Week 8 Flashcards
What type of cells in respitory tract correlate with the following functions
Conduction, gas exchange, host defense, communication, olfaction
- Conduction (the flowing of air) – pseudostratified, columnar, both of which can be ciliated
- Exchange of gases – simple squamous epithelium
- Host defense
- Simple squamous, pseudostratified, columnar, stratified squamous +/- keratinization
- Communication
- Olfaction – cells with chemoreceptors
Function of squamous mucosa
- On the left, stratified squamous with keratinization is in areas with mechanical trauma (i.e. the vocal cords where they slam together)
- Stratified squamous (+/- keratin) are in areas of mechanical trauma – the mouth, the tonsils, the vocal cords, the first portion of the nose
Function of respirtory mucosa
- On the right, the respiratory mucosa have goblet cells which secrete mucous and cilia to move the mucous + antigen/dust/particles out of the respiratory tract
Function of following olfactory cell types..
sustentacular nuclei, olfactry nuclei, Bowman glands
The sustentacular nuclei are for structure/barrier
The olfactory cell nuclei are olfactory neurons that turn over every month
Beneath the surface with chemoreceptors, Bowman’s Glands secrete a fluid that dissolves the chemicals that give scents
How many times do bronchi branch
23
Epithelial type 1 versus 2
- Epithelial type I cells participate in gas exchange
- Epithelial type II cells generate surfactant
Explain this pic
- C is the capillary
- A is the alveolar space
- O2 crosses the plasma membrane of the cells lining the alveolus and the capillary (2 cells with thin plasma membranes) and a basement membrane to diffuse into blood
Identify
right: respiratory mucosa
left: stratified squamous
Triggers for PE
- Trigger for thrombus formation: Virchow’s Triad
- Endothelial damage
- Hypercoagulability
- Stasis
Signs of PE (5)
- Signs
- DVT – common thrombus that can travel to the lung
- Elevated JVD – backup of fluid due to increased pulmonary resistance
- In lung with clot, perfusion decreases
- In lung without clot, perfusion increases because the blood has to go somewhere
- Tachycardia – decreased SV leads to increased HR to maintain CO
- Tachypnea – higher RR compensating for the increased PCO2
- In lung with decreased perfusion, there is a increased V/Q ratio
- The lung will have an area that is ventilated, but not perfused, leading to increased A-a gradient with O2 and increased PaCO2
- Shock – decreased CO due to decreased volume return to left side of heart
Symptoms of PE (3)
- Symptoms
- Chest pain – infarction of lung
- SOB – increased PCO2
- Syncope – decreased CO
Complications of PE (3)
- Complications
- Mortality when untreated: 30%
- Recurrent embolism due to thrombogenicity of first embolism
- Recurrent PEs require lifetime treatment
Explina the rationale behind these PE diagnosistic tests
EKG, CT angiography, scintigrapghy, D-dimer
- EKG shows inverted Tw, showing the possibility for ischemia + tachycardia
- CT pulmonary angiography
- Avoid in renal failure
- Ventilation-perfusion scintigraphy
- Ventilation scan: inhalation of radiotracer
- Perfusion scan: injection of radiotracer albumin
- Can see hypoxic pulmonary vasoconstriction in lung with PE
- D-Dimer – fibrin degradation product
- Highly sensitive (good at ruling diagnosis out) and low specificity (not good at ruling diagnosis in)
- Because of low specificity, you need other diagnostic tests to confirm a PE diagnosis
Acute vs, Longterm tx of PE
- Acutely: enoxaparin or unfractionated heparin
- Long term: oral Xa inhibitors or warfarin
- If unable to anticoagulated: IVC filter
- When serious, give the clot buster! Give systemic thrombolytics: tPA
Varenicline
MOA, Use, AE
MOA:Nicotine receptor agonist
Use: Eases withdrawal symptoms and blocks pleasurable effects
AE:
- Transient nausea
Bupropion
MOA, Use, AE
MOA:Inhibits dopamine reuptake (lasting feeling of pleasure)
Use: Smoking cessation aid
AE:
- Tremors
- Insomnia
Omalizumab
Class, MOA, Use, AE
Class:MAB
MOA:Binds to IgE
Use: allergic asthma
AE:
- expensive
Ipratropium
Tiotropium
Class, MOA, Use, AE
