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CPR 2 Exam 2 > Pathology Of The Respiratory System - Dr. Singh > Flashcards

Pathology Of The Respiratory System - Dr. Singh Flashcards

1
Q

Alveoli walls

A

Thin walls + high vascularity

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2
Q

Epithelium is respiratory tract

A

Have cilia har sticking up

Mucous Blobs = goblet cells

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3
Q

Under respiratory epithelium is what

A
  1. SM and Submucosal glands

2. Cartilage is under that (chondrocytes)= holds open the trachea ridgedly

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4
Q

Type 1 pneumocytes do what

A

Gas exchange (they are very thin and line up with the capillary epithelial cells)

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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)
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6
Q

Alveolar Pores of Kohn

A

Allow Air, bacteria, fluid, cells or travel between alveoli

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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)

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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)

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9
Q

Immediate death from hypoplasia of lung happen at how many %

A

40 % or less lung weight compared to normal lung weight

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10
Q

Foregut cysts are what

A

Outpouching of foregut (respiratory—> ciliated epithelium , esophageal——> squamous epithelium, gastroenteric——> glandular epithelium)
= incidental outpouchings

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11
Q

Foregut cysts risks and complications

A
  • rupture
  • infection
  • airway compression
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12
Q

Foregut cysts look like what on CT

A

Air-fluid level line inside it (shows there is fluid inside)

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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
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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
  1. Communicates with treachebronchal tree
  2. Fetal US detection
  3. Hydrops, pulmonary hypoplasia, infection later in life
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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

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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

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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

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18
Q

Intralobar pulmonary sequestration dx when

A

Usually hides and not until older children or adults

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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

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20
Q

Extralobular pulmonary sequestration dx when

A

Usually after birth with other congenital conditions

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21
Q

Other anomaly that can be present with a extralobular pulmonary sequestration

A

Diaphragmatic hernia

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22
Q

Atelectasis is what

A

Lung parenchyma cant expand and is acquired

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23
Q

Resorption Atelectasis

A 
Airway obstruction (tumor, mucous,….) + gradual resorption of air = reducing lung expansion
= most common 
= obstructive
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24
Q

Compression Atelectasis

A

Material accumulation in pleural cavity = compression of lung parenchyma

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25
Q

Contraction Atelectasis

A

Fibrotic or other restrictive process in pleura or peripheral lung = restricting lung expansion
= pleural fibrosis most common form

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26
Q

Pulmonary edema looks like what on histology

A

A lot of pink more then white, increase in epithelial cells = Left side HF since more P in the BVs + congestion

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27
Q

Pulmonary edema what causes it

A
  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
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28
Q

Gas exchange in Pulmonary edema

A

Alveolar spaces = lower O2 exchange

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29
Q

Heart failure cells

A

After a while of Pulmonary edema , microhemorrhage in alveoli = M accumulate (hemosiderin-laden) ——-> look brown
= in HF and CHF chronic

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30
Q

ALI (Acute Lung Injury)

A

Acute hypoxemia, bilateral infiltrates (PaO2/FiO2 < 300)

= no cardiac failure

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31
Q

ARDS

A

= acute respiratory distress, bilateral infiltrates
= worsening hypoxia ( PaO2/FiO2 < 200)**
= no cardiac problems

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32
Q

DAD (Diffuse Alveolar Damage)

A

The histologically findings of ARDS

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33
Q

What can cause ARDS

A
  1. Sepsis
  2. Diffuse pulmonary infections
  3. Gastric aspirations
  4. Trauma injury (including head)
  5. Pancreatitis
  6. Toxins (like E cigs)
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34
Q

What happens in ARDS from cellular level

A

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

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35
Q

Hyaline membrane form as from what

A

Edema+ Fibrin + cellular debri
= DAD (diffuse Alveolar Damage)
= ventilation - perfusion mismatch

