Respiratory Flashcards
What makes up the Conducting Zone?
Large airways: Nose, Pharynx, Trachea, Bronchi
Small airways: Bronchioles and Terminal Bronchioles
Function of Conducting Zone
Warms and humidifies air but does not participate in gas exchange
Anatomical Dead Space
Cartilage extends until
Bronchi
Goblet cells extend until
End of Bronchi
Pseudostratified, ciliated, columnar cells extend until
What is the cilia’s function?
End of Terminal Bronchioles to beat mucus up and out of lung
Smooth muscle in airway wall extends until
terminal bronchioles
What makes up the respiratory zone?
= Lung Parenchyma. Respiratory bronchioles, alveolar ducts and alveoli
participates in gas exchange
What kind of cells are in the Respiratory zone?
Cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli
Type I Pneumocytes
Percentage of alveolar surface
Kind of cell
Function
97% of alveolar surface. Squamous cells optimal for gas diffusion
Type II Pneumocytes
Kind of cell
Function
Clustered cuboidal cells. Secrete surfactant and act as precursors
Collapsing Pressure Formula
P = 2 (surface Tension) / Radius
When are alveoli most likely to collapse?
On Expiration
Function of surfactant
Decreased alveolar surface tension to prevent atelectasis
Composition of surfactant
Complex mix of lecithins. The most important of which is dipalmitoylphasphatidylcholine
When does surfactant production begin in the fetus? When does it reach mature levels? What indicates maturity?
Begins at week 26. Mature by week 35. Mature when Lecithin/Sphingomyelin > 2
Clara Cells:
Location
Appearance
Function
In Terminal and Respiratory Bronchioles. Non ciliated columnar cells with secretory granules. Secrete components of surfactant, degrade toxins and act as reserve cells
of lobes in each lung?
R: 3, L: 2 + Lingula
Foreign body most likely to be lodged in
R lung because R mainstem bronchus is wider and more vertical than L
Aspirate a peanut:
While upright?
While supine?
Upright: Lower Portion of R Inferior Lobe
Supine: Superior Portion of R Inferior Lobe
Relationship bet Pul Artery to the Bronchus?
RALS
Right: Anterior, Left Superior
Structures perforating the Diaphragm
I ate 10 eggs at 12
T8: IVC
T10: Vagus and Esophagus
T12: Aorta, Azygous, Thoracic duct (Red White and Blue)
What innervates the Diaphragm? Where is pain from the Diaphragm referred?
C3, 4, 5 keeps you alive
Pain referred to shoulder (C5) and Trapezius ridge (C3, C4)
Muscles of respiration (quiet and exercise)
Inspiration: Quiet –> Diaphragm, Exercise –> SCM, Scalene, External Intercostals
Expiration: Quiet –> Passive, Exercise –> Obliques (Internal and External), Abdominis (Rectus and Transversus) Internal Intercostals
Inspiratory Reserve Vol
Air that can be breathed in after normal inspiration
Tidal Vol
500mL. Air that moves into the lung on quiet inspiration
Expiratory Reserve Vol
Air that can still be breathed out after a normal expiration
Reserve Volume
Air left in lung after maximal expiration
Inspiratory capacity
TV + IRV
Function Residual Capacity
RV + ERV
Vital Capacity
TV + IRV + ERV
Total Lung Capacity
IRV + TV + ERV + RV
Physiological Dead Space
Definition
Calculation
Vol of inspired air that does not participate in gas exchange
VD = Anatomical Dead Space of conducting airways + functional dead space in alveoli
VD = TV [(PaCO2 -PECO2)/PaCO2] Taco Paco Peco Paco
Largest contributor to functional dead space?
Apex of Lung
The tendency is for the lung to … and for the chest wall to …
Lung wants to collapse, Chest wall wants to spring outward
@ FRC: What is happening with the lung - chest wall system? What is the P in the alveoli and airway? What is the P in the Intrapleural space?
