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lung Flashcards

1
Q

normal patho

A

Pathology
Congenital
Atelectasis
Acute Pulmonary Injury
Obstructive Pulmonary Disease (COPD)
Restrictive (Infiltrative) Pulmonary Disease
Vascular Pulmonary Diseases
INFECTIONS
NEOPLASMS
PLEURA (effusions, pneumothorax, tumors)

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2
Q

congenital

A

-Agenesis/Hypoplasia
-!!!!!Tracheal/bronchial anomalies, i.e., Tracheo-Esophageal (TE) fistula
-Vascular anomalies
-Congenital Emphysema
-Foregut cysts
-Pulmonary Artery Malformations (CPAM)
-Sequestration (no connection to airways)

-know the 82% picture- food goes back up - emesis -> air goes into stomach

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3
Q

atelectasis

A

-INCOMPLETE EXPANSION

-COLLAPSE
-Resorption can be from a bronchial obstruction, e.g., tumor.
-Compression can be from a pleural effusion.
-Contraction can be from a diffuse lung fibrotic process.

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4
Q

pulmonary edema

A

-FOUR main pathologic mechanisms of pulmonary edema

-IN-creased venous pressure
-DE-creased oncotic pressure
-Lymphatic obstruction
-Alveolar injury

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5
Q

acute respiratory distress syndrome (ARDS or D.A.D., ie., diffuse alveolar damage

A

-Clinical syndrome of progressive respiratory insufficiency caused by !diffuse alveolar damage!
-Sepsis, severe trauma, or diffuse pulmonary infection
-Damage to endothelial and alveolar epithelial cells and secondary inflammation are initiating events and basis of lung damage
-Micro: hyaline membranes lining alveolar walls, accompanied by edema, scattered neutrophils and macrophages, and epithelial necrosis
-COVID
-ventilation does nothing

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6
Q

obstructive vs restrictive lung disease

A

-Obstructive lung diseases: increase in resistance to airflow due to diffuse airway disease (may affect any level of respiratory tract : COPD (obstructive) can’t exhale
-Restrictive diseases: reduced expansion of lung parenchyma and decreased total lung capacity: Fibrosis (restrictive) can’t inhale

-Clinical distinction based primarily on pulmonary function tests
-FEV 1 /FVC ratio of less than 0.7 generally indicates obstructive disease; usually TLC is increased

-Restrictive diseases: proportionate decreases in both total lung capacity and FEV, so that FEV 1 /FVC ratio usually remains normal
-(1) chest wall disorders (e.g., severe obesity, pleural dxs, kyphoscoliosis,etc.)
-(2) chronic interstitial and infiltrative diseases (e.g., pneumoconioses and interstitial fibrosis)

-Overlapping features may occur

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7
Q

obstructive (COPD)

A

-EMPHYSEMA (almost always chronic)
-CHRONIC BRONCHITIS -> emphysema
-ASTHMA
-BRONCHIECTASIS

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8
Q

emphysema

A

-Abnormal permanent enlargement of air spaces distal to terminal bronchioles, accompanied by destruction of alveolar walls without obvious fibrosis
-Leads to reduced gas exchange, changes in airway dynamics that impair expiratory airflow, and progressive air trapping
-Centri-acinar (usually due to cigarette SMOKING), Pan-acinar (usually due to alpha-1-antitrypsin deficiency), Paraseptal, Irregular
-macrophages from smoke
-Role of proteases which break down alveolar walls
-INcreased crepitance, BULLAE (BLEBS)
-Clinically likely to produce recurrent pneumonias, and progressive failure
-wall breakdown due to enzymes

-PANacinar – usually due to alpha-1 antitrypsin (protein that inhibits various proteases) deficiency
intrinsic imbalance in activity of protease/elastase released and an inhibitor of protease - alpha-1 antitrypsin

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9
Q
A

-1) HYPER-expansion
-2) “flattened” diaphragms (blunted),
-3) “bullae” -> can pop
-4) increased lucency (why?)