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36
Q

ARDS can lead to what

A

Fibrosis (irreversible) or resolution

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37
Q

ARDS death rate

A

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

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38
Q

Neonatal RDS

A

= reduced surfactant
= hypoxemia
= pulmonary hypoperfusion —> endothelial damage
= you can see Hyaline membranes *****

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39
Q

Restrictive Lung Disease is what and pulmonary function test you see what

A

Restriction in expanding = V restriction
= FEV1/FVC normal
= FVC reduced
= TLC decreased

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40
Q

Obstructive Lung Disease is what and PFT you see what

A 
Exhalation problem 
= decreased air flow
= Low FEV1/FVC
= TLC increase 
= FEV1 decreased
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41
Q

Restrictive Lung Disease also called

A

Interstitial lung disease (disease between alveoli)

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42
Q

3 common Obstructive Lung Diseases

A
  1. COPD (chronic bronchitis)
  2. Emphysema
  3. Asthma
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43
Q

What happens to cause COPD

A
  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
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44
Q

Chronic Bronchitis is defined as what

A

Cough + sputum production for 3 months in 2 consecutive years
= mucous gland hyperplasia ——> damages the airway

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45
Q

Reed index

A

How hick the submucosal layer is in the respiratory epithelium
= to see if there is chronic bronchitis

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46
Q

What neoplasm can form from chronic bronchitis

A

Squamous metaplasia ——> dysplasia ——> carcinoma

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47
Q

Emphysema is what location

A

Irreversible airspace enlargement distal to terminal bronchiole

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48
Q

Centrilubular emphysema is seen when

A

Smoking

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49
Q

Panlobular emphysema is seen in when

A

A1-antitrypsin deficiency

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50
Q

Chronic bronchitis can cause what in smokers

A

Damages the alveolar walls + alveoli collapse due to contraction upstream = air trapping = centrilobular
= chronic bronchitis traveling down from the bronchus

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51
Q

Reason smokers have contrilobular emphysema

A

Started at terminal bronchus (constricted with mucous)——> dilation starts at respiratory bronchiole and travels down

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52
Q

CXR and physical look of emphysema

A

Black lungs

= barrel chest ( square like chest)

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53
Q

Auscultation of emphysema

A

Exaltation wheezing

= flow graph shows (chair looking graph)

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54
Q

Blue Bloaters

A

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
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55
Q

Pink Puffers

A

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
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56
Q

A1- antirtypsin deficiency what happens

A
  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)
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57
Q

A1-AT deficiency what do you see in location

A

Emphysema is panlobar (starting at the alveoli level), moving up to respiratory bronchus eventually
= also more in the lower lobes
(Where more BF is)

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58
Q

Spontaneous Pneumothorax location

A

Distal acinar (only Alvoli)

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59
Q

A1- AT deficiency hesitance and gene

A

Chr 14 Pi gene = normal
Pizz (homozygous for it)

Autosomal Recessive

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60
Q

Asthma what happens

A

Reversible with bronchodilator
Inflammation + hyper-responsiveness
= muscle constriction
= mucous hypersecreation

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61
Q

Atopic Asthma is from what

A

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
Q

non-Atopic Asthma

A

Intrinsic
1/3 pts
= older pts
= normal IgE levels so not allergy induced
= cold and exercise and infection can cause it

63
Q

Steps of how Asthma comes on

A
  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
Q

Leukotrines do what

A
  1. Bronchoconstrict (also uses PGE, Ach, Histamine)
  2. Mucous secretion
  3. Increase vascular permeability
65
Q

Interleukins do what

A

Recruit inflammatory cells

66
Q

When you go to doctor and the pt has asthma what do they need to do

A

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
Q

Asthma uncontrolled effects

A
  1. Airway remodeling (fibrosis, SM hyperplasia, increased goblet cells + submucosal glands)
    = bronchodilators and corticosteroids stop working on these pts
68
Q