Class:Anticholinergics
MOA:Block M3 receptors (Gq receptors)
Use: Bronchodilation
AE:
- Dry mouth (opposite of SLUD)
Theophylline, caffeine
Class, MOA, Use, AE
Class:Methylxanthines
MOA:
- Inhibits PDE3, activating PKA and causing vasodilation
- Inhibits PDE4, inhibiting inflammatory processes
- Enhance catecholamine secretion to work on beta-2
Use: Used if other drugs do not work, Nocturnal asthma
AE:
- Stimulant
- Diuretic affects
Albuterol (short-acting)
Salmeterol (long-acting)
Class, MOA, Use, AE
Class:Beta-2 agonists
MOA:Beta-2 agonist
Use: Bronchodilation
AE:
- Tachycardia
Montelukast
Class, MOA, Use, AE
Class:Leukotriene modifiers
MOA:Acts on leukotriene receptors C4, D4, E4, decreasing LT effect on Gq receptors
Use: Decreases bronchoconstriction
AE:
- Well Tolerated
Cromyln
Class, MOA, Use, AE
Class:Mast cell inhibitor
MOA:Stabilize plasma membrane of mast cells and basophils and eosinophils to prevent degranulation and release of histamine and leukotrienes
Use: Prevents degranulation and release of histamine and leukotrienes
AE:
- Well Tolerated
Fluticasone
Budesonide
Class, MOA, Use, AE
Class:Glucocorticoid
MOA:Acts as a nuclear transcription factor to antagonize mucous production and inflammatory mediators
Use: Prophylaxis, Upregulation of beta receptor
AE:
- Thrush (can avoid with water)
- Change in vocal chords (can avoid with water)
- Decrease in bone density
- Abruptly stopping drug is bad because cortisol inhibits HPA
What is the pharyngeal pouch made of…
The pharyngeal pouch is made up of cells from the neural crest, endoderm, mesoderm, and ectoderm
What strucutres come form the endoderm, splanchnic mesoderm, somatic mesoderm
- The endoderm forms the pulmonary epithelium and glands of the larynx, trachea, and bronchi
- The splanchnic mesoderm forms the cartilage, connective tissue, visceral pleura, and smooth muscle
- The somatic mesoderm forms the parietal pleura (which is why you can feel pain)
Lung Development
What happens in week 6,7,16,24,32
- Week 6: secondary bronchial buds form, which represent future lung lobes
Week 7: tertiary bronchial buds form, which represent future bronchopulmonary segments
Week 16: terminal bronchioles form
Week 24: vasculature and first primitive alveoli form
Week 32: mature alveoli develop
Lung Development
What happens in week 4 and 5
- Week 4: the laryngotracheal diverticulum from the endoderm and mesoderm forms the respiratory diverticulum (lung bud)
- Endoderm is internal epithelium
- Initial proliferation of internal epithelium occludes larynx, but at week 10, apoptosis leads to larynx recanalization
- Mesoderm is connective tissue and smooth muscle
- Endoderm is internal epithelium
- Week 5: Respiratory diverticulum branches into left and right bronchial buds
- This process creates the carina (septum) in the laryngotracheal tube resulting in the formation of the trachea (which is everything superior to the bronchial buds)
Describe the Pseudoglandular stage
- Pseudoglandular stage – 5 to 17 weeks
- The developing lung at this point resembles a branched, compound gland
- At this point, there are no alveoli, so respiration is not possible
- Also only modest vascularization
- Conductive structures (aka bronchi) are the only ones developed
Describe the Canalicular Stage
- Canalicular Stage – 16 to 26 weeks
- Terminal bronchioles mature
- Alveolar ducts begin to form… prognosis of premature babies is poor at this stage
- Highly vascularized
Describe the Terminal Saccular Stage
- Terminal Saccular Stage – 24 weeks to birth
- Increase in the number of primordial alveoli
- Surfactant production increases
Describe the alveolar stage
- Alveolar Stage – 32 weeks to 8 years old
- Alveolaocapillary membrane forms and proper gas exchange can occur
Laryngeal atresia
- Laryngeal atresia – failure of recanalization –> obstruction of the upper airway
Laryngeal web
- Laryngeal web – partial occlusion due to mucous membrane covering the vocal cords
- Results in a hoarse cry
Tracheo-esophageal fistulas (TEF)
- Tracheo-esophageal fistulas (TEF) – incomplete division of the respiratory diverticulum in week 4