-black bc a lot of air

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10
Q

chronic bronchitis

A

-INHALANTS, POLLUTION, CIGARETTES
-CHRONIC COUGH
-CAN OFTEN PROGRESS TO EMPHYSEMA

-MUCUS hypersecretion, early, i.e. goblet cell increase
-CHRONIC bronchial inflammatory infiltrate

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11
Q

asthma

A

-Similar to chronic bronchitis but:
-Wheezing is hallmark (bronchospasm)
-STRONG allergic role, i.e., eosinophils, IgE, allergens
-Often starting in CHILDHOOD
-ATOPIC (allergic) or NON-ATOPIC
-Chronic small airway obstruction and infection
-1) Mucus hypersecretion with plugging, 2) lymphocytes/eosinophils, 3) lumen narrowing, 4) smooth muscle hypertrophy

-1) Inflammation
-2) Bronchial narrowing
-3) Increased Mucous
-4) Smooth muscle hyperplasia
-5) Eosinophils (if etiology is allergy)

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12
Q

bronchiectasis

A

-DILATATION of the BRONCHUS, associated with, often, necrotizing inflammation
-CONGENITAL
-TB, other bacteria, many viruses
-BRONCHIAL OBSTRUCTION (i.e., LARGE AIRWAY, NOT SMALL AIRWAY)
-Rheumatoid Arthritis, SLE, IBD (Inflammatory Bowel Disease)
-necrotizing

-Bronchiectasis is not a specific disease, but a condition in which LARGE bronchi are damaged and DILATED due to a variety of causes.
“-ectasis” is the root word for “dilatation”

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13
Q

restrictive (infiltrative)

A

-REDUCED COMPLIANCE, reduced gas exchange)
-Are also DIFFUSE
-HETEROGENEOUS
-FIBROSING
-GRANULOMATOUS
-EOSINOPHILIC
-SMOKING RELATED
-PAP (Pulmonary Alveolar Proteinosis

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14
Q

lung with restrictive disease: compliance

A

-less “spongy”
-reduced compliance.
-In contrast to “obstructive” lung diseases, the chest x-ray shows diffuse INCREASE in density, NOT DECREASED, density.
-“restrictive” lung diseases = anatomic/functional barriers to the classic gas exchange between an endothelial cell and a type-1 pneumocyte

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15
Q

FIBROSING

A

-!!!“IDIOPATHIC” PULMONARY FIBROSIS (IPF)- -cant inhale -> need lung transplant
-NONSPECIFIC INTERSTITIAL FIBROSIS
-“CRYPTOGENIC” ORGANIZING PNEUMONIA
-“COLLAGEN” VASCULAR DISEASES
-!!!PNEUMOCONIOSES
-DRUG REACTIONS
-RADIATION CHANGES

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16
Q

idiopathic pulmonary fibrosis (usually interstitial penumonia)

A

-IDIOPATHIC, i.e., not from any usual causes, like lupus, scleroderma)
-FIBROSIS- scarring
-Usual Interstitial Pneumonia
-refers to histology of IPF

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17
Q

etiology pathogenesis of IPF

A

-Unknown
-Injured epithelial cells may be source of profibrogenic factors, such as TGF-beta
-Innate and adaptive immune cells produce profibrogenic factors as a host response to epithelial cell damage
-Genetic role suggested by familial IPF
-20% of cases are associated with collagen vascular disease including RA, SLE and progressive systemic sclerosis – suggests immune system involvement
-UIP (histological hallmark may) – usual interstitial pneumonia

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18
Q

pneumoconioses

A

-“OCCUPATIONAL”
-“COAL MINERS LUNG”
-DUST OR CHEMICALS OR ORGANIC MATERIALS:
-Coal (anthracosis)
-Silica
-Asbestos
-Be, FeO, BaSO4, CHEMO
-HAY, FLAX, INSECTICIDES, etc.

