should be on left done by cilia in fetus)
= often male infertility is also another problem
78
CF infertility
X vas deferons
79
Allergic Bronchopulmonary Aspergillosis
= lives in airspace’s ——> exagggerated hypersensitivity response
= IgE is made and try to destroy it
= usually in pts with asthma or CF
= thick dark mucous in bronchi ——> bronchiectasis in advanced disease
80
Allergic Bronchopulmonary Aspergillosis DX
+ skin test
Septal hyphae with acute angle (like a tree)
(Aspergillosis does many more things like fungal ball)
81
what causes Bronchiectasis
1. CF
2. Allergic Bronchopulmonary Aspergillosis
3. Primary Ciliary Dyskinesia
82
Idiopathic Pulmonary Fibrosis
1. Waves in inflammation
| 2. Usual Interstitial Pneumonia * pattern in histology , normal + inflammation + organizing pneumonia + fibrosis areas
83
4 things seen in usual Interstitial Pneumonia
1. Normal areas
2. Inflammation
3. Fibroblast foci (fibrosis) (pink)
4. Peripheral honeycombing (circular thing looking)
84
Factors that lead to Idiopathic Pulmonary Fibrosis
1. Smoking, industrial societies
2. Genetics
3. Over 50yo (with increasing dyspnea)
85
Idiopathic Pulmonary Fibrosis DX and type of lung disease
RESTRICTIVE LUNG DISEASE
= biopsy and see the usual Interstitial Pneumonia pattern
= CT scan
86
Idiopathic Pulmonary Fibrosis SX
1. Velcro- like crackles (both inspiratory and expiratory)
2. SOB
3. PFT restrictive pattern (decreased FEV1 and TPV, normal FEV1/FCV)
4. Honeycomb lung from basilar infiltrates ****
87
End stage Idiopathic Pulmonary Fibrosis is seen how
Basilar infiltrates = honeycomb fibrosis (spaces with thick areas around them)
88
Idiopathic Pulmonary Fibrosis TX
TGF-B inhibitors
Lung transplant
(3-5 years)
89
Non-Specific Interstitial Pneumonia compare to UIP
Only uniform infiltrates no fibrosis (higher prognosis then UIP)
Also idiopathic
90
Non-Specific Interstitial Pneumonia histology
Uniform pattern
| Fibrosis and inflammation = thickening spaces between alveoli (plasma cells and lymphocytes)
91
Non-Specific Interstitial Pneumonia risks
Can go on and become more fibrotic = harder to treat
| Otherwise just treat with steroids and ant inflammatory agents
92
Cryptogenic Organizing Pneumonia what happens
Called bronchiolitis obliterans organizing pneumonia
| = from a previous infection or inflammatory process
93
Cryptogenic Organizing Pneumonia SX
1. Pneumonia like consolidation
| 2. 5th and 6th decade in life
94
Histology of Cryptogenic Organizing Pneumonia
1. White loose fibro-CT tissue plugs = circular fibroblasic foci (MASSON BODIES)
= one component of UIP
95
Cryptogenic Organizing Pneumonia can be confused with what
You see the Masson bodies and that is what you see in infection, tumor, drug/toxin induced lung injury
= however rule this out by seeing no inflammation and widespread fibroblastic foci areas
96
Cryptogenic Organizing Pneumonia to
Oral steroids cures it
97
Autoimmune lung disease is in what category
CT disease (Interstitial lung disease)
1. RA
2. Systemic sclerosis
3. SLE
98
Sarcoidosis histology
Non-caseating non-necrotising granulomata
99
Sarcoidosis
Histiocytes making granulomas
| = multinucleated giant cells
100
How to you see Sarcoidosis in CXR
1. Hilar lymphadenopathy (white consolidation next to the branching of the lobes)
2. There can also be in pulmonary infiltration also
101
Sarcoidosis risk
Stage 4 pulmonary fibrosis
102
Sarcoidosis histology
1. Granulomas + giant cells