- Results in an abnormal connection between the esophagus and trachea, allowing food to enter the lungs (depending on the type of TEF)
Tracheal bronchus
Tracheal bronchus – extra branches off of the trachea
Respiratory Distress Syndrome (RDS)
Respiratory Distress Syndrome (RDS) – inadequate surfactant function, causing lungs to collapse and inadequate ventilation of some alveolar sacs
obstructive lung diseases
symptoms (4)
Dyspnea (at rest)
Wheezing
Cough
Episodic
obstructive lung diseases
Pathophysiology
- Obstruction of air flow → air trapping in lungs→ FRC, TLC, and RV increases → barrel chest
- Pulmonary Function Tests: large decrease in FEV1, smaller decrease in FVC→ hallmark decrease in FEV1/FVC ratio
obstructive lung diseases
signs (3)
Diminished air flow
Wheezes/rhonchi
Chest hyperinflation
asthma
triggers, patho. epidemiology, pathphysiology
- Triggers: viral URIs, allergens, stress, exercise
- Pathology: smooth muscle hypertrophy and hyperplasia due to eosinophilia
- Epidemiology: 5 to 20% of population depending on age
- Pathophysiology:
- Reversible bronchoconstriction due to hyperresponsiveness
- FEV1 decreases: bronchoconstriction leads to decreased flow of air during expiration
chronic bronchitis COPD
presentation, epidemiology, patho
- Presentation: “blue bloater” – hypoxemia due to right to left shunt of blood, cough with sputum
- Epidemiology of COPD as a whole: 6-8% and is the only major cause of death that is increasing in prevalence
- Pathology: hypertrophy and hyperplasia of mucus-secreting glands due to neutrophilia
emphysema COPD
types
Centrialobular – associated with smoking
Panlobular – associated with alpha-1 antitrypsin deficiency
emphysema COPD
presentation, patho, pathogensis, epidemiology
- Presentation: “pink puffer” – pink complexion and pursed lips
- Pathology: enlargement of air spaces due to collapse of alveoli
- Loss of elastic fibers leads to decreased lung recoil à barrel chest
- Pathogenesis: inflammation of the lungs normally leads to release of proteases by neutrophils and macrophages à protease damage causes destruction of alveolar air sacs
- Smoking: excessive inflammation and protease mediated damage
- Alpha-1 antitrypsin: neutralizes proteases
- Epidemiology of COPD as a whole: 6-8% and is the only major cause of death that is increasing in prevalence
Broncheictasis
CF vs. non-CF
- Cystic Fibrosis Pathogenesis: impaired ciliary movement → mucus plug→ bronchodilation → mucus buildup → infection → chronic necrotizing infection → permanent dilation of bronchioles → loss of airway tone → air trapping
- Non-CF Pathogenesis: immunodeficiency → infection → chronic necrotizing infection → increased cytokine production → increased mucus production → obstruction of airway → permanent dilation of bronchioles → loss of airway tone → air trapping
Bronchiolitis
pathogensis, etiology
Pathogenesis: inflammatory disorder of small bronchioles
Etiology: often viral but can be idiopathic
restrictive lung diseases
descritpion and PFT results
- Restricted lung expansion (increased elastic recoil) causes decrease in forced vital capacity and total lung capacity
- Pulmonary Functional Tests: proportional decrease in both FEV1 and FVC leads to relatively stable FEV1/FVC ratio
restrictive lung diseases
pathogensis, symptoms, signs, lab findings
- Pathophysiology
- Antigen is picked up by the macrophages in the alveolar sacs à recruitment of fibroblasts à laying down of collagen à fibrosis
- Symptoms
- Short, shallow breaths
- Dry cough
- Flu-like illness may precede disease
- Signs
- Tachypneic
- Cyanosis à clubbing
- Chest CT: honeycomb appearance of lungs
IDK WHAT TO DO ABOUT THIS PIC BUT HERE IT IS
MEMORIZE IT I GUESS
Pneumoconiosis - Coal
Clinical Description, Pathological features
CD: Silicosis – Coal Workers’ Pneumoconiosis – inhalation of coal particles
PF:Anthracosis – small collections of dust-laden macrophages near respiratory bronchioles
Pneumoconiosis - Silicosis
Clinical Description, Pathological features
CD: Silicosis – decades exposure to sand in mining industry with increased incidence of TB