Status Asthmaticus what is it and what do you see

A
  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
Q

Genetics + environment associated with atopic Asthma

A
  • seasonal allergies
  • eczema
    = pollution
    = X allergen exposure at early age
    = early infections
70
Q

Aspirin Sensitive Asthma

A

BLOCKED COX 1 + 2 = Arachidonic Acid goes towards 5-Lipoxygenase pathway which increases leukotreins
= increased bronchospasm
= increased chemotaxis
= SAMTERS TRIAD

71
Q

SAMTERS Triad

A
  1. Nasal polyps
  2. Recurrent rhinitis
  3. Aspirin sensitive Asthma
72
Q

Bronchiectasis

A

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
Q

What can cause Bronchiectasis

A
  1. Allergic Bronchopulmonary Aspergillosis (ABPA)
  2. CF
  3. TB
  4. Primary Ciliary dyskinesia
74
Q

CF in lung

A

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
Q

Bronchiectasis what do you see on the lung

A

The bronchioles are so dilated they go all the way to the periphery of the lungs

76
Q

Kartageners Syndrome

A

Primary Ciliary Dyskinesia

= dynein arm not working (in microtubules ——> X flagella and cilia) = X cilia in respiratory tract

77
Q

Kartageners Syndrome TRIAD

A
  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
Q

CF infertility

A

X vas deferons

79
Q

Allergic Bronchopulmonary Aspergillosis

A

= 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
Q

Allergic Bronchopulmonary Aspergillosis DX

A

+ skin test
Septal hyphae with acute angle (like a tree)
(Aspergillosis does many more things like fungal ball)

81
Q

what causes Bronchiectasis

A
  1. CF
  2. Allergic Bronchopulmonary Aspergillosis
  3. Primary Ciliary Dyskinesia
82
Q

Idiopathic Pulmonary Fibrosis

A
  1. Waves in inflammation

2. Usual Interstitial Pneumonia * pattern in histology , normal + inflammation + organizing pneumonia + fibrosis areas

83
Q

4 things seen in usual Interstitial Pneumonia

A
  1. Normal areas
  2. Inflammation
  3. Fibroblast foci (fibrosis) (pink)
  4. Peripheral honeycombing (circular thing looking)
84
Q

Factors that lead to Idiopathic Pulmonary Fibrosis

A
  1. Smoking, industrial societies
  2. Genetics
  3. Over 50yo (with increasing dyspnea)
85
Q

Idiopathic Pulmonary Fibrosis DX and type of lung disease

A

RESTRICTIVE LUNG DISEASE
= biopsy and see the usual Interstitial Pneumonia pattern
= CT scan

86
Q

Idiopathic Pulmonary Fibrosis SX

A
  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
Q

End stage Idiopathic Pulmonary Fibrosis is seen how

A

Basilar infiltrates = honeycomb fibrosis (spaces with thick areas around them)

88
Q

Idiopathic Pulmonary Fibrosis TX

A

TGF-B inhibitors
Lung transplant
(3-5 years)

89
Q

Non-Specific Interstitial Pneumonia compare to UIP

A

Only uniform infiltrates no fibrosis (higher prognosis then UIP)
Also idiopathic

90
Q

Non-Specific Interstitial Pneumonia histology

A

Uniform pattern

Fibrosis and inflammation = thickening spaces between alveoli (plasma cells and lymphocytes)

91
Q

Non-Specific Interstitial Pneumonia risks

A

Can go on and become more fibrotic = harder to treat

Otherwise just treat with steroids and ant inflammatory agents

92
Q

Cryptogenic Organizing Pneumonia what happens

A

Called bronchiolitis obliterans organizing pneumonia

= from a previous infection or inflammatory process

93
Q

Cryptogenic Organizing Pneumonia SX

A
  1. Pneumonia like consolidation

2. 5th and 6th decade in life

94
Q

Histology of Cryptogenic Organizing Pneumonia

A
  1. White loose fibro-CT tissue plugs = circular fibroblasic foci (MASSON BODIES)
    = one component of UIP
95
Q