@ FRC: Inward pull of lung = outward pull of chest wall and system pressure is atmospheric. P in the alveoli and airway = 0. P in the Intrapleural space is negative to prevent pneumothorax
Alveolar transmural pressure is …
Always positive. Meaning always tending to collapse
What determines the elastic properties of both the chest wall and lungs?
Their combined volume
What is compliance?
What increases compliance?
What decreases compliance?
Change in lung vol for a given change in pressure
Increases in emphysema and normal aging
Decreases in fibrosis, pneumonia and edema
Hemoglobin
Composed of
Exists in 2 forms
Exhibits
Composed of 2 alpha and 2 beta subunits
Exists in Taut form in tissues (low affinity) and Relaxed form in lungs (high affinity)
Exhibits positive cooperativeity and negative allostery
What shifts Hemoglobin dissociation curve to the R (towards T form)
CADET! Turn R!
CO2 and Cl, Acidosis and Altitude, BPG, Exercise, Increased Temp
Fetal Hemoglobin
Consists of
Different affinities?
Consists of 2 alpha and 2 gamma subunits
Lower affinity for BPG = higher affinity for O2 –> curve shifted to the L
Methemoglobin What is it ? Change in affinity? Shift in curve? Treat with
Oxidized Iron 3+ (ferric) instead of Iron 2+ (ferrous)
Lower affinity for O2, Higher affinity for cyanide
Shifts curve to R
Treat with Methylene Blue
Nitrite poisoning causes
Oxidization of Fe2+ to Fe3+
How to treat cyanide poisoning?
Use nitrites to oxidize Hemoglobin to methemoglobin. MetHem with bind cyanide and allow cytochrome oxidase to function. Then use Thiosulfate to bind cyanide –> forms thiocynate which is renally excreted
Carboxyhemoglobin
What is it
Affect on O2 binding curve
Hemoglobin bound to CO
Shifts curve to L –> decreased O2 unloading in tissues
Appearance of Hemoglobin O2 binding curve?
Sigmoidal because of cooperativity
Pulmonary Circulation Re Resistance and Compliance
Low Resistance and High Compliance
How does a decrease in PA02 (= increase in PACO2) affect pulmonary circulation?
Vasoconstriction to shift blood away from poorly ventilated areas
Which gases are perfusion limited? What does that mean?
O2 (normally), CO2, N2O. Diffusion Increases if Blood Flow Increases
Which gasses are diffusion limited? What does that mean?
O2 (in fibrosis or emphysema), CO. Gas does not equilibrate by the time the blood reaches the end of the capillary.
Gas diffusion equation
What happens in Emphysema?
What happens in Fibrosis?
Vgas = (A/T) x D(P1-P2)
Emphysema –> Area decreases
Fibrosis –> Thickness increases
Pulmonary artery pressure: Normal? PHTN?
Normal: 10-14mmHg, PHTN: >/= 25 (rest) or >/= 35 (exercise)
PHTN affect on pulmonary artery
Arteriosclerosis, Medial Hypertrophy, Intimal Fibrosis
Cause of Primary PHTN
Inactivation of BMPR2 gene which normally functions to inhibit vascular smooth muscle proliferation
What causes secondary PHTN? What is the course of the disease?
COPD (destruction of lung parenchyma), Mitral Stenosis (Increased resistance –> increased P), Recurrent thromboemboli (decreased cross sectional area of pulmonary vascular bed), autoimmune disease, L –> R shunt (increased sheer stress –> endothelial injury), Sleep Apnea, Living at high altitude
Respiratory distress –> Cyanosis and RVH –> cor pulmonale –> death
Pulmonary Vascular Resistance formula
PVR = (P pulmonary artery - P left atrium) / CO
O2 content of blood formula
What is normal O2 binding capacity?
O2 binding capacity x saturation + dissolved O2
O2 binding capacity normally 20ml/dL
1g Hb can bind how much O2?
How much Hb is normally in blood?
When does cyanosis occur?
1.34mL
15 g Hb/dL
Cyanosis occurs when deoxygenated Hb > 5g/dL
What happens to O2 content of blood, O2 sat and PaO2 when Hb decreases?