2. Asteroid Body (pink fuzz ball inside the Giant cell) = debri
3. Schaumann body (purplish blob inside the giant cell) = calcification
103
Sarcoidosis prevalence
- under 40yo
- AA
- involves lungs usually
- elevated ACE levels
104
Sarcoidosis development
Not in stages (some are progressive to fibrosis)
105
Hypersensitivity Pneumonitis histology
1. A bunch of inflammation everywhere (purple dots all over)
106
Hypersensitivity Pneumonitis is what
1. Immune reaction to inhaling Ag
- Pigeon -breeder lung (bird poop protein)
- Farmers lung (Actinomycetes spores)
- Hot tub lung (MAC reaction)
= not infection, hypersensitivity
(Vape, hairspray, work inhalants, wind instrument bagpipes)
107
Hypersensitivity Pneumonitis causes
Airway centered granulomata associated with lymphocytes
108
4 smoking related lung diseases
1. Idiopathic Pulmonary Fibrosis
2. Desquamative Interstitial Pneumonia
3. Respiratory Bronchiolitis - Interstitial Pneumonia
4. Langerhans Cell Histiocytosis
109
Desquamative Interstitial Pneumonia Histology and type of lung disease
```
RESTRICTIVE
1. Stuffed alveolar spaces
2. Alveoli FULL OF M cells = plug the alveoli
= 5th-6th decade
= from smoking
```
110
Desquamative Interstitial Pneumonia TX
Corticosteroids
Stop smoking
Good prognosis (survive at 5years)
111
RB-ILD (Respiratory Bronchiolitis Interstitial Lung Disease) is what
3rd -4th decade in life
= smoking related
= baby part of DSIP less symptomatic
112
RB-ILD (Respiratory Bronchiolitis Interstitial Lung Disease)DX
CT scan = early interstitial lung disease seen
1. M some
2. Peribronchial metaplasia (abnormally located ciliated cells)
3. Some fibrosis if advanced
113
RB-ILD (Respiratory Bronchiolitis Interstitial Lung Disease)TX
Stop smoking + steroids
114
Langerhans Cell Histocytosis is what
= Stellate lung lesions *****
| = scarring ——> big many cysts that can rupture and cause pneumothorax
115
Langerhans Cell Histocytosis histology
1. E*
2. Langerhans cells*
3. Fibrosis and cysts
= stain with S-100 and CD1a+ ********
116
Langerhans Cell Histocytosis TX
Stop smoking
117
Pulmonary Alveolar Proteinosis what happens
= X surfactant metabolism = defected granulocyte-M colony stimulating factor (GM-CSF)
= autoimmune, secondary, hereditary
= surfactant Protein accumulates throughout the alveoli and airspaces
118
Pulmonary Alveolar Proteinosis prevalence
Young -mileage female autoimmune prone
119
Pulmonary Alveolar Proteinosis TX
GM- CSF given SubQ
| Steroids or IVIG
120
Pulmonary Alveolar Proteinosis histology
Alveoli full of surfactant protein (light pink stuff) looking like edema
121
Pulmonary Alveolar Proteinosis DX
Bronchioloalveolar lavage is done and pulling out a bunch of milky looking surfactant and protein from it fluid, from the alveolar spaces
122
Pneumoconiosis happens from what
1. Occupational exposure (in this case I have to find out all who have been exposed)
2. Air pollution
= some pts have more exaggerated response
123
Pneumoconiosis is worse in who
Smokers (ciliary clearance)
Smaller particles
High and repetitive exposure to toxins
124
Coal Workers Pneumoconiosis 3 conditions that these patients can get
1. Anthracosis (accumulation of coal pigment)
2. Coal Macules / Nodules
3. Progressive Massive Fibrosis (advanced and fatal stage, usually does not progress there unless Smokey Coal to heat cabins and homes DO PROGRESS)
125
Silicosis comes from what
Inhaling silicon dioxide (mining , concrete repair, demolition) = HIGH CHANCE CANCER