Cryptogenic Organizing Pneumonia can be confused with what

A

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
Q

Cryptogenic Organizing Pneumonia to

A

Oral steroids cures it

97
Q

Autoimmune lung disease is in what category

A

CT disease (Interstitial lung disease)

  1. RA
  2. Systemic sclerosis
  3. SLE
98
Q

Sarcoidosis histology

A

Non-caseating non-necrotising granulomata

99
Q

Sarcoidosis

A

Histiocytes making granulomas

= multinucleated giant cells

100
Q

How to you see Sarcoidosis in CXR

A
  1. Hilar lymphadenopathy (white consolidation next to the branching of the lobes)
  2. There can also be in pulmonary infiltration also
101
Q

Sarcoidosis risk

A

Stage 4 pulmonary fibrosis

102
Q

Sarcoidosis histology

A
  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
Q

Sarcoidosis prevalence

A
  • under 40yo
  • AA
  • involves lungs usually
  • elevated ACE levels
104
Q

Sarcoidosis development

A

Not in stages (some are progressive to fibrosis)

105
Q

Hypersensitivity Pneumonitis histology

A
  1. A bunch of inflammation everywhere (purple dots all over)
106
Q

Hypersensitivity Pneumonitis is what

A
  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
Q

Hypersensitivity Pneumonitis causes

A

Airway centered granulomata associated with lymphocytes

108
Q

4 smoking related lung diseases

A
  1. Idiopathic Pulmonary Fibrosis
  2. Desquamative Interstitial Pneumonia
  3. Respiratory Bronchiolitis - Interstitial Pneumonia
  4. Langerhans Cell Histiocytosis
109
Q

Desquamative Interstitial Pneumonia Histology and type of lung disease

A 
RESTRICTIVE 
1. Stuffed alveolar spaces 
2. Alveoli FULL OF M cells = plug the alveoli
= 5th-6th decade
= from smoking
110
Q

Desquamative Interstitial Pneumonia TX

A

Corticosteroids
Stop smoking
Good prognosis (survive at 5years)

111
Q

RB-ILD (Respiratory Bronchiolitis Interstitial Lung Disease) is what

A

3rd -4th decade in life
= smoking related
= baby part of DSIP less symptomatic

112
Q

RB-ILD (Respiratory Bronchiolitis Interstitial Lung Disease)DX

A

CT scan = early interstitial lung disease seen

  1. M some
  2. Peribronchial metaplasia (abnormally located ciliated cells)
  3. Some fibrosis if advanced
113
Q

RB-ILD (Respiratory Bronchiolitis Interstitial Lung Disease)TX

A

Stop smoking + steroids

114
Q

Langerhans Cell Histocytosis is what

A

= Stellate lung lesions *****

= scarring ——> big many cysts that can rupture and cause pneumothorax

115
Q

Langerhans Cell Histocytosis histology

A
  1. E*
  2. Langerhans cells*
  3. Fibrosis and cysts
    = stain with S-100 and CD1a+ **
116
Q

Langerhans Cell Histocytosis TX

A

Stop smoking

117
Q

Pulmonary Alveolar Proteinosis what happens

A

= X surfactant metabolism = defected granulocyte-M colony stimulating factor (GM-CSF)
= autoimmune, secondary, hereditary
= surfactant Protein accumulates throughout the alveoli and airspaces

118
Q

Pulmonary Alveolar Proteinosis prevalence

A

Young -mileage female autoimmune prone

119
Q

Pulmonary Alveolar Proteinosis TX

A

GM- CSF given SubQ

Steroids or IVIG

120
Q

Pulmonary Alveolar Proteinosis histology

A

Alveoli full of surfactant protein (light pink stuff) looking like edema

121
Q

Pulmonary Alveolar Proteinosis DX

A

Bronchioloalveolar lavage is done and pulling out a bunch of milky looking surfactant and protein from it fluid, from the alveolar spaces