-Development depends on
-Amount in lungs
-Size, shape, buoyancy
-Solubility and physiochemical reactivity
-Additional irritants (smoking)

-Most dangerous 1 – 5 um
-Macrophages ingest particles and immune system is stimulated

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19
Q

granulomatous

A

-sarcoidosis, ie. NON-caseating granulomas (idiopathic)
-hypersensitivity (DUSTS, bacteria, fungi, FARMERS lung, PIGEON BREEDERS lung)

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20
Q

sardoidosis

A

-Mainly LUNG, but eye, skin or ANYWHERE - systemic
-UNKNOWN ETIOLOGY
-IMMUNE, GENETIC factors
-Usually female > male and African American > Caucasian

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21
Q

hypersensitivity pneumonitis

A

-Interstitial lung disorders - immune mediated, caused by intense, usually long-term exposure to inhaled organic dusts
-Organic dust usually contains Ags made of spores of thermophilic bacteria, fungi, animal proteins, bacterial products
-Patients have abnormal sensitivity or reactivity to Ag mainly involving alveoli; Most patients have specific Abs against causative agent in serum
-Symptoms 4 – 6 hrs after exposure; may last 12 hrs to days; recur with re-exposure
-non-caseating granulomas (2/3 rds of patients)

-Examples –
-farmer’s lung (exposure to dusts from humid, warm, newly harvested hay, permits proliferation of spores of thermophilic actinomycetes)
-pigeon breeder’s lung (provoked by proteins from serum, excreta, or feather of birds)
-air conditioner lung (caused by thermophilic bacteria in heated water reservoirs)

-goes away once they move away from it

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22
Q

vascular pulmonary diseases

A

-PULMONARY EMBOLISM (with or usually WITHOUT infarction)
-PULMONARY HYPERTENSION, leading to cor pulmonale

-HEMORRHAGIC SYNDROMES:
-GOODPASTURE SYNDROME
-HEMOSIDEROSIS, idiopathic
-Granulomatosis with polyangiitis

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23
Q

pulmonary embolism

A

-Usually secondary to debilitated states with immobilization, or following surgery
-Usually deep leg and deep pelvic veins (DVT), NOT superficial veins
-Follows Virchow’s triad, i.e., 1) flow problems 2) endothelial disruption, 3) hypercoagulabilty
-Usually do NOT infarct, usually ventilate -> 2 blood supplies
-When they DO infarct, the infarct is hemorrhagic (why?)
-Decreased PO2, acute chest pain, V/Q MIS-match
-DX: Chest CT, V/Q scan, angiogram

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24
Q

pulmonary HTN

A

-May occur with:
-COPD- As the alveoli become wider, the arterioles become narrower
-CHD (Congenital HD, increased left atrial pressure)
-Recurrent PEs
-Autoimmune, e.g., PSS (Scleroderma), i.e., fibrotic pulmonary vasculature
-congenital vs acquired (RHF)