O2 content decreases but O2 sat and PaO2 remain the same
Formula for oxygen delivery to tissues
CO x O2 content of blood
Alveolar gas equation
PAO2 = PIO2 - PaCO2/R PAO2 = 150 - PaCO2/.8 R = CO2 produced/O2 consumed
A-a gradient
Normal value
Increased in?
Causes?
Normal A-a gradient = 10-15mmHg
Increased in hypoxemia due to lesion in Lung
Causes: Shunting, V/Q mismatch, Fibrosis
Causes of hypoxemia with normal A-a gradient?
High altitude, hypoventilation
What causes hypoxemia with increased A-a gradient?
V/Q mismatch, Diffusion limitation, R-L shunt
Causes of Hypoxia
Decreased cardiac output, Hypoxemia, Anemia, CO poisoning
What can cause ischemia?
Arterial flow or venous drainage blocked
V/Q at apex? base?
apex = 3 (wasted ventilation). base = .6 (wasted perfusion)
Where in the lung is ventilation greatest? Where is perfusion greatest?
Both at base
What happens to V/Q during exercise?
Vasodilation of apical capillaries –> V/Q approaches 1 at apex
What kind of organisms thrive in the apex of the lung?
Those that thrive on high O2 like TB
V/Q = 0
Shunt (airway obstruction). 100% O2 wont help
V/Q = infinity
Blood flow obstruction (physiological dead space) Assuming <100% dead space, O2 will help
PAO2, PaO2, and PvO2 in apex, middle and base
Apex: PA>Pa>Pv
Middle: Pa>PA>Pv
Base: Pa>Pv>PA
In what forms is CO2 transported in the blood?
Bicarb: 90%, CarbaminoHb (binds at N terminus and binding favors T form): 5%, Dissolved CO2: 5%
How does oxygenation of Hb affect CO2 in blood?
Oxygenation –> dissociation of H from Hb. H + bicarb = CO2 thus more CO2 is released from RBC
Haldane Effect
Bohr Effect
Increased H in periphery –> Hb O2 curve shifted to R and O2 unloading favored
Response to high altitude?
Increased Mito, Increased renal excretion of bicarb (to combat alkalosis) Increase in ventilation, decreased PO2 + PCO2, Increased EPO –> Increased Hb and Hc, Increased BPG, RVH
“Mr. V. Deb”
Response to exercise CO2 production O2 consumption Ventilation V/Q Pulmonary blood flow pH PaO2, PaCO2, venous CO2, venous O2
CO2 production increases, O2 consumption increases, Ventilation increases, V/Q becomes more uniform, Pulmonary blood flow increases, pH decreases (lactic acidosis), PaO2 NC, PaCO2 NC, venous CO2 increase, venous O2 decreases
DVT What predisposes to it? What can it lead to? Physical Exam sign? Treatment and prevention?
Virchow’s triad of Vascular damage (exposed collagen), Increased coagulability (defect in coagulation cascade, most commonly factor V Leiden), Reduced flow [VIR]
Leads to Pul embolus
Homan’s Sign –> Dorsiflexion of foot –> calf pain
Heparin for prevention and acute management. Warfarin for long-term prevention of recurrence
Sudden onset of dyspnea, chest pain, and tachypnea
Pulmonary embolism
Types of PE?
FAT BAT
Fat, Air, Thrombus, Bacteria, Amnionic fluid, Tumor
Fat embolus associated with…
Presents as…
Long bone fracture and liposuction
Presents as hypoxemia, neurological abnormalities, petechial rash
Major risk with Amnionic fluid embolus?
Can lead to DIC especially post partum
Imaging test of choice for PE?
CT pulmonary angiography
Where do most PEs arise from?
95% from deep leg veins
Most dangerous location for PE?
Saddle Embolus of Pulmonary Artery
Histology of thromboembolus formed premortem?