122
Q

Pneumoconiosis happens from what

A
  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
Q

Pneumoconiosis is worse in who

A

Smokers (ciliary clearance)
Smaller particles
High and repetitive exposure to toxins

124
Q

Coal Workers Pneumoconiosis 3 conditions that these patients can get

A
  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
Q

Silicosis comes from what

A

Inhaling silicon dioxide (mining , concrete repair, demolition) = HIGH CHANCE CANCER

126
Q

Silicosis what happens

A 
SLOW progressive (even after exposure is gone) fibrosis 
= silica deposits in collagenous nodules* + calcification (EGGSHELL CALCIFICATIONS)*
127
Q

Silicosis on CXR or CT

A

Circles at the hilum are seen = eggshell calcifications

CT : rings white that are seen in the fibrotic area

128
Q

Silicosis location

A

Fibrosis is more upper lobular location

129
Q

Coal miner pneumoconiosis and cancer

A

No link unless bituminous coal

130
Q

Asbestosis caused by what

A 
Inhaling asbestos fibers 
= Insulation workers 
= shipyard navy workers
= paper mill workers
= Oil or chemical refinery worker
131
Q

Asbestosis diseases it causes

A
  1. Pleural fibrosis, effusion, mesothelioma
  2. Lung interstitial fibrosis, carcinoma
  3. Other cancers (like liver)
132
Q

Asbestos fibers are dangerous for hat reason and histology

A

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
Q

Pleural plaque formation happens in what condition and what does it look like on histology

A

Asbestos

= Candlewax dripping on pleura , hyalinized collagen

134
Q

Mesothelioma associated with what

A

Asbestos even after decades after exposure
= cancer in the lungs
= can come from the pleural plaques

135
Q

What does a PE look like in the CXR

A
  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
Q

Lines of Zahn

A

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
Q

Angiography of PE

A

Contrast does not go down all the way to the smallest vessels only in big branches

138
Q

BM emboli

A

Cause PE from trauma or chest compressions (you see fat and lymph cells)

139
Q

Talc Embolism

A

Drugs takes by IV can cause a shiny looking PE

140
Q

Septic emboli

A 
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
Q

Pulmonary HTN is what

A

Pulmonary Artery P > 20mmHg

142
Q

Pulmonary HTN happens when

A
  1. More genetic young pts primary vascular disease
  2. Left HF
  3. . hypoxia or Chronic Pulmonary parenchymal disease
  4. From PE
143
Q

Pulmonary HTN histology

A
  1. Knotted BVs = PLEXIFORM LESION

2. Medial hypertrophy (SM in vessels)

144
Q

3 Pulmonary Hemorrhage Syndromes

A
  1. Goodpasture Syndrome
  2. Granulomatosis with Polyangitis (Wagner granulomatosis)
  3. Idiopathic Pulmonary Hemosiderosis
145
Q

Pulmonary Hemorrhage Syndrome histology

A

Hemosiderine stained M in lungs and blood hemorrhaging

146
Q

Goodpasture Syndrome what happens and histology

A

ABs attacking collagen4 on BM = linear immunofluorescence study
+ you see the RBCs around the linear staining in histology
= TYPE 2 hypersensitivity

147
Q

Goodpasture Syndrome prevalence

A

Male younger age 2nd-3rd decade

= AB against collagen 4 on BM

148
Q

Goodpasture Syndrome attacks what organs

A

Lungs and Kidneys

149
Q

Granulomatosis With Polyangiitis

A

Wagners Disease
= granulomatous inflammation that can hemorrhage (can look like pneumonia)
= a lot of bleeding in the lung
= BV necrotizing granuloma

150
Q

Granulomatosis With Polyangiitis prevalence

A

Male over 40yo
= ANCA +
= saddle nose necrotizing granulomatous
= bleeding in lung alveoli

CPR 2 Exam 2 (12 decks)

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