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25
hemorrhagic syndromes
-GOODPASTURE Syndrome: Ab’s to the alpha-3 chains of collagen IV, glomerular basement membrane deposits also (kidneys) -IDIOPATHIC PULMONARY HEMOSIDEROSIS -Granulomatosis with polyangiitis (Wegener's granulomatosis): form of vasculitis that affects the lungs, kidneys and other organs. Due to its end-organ damage, it can be a serious disease that requires long-term immunosuppression
26
pulmonary infections
-COMMUNITY-ACQUIRED BACTERIAL ACUTE PNEUMONIAS: -Streptococcus Pneumoniae -Haemophilus Influenzae -Moraxella Catarrhalis -Staphylococcus Aureus -Klebsiella Pneumoniae -Pseudomonas Aeruginosa -Legionella Pneumophila -COMMUNITY-ACQUIRED ATYPICAL (VIRAL AND MYCOPLASMAL) PNEUMONIAS -Morphology. -Clinical Course. -Influenza Infections -Severe Acute Respiratory Syndrome (SARS) -atypical - interstitial -NOSOCOMIAL PNEUMONIA -ASPIRATION PNEUMONIA -LUNG ABSCESS- Etiology and Pathogenesis. -CHRONIC PNEUMONIA -Histoplasmosis, Morphology -Blastomycosis, Morphology -Coccidioidomycosis, Morphology -PNEUMONIA IN THE IMMUNOCOMPROMISED HOST -PULMONARY DISEASE IN HUMAN IMMUNODEFICIENCY VIRUS INFECTION
27
predisposing factors
-LOSS OF COUGH REFLEX -DIMINISHED MUCIN or CILIA FUNCTION -ALVEOLAR MACROPHAGE INTERFERENCE -VASCULAR FLOW IMPAIRMENTS -BRONCHIAL FLOW IMPAIRMENTS
28
classification on pneumonias
-COMMUNITY ACQUIRED -COMMUNITY ACQUIRED, ATYPICAL -NOSOCOMIAL -ASPIRATION -CHRONIC -NECROTIZING/ABSCESS FORMATION -PNEUMONIAS in IMMUNOCOMPROMISED HOSTS
29
community acquired pneumonia
-STREPTOCOCCUS PNEUMONIAE (i.e., “diplococcus”) -HAEMOPHILUS INFLUENZAE (“H-Flu”) -STAPHYLOCOCCUS (STAPH) -KLEBSIELLA PNEUMONIAE -PSEUDOMONAS AERUGINOSA- cystic fibrosis -LEGIONELLA PNEUMOPHILIA
30
streptococcus pneumonia
-Classic LOBAR pneumonia -Normal flora in 20% of adults -Only 20% of victims have + blood cultures -“Penicillins” are often curative -Vaccines are often preventive
31
lobar pneumonia
-only affects one lobe -she barely went over this slide -Four stages: congestion, red hepatization, gray hepatization, and resolution -Congestion: heavy, boggy, red lung with vascular engorgement, intra-alveolar edema fluid with few neutrophils, bacteria -Red hepatization: massive confluent exudation, as neutrophils, red cells, and fibrin fill the alveolar spaces; grossly lung lobe red, firm, airless with liver-like consistency -Gray hepatization: progressive disintegration of red cells and persistence of a fibrinosuppurative exudate; results in color change to grayish-brown. -Resolution: exudate within alveolar spaces broken down by enzymatic digestion to produce granular, semifluid debris that is resorbed, ingested by macrophages, expectorated, or organized by fibroblasts
32
staph aureus pneumonia
-Associated with high incidence of complications (e.g., lung abscess and empyema) -IV drug users are at high risk for development of staphylococcal pneumonia in association with endocarditis -Also an important cause of hospital-acquired pneumonia
33
klebsiella pneumoniae pneumonia
-Commonly afflicts debilitated and malnourished people, especially chronic alcoholics -Thick, mucoid (often blood-tinged) sputum characteristic - organism produces an abundant viscid capsular polysaccharide, which the patient may have difficulty expectorating
34
pseudomonas aeruginosa pnuemonia
-Most commonly causes hospital-acquired infections -Especially occurs in cystic fibrosis and immunocompromised patients -Tends to invade blood vessels causing dangerious septicemia
35
legionella (pneumophila) pneumonia
-Present in water-cooling towers and the tubing systems of water supplies -Transmitted by either inhalation of aerosolized organisms or aspiration of contaminated drinking water -Common in individuals with predisposing conditions (e.g., cardiac, renal, immunologic, or hematologic disease, and especially organ transplant recipients) -May be severe, frequently requiring hospitalization; immunosuppressed patients have fatality rates up to 50% -Diagnosis made rapidly by detecting Legionella DNA in sputum using !PCR–based test or by identification of Legionella antigens in the urine; culture remains diagnostic gold standard, but takes 3 to 5 days!
36
community acquired (atypical) pneumonia