Lines of Zahn: interdigitating areas of pink (platelets, fibirn) and red (RBCs)
Obstructive Lung Disease: Names, RV, FVC, PFTs, V/Q, PO2, PCO2
Chronic Bronchitis, Emphysema, Asthma, Bronchiectasis
RV: Increases, FVC: Decreases
FEV1 decrease, FVC decreases, FEV1/FVC decreases
V/Q decreases, PO2 decreases, PCO2 increases
Chronic Bronchitis: Clinical definition
Productive Cough for >3 months (not necessarily consecutive) for >2 years
Chronic Bronchitis: Pathology and Physical Findings
Harry Reid Won 50% Securing Complete Democratic Control
Hypertrophy of Mucus secreting glands in bronchi, Reid Index > 50%, Wheezing, Small airway disease, Crackles (early) Dyspnea (late), Cyanosis (early onset hypoxemia due to shunting)
Emphysema: pathology and findings
PERCE
Pursed lip breathing (increased airway pressure prevents collapse), Enlarged airspace, Recoil decreased, Compliance increased, Elastase activity increased
Two types of emphysema
Centriacinar = smoking Panacinar = alpha-1-antitrypsin deficiency
Alpha Agonists
Names
Uses
Tox
Pseudoephedrine, Phenylephrine
Reduce hyperemia, edema, nasal congestion.
Open up Eustachian tube.
Pseudoephedrine is a stimulant. Can cause HTN. Pseudoephedrine can cause CNS stimulation/anxiety
Dextromethorphan Class MoA Uses Risk Antidote
Opioid (synthetic codeine analog) Antagonizes NMDAR Antitussive Mild abuse potential Naloxone treats OD
Bosentan
MoA
Uses
Competative antagonist of endothelin 1 receptor
Decreases Pulmonary Vascular Resistance
Used to treat Pulmonary Arterial HTN
N Acetylcysteine
Type of drug
Action
Uses
Mucolytic expectorant
Loosens mucus plugs in CF
Antidote for acetaminophen OD
Guaifenesin
Type of drug
Action
Expectorant that thins the respiratory secretions but does not suppress the cough reflex
Molecules that cause bronchoconstriction?
Adenosine, ACh
Molecules that cause Bronchodilation
cAMP
Ab Asthma therapy
Name
MoA
Uses
Omalizumab
Monoclonal IgE Ab that binds up serum IgE
Used in allergic asthma resistant to steroids and long acting beta2 agonists
Anti Leukotrienes
Names
MoA
Uses
Montelukast, Zafirlukast --/ leukotriene receptor. Especially good in aspirin induced asthma Zileuton --/ 5 lipoxygenase pathway. Blocks arachidonic acid --> leukotrienes Both used to treat Asthma
Corticosteroids used to treat Asthma
Names
MoA
Beclomethasone, Fluticasone
- -/ cytokine production
- -/ NFkB (NFkB –> TNF alpha)
Antimuscarinics
Name
MoA
Uses
Ipratropium (short), Tiotropium (long)
–/ muscarinic receptors thereby preventing bronchoconstriction
Asthma and COPD
Methylxanthines Names MoA Use Tox Metabolism Blocks actions of
Theophylline–/ PDE leading to increased cAMP
Asthma treatment
Narrow therapeutic index –> cardiotoxic, neurotoxic
P450 metabolism
Blocks actions of Adenosine
Pneumothorax presentation
PTHORAX
Pleuritic pain, Tracheal deviation, Hyperresounant, sudden Onset, Reduced breath sounds, Absent Fremitus, XR –> Collapse
Beta 2 agonists
Short
Long (uses, tox)
Short: Albuterol –> Beta2 –> SM relaxation
Long: Salmeterol, Formoterol.
Used for prophylaxis.
Can cause tremors and arrhythmias
Asthma drug targets
Classes of drugs
Antiinflammation + Anti parasympathetic tone
First Line Therapy: Corticosteroids
Beta 2 agonists, Methylxanthines, Anti Muscarinic, Antileukotrienes, Abs
H1 Blockers 2nd Gen
Names
Use
Tox
Loratadine, Fexofenadine, Desloratadine (adine)
Allergy
Much less sedating because do not enter CNS
H1 Blockers, 1st Gen
Names
Use
Tox
Diphenhydramine, dimenhydrinate, chlorpheniramine (en/ine, en/ate)
Allergy, motion sickness, sleep aid
Sedation, antimuscarinic, anti alpha adrenergic
Kinds of antihistamines used in the lung?