PF:Dense pink fibrosis surrounded by histiocytes that have polarizable birefringent crystals
Pneumoconiosis - asbestos
Clinical Description, Pathological features
CD: Asbestos – silicate mineral with heaviest exposures in industries
PF:Lung adenocarcinoma, malignant mesothelioma, pleural plaques (fibrocalcific formation on parietal pleura), and asbestosis (long-thin crystal-like finding)
Hypersensitivity pneumonitis
Clinical Description, Pathological features
CD: Type III or Type IV hypersentitivity reaction that produces granulomas
PF:Chronic inflammation of the bronchioles, granulomas, and fibrosis
Interstitial pneumonia/follicular bronchiolitis from Collagen Vascular Disease
Clinical Description, Pathological features
CD: Common in Rheumatoid Arthritis, SLE, and Sjogren’s Syndrome
PF:
Interstitium is thick but architecture is respected and there is not a lot of fibrosis
- Interstitial pneumonia (top) – many lymphocytes have invaded the interstitium but it is more cellular without fibrous tissue
- Follicular bronchiolitis (bottom) – chronic inflammation with dark lymphoid aggregates
Sarcoidosis
Clinical Description, Pathological features
CD: Systemic non-necrotizing granulomatous disease with bilateral hilar and mediastinal lymphadenopathy
PF:
Multinucleated giant cell due to fused histiocytes forming small nodules in interstitium
- Schaumann body – Ca2+ and protein deposit in the giant cell
- Asteriod body – cytoskeletal proteins in the giant cell
Usual Interstitial Pneumonia (UIP)
Clinical Description, Pathological features
CD:
- Diagnosis if there is no other explanation
- Chronic symptoms upon presentation
PF:
- Area of many inflammatory cells
- Fibroblast foci with significant proliferation and collagen deposition
Usual Interstitial Pneumonia (UIP)
Sarcoidosis
Interstitial pneumonia
Follicular bronchiolitis
Hypersesntivity pneumonitis
Asbestos
Silicosis
Coal Workers’ Pneumoconiosis
Spiromentry versus complete PFTs
- Spirometry and complete PFTs provide information on lung volumes and capacities
- PFTS give FRC, RV, TLC, and DLCO, which spirometry cannot
- Spirometry can only “suggest” restrictive disease, which PFTs can confirm
- Useful for diagnosis and disease monitoring
Explain this pic
- Extrathoracic airway obstruction
- Flow becomes obstructed during inspiration because atmospheric pressure is greater than tracheal pressure
- Variable intrathoracic airway obstruction
- Flow becomes more obstructed during expiration because the difference between the intrapleural pressure and the alveolar pressure is less than normal
process, focus and exampls of
asphyxiation, COPD, asthma, granulomatous lung disease, pneumoconiosis
Anterior Mediastinal Diseases:
- The Four Ts + Other:
- Thymoma
- Thyroid – goiters
- Teratoma
- Terrible Lymphoma
- Congenital Diaphragmatic Hernia
Middle Mediastinal Disease:
- Cardiac/Great Vessels
- Superior Vena Cava Syndrome
Superior Vena Cava Syndrome
Patterns of Differentiation in Etiological Causes
Tumor – will cause dilated veins of chest
Trauma – will cause demarcated cyanosis of upper body
Posterior Mediastinum Diseases:
- Neurogenic tumors
- Spine tumors
- Descending aortic aneurysm/dissection
- Bochdalek or hiatal hernias
- Esophageal tumors
Pneumomediastinum
some characteristics and ways to treat
- You may or may not feel air under the skin around the neck region or chest on physical exam (“subcutaneous emphysema”)
- Ability to palpate gas under the skin
- Think crepitus around neck
- You need to find the origin of the hole so as to control the leak; the differential includes anything along the aero-digestive track (esophagus, trachea, etc.)
- Trauma of upper airway
- Perforation of the stomach
- Rupture of the esophagus
- Rupture of the trachea
Pancoast tumore
description and complications
- Tumor near the apex of the lung that compresses the brachial plexus
- Result is Horner’s Syndrome:
- Anhidrosis – lack of facial sweating
- Miosis – constricted pupil
- Ptosis – dropping of eyelid
Pneumomediastinum
pancoast tumor
small vessel vasculitis
excess of neutriphils in interstitial space
fibrinous pleuritis
(right side) look at the extra fiberous layer - not normal