-not bacteria -VIRAL (INFLUENZA) -MYCOPLASMAL (MYCOPLASMA PNEUMONIAE (obligate intracellular)) -NOT BACTERIAL -CULTURES NOT HELPFUL -can become problematic - ARDs -> stuffed with bacteria -> no diffusion
37
viral pneumonias
-Viral pneumonias, generally interstitial, bacterial pneumonias generally alveolar -Frequently “interstitial”, NOT alveolar
38
influenza virus (i think she skipped this)
-Types A, B, C -Single subtype of influenza virus A predominates throughout world at a given time -Epidemics caused by spontaneous mutations that cause antigenic changes (antigenic drift) resulting in new viral strains – yearly vaccine needed -Shortly after entry into pneumocytes, the viral infection inhibits sodium channels, producing electrolyte and water shifts leading to fluid accumulation in the alveolar lumen -Infected cells then die which worsens the fluid accumulation and release signals that activate resident macrophages -Before their death, infected epithelial cells release inflammatory mediators, including several chemokines and cytokines -Some cases cause enough lung injury to produce ARDS, but more often severe pulmonary disease results from superimposed bacterial pneumonia, esp. S. aureus
39
COVID-19
-Broad clinical spectrum, ranging from asymptomatic infection or mild upper respiratory tract illness to multifocal pneumonia, respiratory failure, and death. -The most severe cases develop pneumonia and acute respiratory distress syndrome (ARDS) -can cause interstitial pneumonia -Symptoms may appear 2-14 days after exposure to the virus -Fever or chills -Cough -Shortness of breath or difficulty breathing -Fatigue -Muscle or body aches -Headache -New loss of taste or smell -Sore throat -Congestion or runny nose -Nausea or vomiting -Diarrhea -Effects its cellular entry via attachment of its virion spike protein (a.k.a. S protein) to the angiotensin-converting enzyme 2 (ACE2) receptor, commonly found on alveolar cells of the lung epithelium -Cardiovascular effects may also be via same ACE2 receptor, also commonly expressed on cells of cardiovascular system
40
covid imaging findings
-X RAY -airspace opacities, whether described as consolidation or ground glass opacities; distribution is most often bilateral, peripheral, and lower zone predominant -CT -Ground-glass opacities (GGO): bilateral, subpleural, peripheral -crazy paving appearance (GGOs and inter-/intra-lobular septal thickening) -air space consolidation -bronchovascular thickening in the lesion -traction bronchiectasis -The ground-glass and/or consolidative opacities are usually bilateral, peripheral, and basal in distribution
41
nosocomial pneumonia
-Acquired in HOSPITALS, also called “hospital acquired”, versus “community acquired” pneumonias. -DEBILITATION -CATHETERS, VENTILATORS -ENTEROBACTER, PSEUDOMONAS -STAPH (MRSA) -MRSA (MR=Methicillin Resistant) -OTHER Common causes -P. aeruginosa -Klebsiella -E. coli -S. pneumoniae -H. influenzae
42
aspiration pneumonias
-UNCONSCIOUS PATIENTS -PATIENTS IN PROLONGED BEDREST -LACK OF ABILITY TO SWALLOW OR GAG -USUALLY CAUSED BY ASPIRATION OF GASTRIC CONTENTS -POSTERIOR LOBES (gravity dependent) MOST COMMONLY INVOLVED, ESPECIALLY THE SUPERIOR SEGMENTS of the LOWER LOBES -Often lead to ABSCESSES
43
lung abscesses
-ASPIRATION -SEPTIC EMBOLIZATION -NEOPLASIA -From NEIGHBORING structures: -ESOPHAGUS -SPINE -PLEURA -DIAPHRAGM -Abscess - localized “pneumonia” - normal lung outline can no longer be seen, 100% pus. Increasing destruction of alveolar framework progressing closer to center of abscess
44
chronic pneumonias: fungal
-TB -HISTOPLASMOSIS -BLASTOMYCOSIS -COCCIDIOMYCOSIS -“Chronic” by classification, but “granulomatous” by histology.
45
histoplasmosis
-Spores in bird or bat droppings -Mimics TB -Histoplasma CAPSULATUM -Pulmonary granulomas, often large and calcified -Tiny organisms live in macrophages -Ohio, Mississippi valley -MANY other organs
46
blastomycosis
-Spores in soil -Mimics TB, like all granulomatous lung diseases -Blastomyces DERMATIDIS -Pulmonary granulomas, often large and calcified -Large distinct SPHERULES -Ohio, Mississippi valley, Great Lakes, WORLDWIDE -MANY other organs can be affected, especially SKIN
47
coccidiomycosis
-Spores in soil -Mimics TB -Coccidioides IMMITIS -Pulmonary granulomas, often large and calcified -Tiny organisms live in macrophages -American SOUTHWEST -MANY other organs can be affected
48
TB