H1 blockers
Pleural Effusion: Lymphatic
Name
Due to
Appearance
Chylothorax. Due to thoracic duct injury from trauma or malignancy.
Appears milky with high triglyceride content
Pleural Effusion: Exudate
Caused by
Action that must be taken?
High Protein content, appears cloudy
“CAPTAIN”
Due to Collagen Vascular Disease, Abdominal pathology, Pneumonia, TB, Trauma (occurs in states of increased vascular permeability), Asbestos, Infection (Pneumonia), Malignancy
Must be drained to prevent infection
Pleural Effusion: Transudate
Caused by
Low protein content
“CHEMN”
Due to CHF, Hepatic cirrhosis (Hypoalbuminia), Embolism, Meig Syndrome, Nephrotic syndrome
Hypersensitivity Pneumonitis
Type of Rxn
Presentation
Seen in what kind of pt?
Mixed Type III/IV hypersensitivity rxn to environmental antigen
“Holding Down Tough Cows on a Farm”
Presents with headache, dyspnea, tight chest, cough
Seen in farmers and bird owners
Interstitial (atypical) pneumonia Organisms Characteristics Distribution Course
Viruses (influenza, RSV, adenovirus), Mycoplasma, Legionella, Chlamydia
Diffuse, patchy inflammation in interstitial areas
Involves ≥ 1 lobe.
Indolent course
Bronchopneumonia Organisms Characteristics Histo Distribution
S pneumoniae, S aureus, H influenzae, Klebsiella
Acute inflammatory infiltrates from bronchioles into adjacent alveoli
Neutrophils in alveolar spaces
Patchy distribution involving ≥ 1 lobe
Lobar Pneumonia
Organisms
Characteristics
S. pneumoniae, KlebsiellaIntra
alveolar exudate –> consolidation
May involve entire lung
SVC syndrome Def Presentation Causes Can lead to...
Obstruction of SVC impairs blood drainage from Head (Facial Plethora) Neck (JVD) and Arms (Edema)
Caused by malignancy, thrombosis (from indwelling catheters)
Can lead to Increased ICP –> headache, dizziness, aneurysm, cranial artery rupture
Pancoast Tumors
Carcinomas in apex of lung affect cervical sympathetic plexus resulting in Horner’s Syndrome (Ipsilateral Miosis, Anhidrosis, Ptosis)
Mesothelioma Location Associated with Results in Histology
Pleural. Associated with asbestosis.
Results in Hemorrhagic pleural effusions and pleural thickening.
Psommoma bodies
Bronchial Carcinoid Tumor Prognosis Metastasis Symptoms due to Can lead to Histology
Excellent Prognosis.
Metastasis: rare.
Symptoms due to mass effect
Can lead to CARCinoid syndrome (5HT release –> Cutaneous flushing, Asthmatic wheezing, Right valve lesions, Cramps, Diarrhea, Salivation)
Nests of neuroendocrine cells. Chromogranin +
Large Cell Carcinoma Location Differentiation Prognosis Treatment Histology
Peripheral, highly anaplastic undifferentiated tumor Poor Prognosis Surgery. Poor response to chemo Pleomorphic giant cells
Small Cell (Oat Cell) Carcinoma Location Differentiation May produce Genetics Treatment Histology
Central, undifferentiated, aggressive
May produce ACTH, ADH, Abs against presynaptic Ca channels (Lambert Eaton)
Genetics: amplification of myc oncogenes
Chemotherapy.