126
Silicosis what happens
```
SLOW progressive (even after exposure is gone) fibrosis
= silica deposits in collagenous nodules* + calcification (EGGSHELL CALCIFICATIONS)*
```
127
Silicosis on CXR or CT
Circles at the hilum are seen = eggshell calcifications
| CT : rings white that are seen in the fibrotic area
128
Silicosis location
Fibrosis is more upper lobular location
129
Coal miner pneumoconiosis and cancer
No link unless bituminous coal
130
Asbestosis caused by what
```
Inhaling asbestos fibers
= Insulation workers
= shipyard navy workers
= paper mill workers
= Oil or chemical refinery worker
```
131
Asbestosis diseases it causes
1. Pleural fibrosis, effusion, mesothelioma
2. Lung interstitial fibrosis, carcinoma
3. Other cancers (like liver)
132
Asbestos fibers are dangerous for hat reason and histology
They are thin and straight = easy to travel down and are nerves removed
= Asbestos Bodies (FERRUGINOUS BODIES)
= look like brown straight lines with some beads on it (M that is the beading on it)
133
Pleural plaque formation happens in what condition and what does it look like on histology
Asbestos
| = Candlewax dripping on pleura , hyalinized collagen
134
Mesothelioma associated with what
Asbestos even after decades after exposure
= cancer in the lungs
= can come from the pleural plaques
135
What does a PE look like in the CXR
1. Wedge shaped lesion that’s white = small PE
Or a red infect that’s also wedged shaped
2. Saddle PE = fatal right HF from big PE
136
Lines of Zahn
How you can tell if pt died from coagulation from death or if it was the cause of death
= IF CAUSE OF DEATH ——> lines of alternating red (RBCs) and white (plt, fibrin)
137
Angiography of PE
Contrast does not go down all the way to the smallest vessels only in big branches
138
BM emboli
Cause PE from trauma or chest compressions (you see fat and lymph cells)
139
Talc Embolism
Drugs takes by IV can cause a shiny looking PE
140
Septic emboli
```
Can happen form IV drug use
Can also happen from endocarditis
= infective material ABSCESSES in blood ——> PE
= valve vegetation ——> PE
1. Jane way lesions
2. Roth spots
3. Splinter hemorrhages
```
141
Pulmonary HTN is what
Pulmonary Artery P > 20mmHg
142
Pulmonary HTN happens when
1. More genetic young pts primary vascular disease
2. Left HF
3. . hypoxia or Chronic Pulmonary parenchymal disease
4. From PE
143
Pulmonary HTN histology
1. Knotted BVs = PLEXIFORM LESION
| 2. Medial hypertrophy (SM in vessels)
144
3 Pulmonary Hemorrhage Syndromes
1. Goodpasture Syndrome
2. Granulomatosis with Polyangitis (Wagner granulomatosis)
3. Idiopathic Pulmonary Hemosiderosis
145
Pulmonary Hemorrhage Syndrome histology
Hemosiderine stained M in lungs and blood hemorrhaging
146
Goodpasture Syndrome what happens and histology
ABs attacking collagen4 on BM = linear immunofluorescence study
+ you see the RBCs around the linear staining in histology
= TYPE 2 hypersensitivity
147
Goodpasture Syndrome prevalence
Male younger age 2nd-3rd decade
| = AB against collagen 4 on BM
148
Goodpasture Syndrome attacks what organs
Lungs and Kidneys
149
Granulomatosis With Polyangiitis
Wagners Disease
= granulomatous inflammation that can hemorrhage (can look like pneumonia)
= a lot of bleeding in the lung
= BV necrotizing granuloma
150
Granulomatosis With Polyangiitis prevalence
Male over 40yo
= ANCA +
= saddle nose necrotizing granulomatous
= bleeding in lung alveoli