-TB: Chronic pulmonary and systemic disease caused most often by M. tuberculosis, leading infectious cause of death worldwide -Infection signifies presence of bacteria in body, may be symptomatic (active disease) or not (latent infection) -Most infections acquired by person-to-person transmission of airborne organisms from an active case to susceptible host -In most healthy people primary tuberculosis is asymptomatic, may cause fever and pleural effusion; however, viable organisms may remain dormant in for decades -If immunity is compromised, the infection may be reactivated, producing communicable and potentially life-threatening disease
49
TB
-Mycobacteria enter into macrophages and replicate; after about 3 weeks a Th1 response activates macrophages -Th1 cells produce IFN-γ, important mediator activates macrophages and enables them to contain the M. tuberculosis infection; Th1 response orchestrates formation of granulomas and caseous necrosis -In many people the infection is contained before significant tissue destruction occurs; however, if immunocompromised, infection progresses -Inhaled bacilli implant in distal airspaces of lower part of the upper lobe or the upper part of the lower lobe, -As sensitization develops, a 1- to 1.5-cm area of gray-white inflammation with consolidation emerges, the Ghon focus, which usually undergoes caseous necrosis in center; also either free or within phagocytes bacilli, drain to regional nodes, which also often caseate. -Combination of lung lesion and nodal involvement referred to as the Ghon complex
50
primary vs secondary TB
Primary tuberculosis develops in previously unexposed, unsensitized person; usually, primary infection is contained, but sometimes progressive. Secondary tuberculosis arises in a previously sensitized host, more commonly months to years after the initial infection, usually when host resistance is weakened
51
compromised hosts
-PNEUMOCYSTIS Jiroveci -CYTOMEGALOVIRUS (CMV) -FUNGI
52
PCP
-tea cupping found on imaging -cysts -Methenamine SILVER stain for Pneumocystis jiroveci
53
lung tumors
-90% are CARCINOMAS -Tobacco, radiation, asbestos, radon -Different genetic mutations important
54
lung tumor pathogenesis
-NORMAL BRONCHIAL MUCOSA -METAPLASTIC/DYSPLASTIC MUCOSA -metaplasia becomes dysplasia if you continue to smoke -CARCINOMA-IN-SITU (squamous, adeno) -INFILTRATING (i.e., “INVASIVE”) cancer
55
two types of lung cancer
-NON-SMALL CELL -SQUAMOUS CELL CARCINOMA (smoking) -ADENOCARCINOMA (can be seen in non-smoking females) -LARGE CELL CARCINOMA -SMALL CELL CARCINOMA (smoking) -* Adenocarcinoma (50%) * Squamous cell carcinoma (20%) * Small cell carcinoma (15%) * Large cell carcinoma (2%) * Other (13%)
56
local effects of lung cancer
-
57
systemic effects of lung cancer (para-neoplastic syndromes)- 5%
-usually small cell carcinoma -ADH (hyponatremia) – ectopic production of hormone esp. in small cell carcinoma -> hyponatremia -ACTH (Cushing) - same -PTH-RP (Hyper-CA) - esp squamous cell CA -> hypercalcemia -> get x ray
58
metastatic tumors
-LUNG is MOST COMMON site for all metastatic tumors, regardless of site of origin -Often first site for metastatic sarcomas
59
pleura
-PLEURITIS -PNEUMOTHORAX -EFFUSIONS -HYDRO-THORAX -HEMO-THORAX -CHYLO-THORAX -MESOTHELIOMAS
60
pleuritis
-Usual bacteria, viruses, etc. -Infarcts -Lung abscesses, empyema -TB -“Collagen” diseases, e.g., RA, SLE -Uremia -Metastatic
61
pneumothorax
-SPONTANEOUS, TRAUMATIC -OPEN or CLOSED -“TENSION” pneumothorax - pleural defect acts as a flap valve and permits entrance of air during inspiration but does not allow air to escape during expiration; progressively increasing intrapleural pressure may compress vital mediastinal structures and the contralateral lung -“Bleb” rupture -Perforating injuries -Post needle biopsy
62
effusions
-TRANSUDATE (HYDROTHORAX) EXUDATE (HYDROTHORAX) BLOOD (HEMOTHORAX) LYMPH (CHYLOTHORAX) -How would you differentiate a pleural transudate from an exudate? Ans: Specific gravity, cells, protein
63
mesotheliomas
-Visceral or parietal pleura, pericardium, or peritoneum -Most are regarded as asbestos caused or asbestos “related” -Typical growth appearance of a malignant mesothelioma, it compresses the lung from the OUTSIDE -IF YOU HAVE THIS ITS MOST LIKELY ASBESTOS -IF YOU HAVE ASBESTOS EXPOSURE IT DOESNT MEAN YOU HAVE MESOTHELIOMA

patho (11 decks)

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