Inoperable
Kulchitsky cells (small dark blue cells). Salt and Pepper neuroendocrine chromatin
Squamous Cell Carcinoma Location Arise from Characteristics Histology
Central
Hilar mass arises from bronchus
Cavitation, Cigarettes, hyperCa (produces PTH)
Dysplastic squamous cells with Keratin Pearls and Intracellular Bridges
Lung Abscess
Definition
Caused by
CXR
Localized collection of pus within parenchyma
Caused by bronchial obstruction (cancer), aspiration of oropharyngeal contents (pts predisposed to LOC i.e. alcoholics), infection of S aureus or anaerobes (Bacteroides, Fusobacterium, Peptostretococcus)
Air-Fluid levels often seen on CXR
Bronchioloalveolar adenocarcinoma Derived from CXR Histology Prognosis
Derived from Clara Cells
Hazy infiltrates similar to pneumonia
Grows along alveolar septa –> apparent thickening of alveolar walls
Excellent prognosis
Adenocarcinoma Can present as... Location Most common lung cancer in Genetics Physical Exam Findings
Can present as pneumonia
Peripheral.
Develops in scars (old Tuberculous Granulomas)
Most common lung cancer in nonsmokers and females
Activating k-ras mutation
Osteoarthropathy (clubbing)
Where do Lung Cancers metastasize to?
Brain, Liver (jaundice, hepatomegaly), Adrenals, Bone (pathologic fracture)
Most common cause of Lung Cancer?
Metastasis from Breast, Bladder, Colon, or Prostate
Lung Cancers Not Associated with Smoking?
Bronchioloalveolar and bronchial carcinoid
Complications of Lung Cancer
SPHERE
SVC syndrome, Pancoast tumor, Hornerns, Endocrine (paraneoplastic), Recurrent laryngeal symptoms (hoarseness), Effusions (pleural or pericardial)
Lung Cancer Presentation
ABCDE
Avalanche, Bloody cough, Cough, Coin Lesions on XR, nonCalcified nodules on CT, Disrupted bronchi (bronchial obstruction), whEezing
Consolidation (Lobar Pneumonia, Pulmonary Edema) Breath sounds Percussion Fremitus Tracheal deviation
Breath sounds: Bronchial, Late inspiratory Crackles
Percussion: dull
Fremitus: increased
Tracheal deviation: none
Tension Pneumothorax Presentation Pathology Breath sounds Percussion Fremitus Tracheal deviation Most common pt
Unilateral chest pain, dyspnea, unilateral chest expansion Air enters pleural space but cannot exit Breath sounds: decreased Percussion: hyperresonant Fremitus: decreased Tracheal deviation away from lesion Trauma or lung infection
Spontaneous Pneumothorax Presentation Pathology Breath sounds Percussion Fremitus Tracheal deviation Most common pt
Unilateral chest pain, dyspnea, unilateral chest expansion
Rupture of apical bleb –> accumulation of air in pleural space
Breath sounds: decreased
Percussion: hyperresonant
Fremitus: decreased
Tracheal deviation towards side of lesion
Tall thin young male
Atelectasis (Bronchial Obstruction) Breath sounds Percussion Fremitus Tracheal deviation
Breath sounds: decreased
Percussion: dull
Fremitus: decreased
Tracheal deviation toward side of lesion
Pleaural Effusion Breath sounds Percussion Fremitus Tracheal deviation
Breath sounds: decreased
Percussion: dull
Fremitus: decreased
Tracheal deviation: none
Obstructive Sleep Apnea
Description
Associations
Respiratory effort against airway obstruction. Associated with obesity, snoring, HTN, PHTN, Arrhythmias, Sudden Death
Sleep Apnea Definition Types Results in Treatment
Cessation of breathing for >10 sec
Central (no respiratory effort) vs Obstructive
Results in Hypoxia –> EPO release –> Erythropoiesis
Wt loss, CPAP, Surgery
ARDS Causes Pathology Initial damage caused by Histology
Caused by Aspiration, Acute pancreatitis, Air or Amnionic emboli, Radiation, DIC, Drugs, Dialysis, Diffuse Infection, Sepsis, Shock, Trauma, Uremia
Diffuse alveolar damage –> Increased capillary permeability –> protein rich exudate into alveoli –> Intraalviolar hyaline membane
Initial damage caused by release of substances toxic to alveolar wall by neutrophils, activation of coagulation cascade, ROS
Histo: Alveolar fluid and hylaline membranes
NRDS Pathology Lechithin/Sphingomyelin ratio Because of low O2 tension --> Therapeutic O2 --> Risk factors Treatment
Surfactant deficiency –> Increased Surface Tension –> alveolar collapse
L/S < 1.5 predictive
Because of low O2 tension –> risk of PDA
Therapeutic O2 –> ROP and Bronchopulmonary Dysplasia
Risk factors: Prematurity, Maternal Diabetes, Cesarean delivery (decreased release of glucocorticoids)
Treatment: maternal steroids before birth. Artificial surfactant for the infant
Asbestosis Associated with what kind of jobs? Associated with what other diseases Histology? Appearance?
Associated with shipbuilding, roofing, plumbing
Associated with Bronchogenic Carcinoma and Mesothelioma
Asbestos bodies are golden brown fusiform rods (dumbbells) in Macs Ivory White calcified pleural plaques are pathognomonic but not precancerous
Silicosis Associated with what kind of jobs? Pathology Increased risk for Affects which lobes? Appearance?
Associated with foundries, sandplansting, mines
Si –> Macs –> release fibrogenic factors
Increased risk for TB because Si –/ phagolysosomes thereby –/ macs.
Also increased risk for Bronchogenic Carcinoma
Affects Upper Lobes
Eggshell calcifications on hilar lymph nodes
Anthracosis
Associated with what kind of pt?
Which lobes are affected?
Coal Miners Lung. Affects Upper Lobes
Names of Pneumoconioses
Anthracosis, Silicosis, Asbestosis
Pneumoconioses + RA
Caplan Syndrome which can lead to Cor Pulmonale
Drugs that cause restrictive lung disease
Bleomycin, Busulfan, Amiodarone, Methotrexate
Interstitial Restrictive Lung Disease
Characterized by
Names
Decreased Diffusion Capacity and Increased A-a Gradient
“A Good Physician Would Never Speak Hateful, Disgusting Epithets Intentionally”
ARDS, Goodpasture, Pneumoconioses, Wegeners (granulomatosis with polyangiitis), NRDS (hyaline membrane disease), Sarcoidosis (bilateral hilar lymphadenopathy, noncaseating granulomas, Increased ACE and Ca), Hypersensitivity pneumonitis, Drugs, Eosinophilic Granulomas (Langerhans cell histiocytosis), Idiopathic (repeat injury with collagen deposition)
Extra-pulmonary restrictive lung disease
Muscles: Polio, MG.
Structural: Scoliosis, Morbid Obesity
Restrictive Lung Disease: Lung Volumes, PFTs
FVC: decreased, TLC: decreased, FEV1/FVC > 80%
Bronchiectasis Pathology and Associations
“No Hot Days Post September, Onto KA”
chronic Necrotizing infection of bronchi, Hemoptasis, permanently Dilated airways, Purulent Sputum, Smoking (poor ciliary motility), bronchial Obstruction, Kartageners’s (Dynein arm), Allergic bronchopulmonary Aspergillosis, CF
Asthma physical exam findings:
“His Majesty Coughed and Wheezed In Excruciating Pain ‘Till Dawn”
Hypoxia, Mucus plugging, Cough, Wheeze, I/E ratio decreased, Pulsus Paradoxus (decrease in Systolic Pressure), Tachypnea, Dyspnea
Test given to prove asthma
Methacholine challenge. Muscarinic agonist
Asthma pathological causes and course
Bronchial hyper-responsiveness causes reversible Bronchoconstriction + Smooth Muscle hypertrophy
Antigen –> IgE on mast cell. Mast cell releases inflammatory mediators (leukotrienes, histamine, etc.)
Early response to inflammation = bronchoconstriction
Late response to inflammation = Bronchial hyper-reactivity
Asthma triggers
URI, stress, allergens
Asthma histology
Cushmann’s Spirals (shed epithelium from mucus plugging). Charcot-Leyden Crystals (Formed from breakdown of eosinophils in sputum)
