Week 8 Flashcards

Question

What strucutres come form the endoderm, splanchnic mesoderm, somatic mesoderm

Answer 1

* 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)

Answer 2

* 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

Answer 3

* 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 * 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)

Answer 4

* 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

Answer 5

* 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

Answer 6

* Terminal Saccular Stage – 24 weeks to birth * Increase in the number of primordial alveoli * Surfactant production increases

Answer 7

* Alveolar Stage – 32 weeks to 8 years old * Alveolaocapillary membrane forms and proper gas exchange can occur

Answer 8

* Laryngeal atresia – failure of recanalization --\> obstruction of the upper airway

Answer 9

* Laryngeal web – partial occlusion due to mucous membrane covering the vocal cords * Results in a hoarse cry

Answer 10

* 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)

Answer 11

Tracheal bronchus – extra branches off of the trachea

Answer 12

Respiratory Distress Syndrome (RDS) – inadequate surfactant function, causing lungs to collapse and inadequate ventilation of some alveolar sacs

Answer 13

Dyspnea (at rest) Wheezing Cough Episodic

Answer 14

* 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

Answer 15

Diminished air flow Wheezes/rhonchi Chest hyperinflation

Answer 16

* 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

Answer 17

* 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

Answer 18

Centrialobular – associated with smoking Panlobular – associated with alpha-1 antitrypsin deficiency

Answer 19

* 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

Answer 20

* 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

Answer 21

Pathogenesis: inflammatory disorder of small bronchioles Etiology: often viral but can be idiopathic

Answer 22

* 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

Answer 23

* 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

Answer 24

CD: Silicosis – Coal Workers’ Pneumoconiosis – inhalation of coal particles PF:Anthracosis – small collections of dust-laden macrophages near respiratory bronchioles

Answer 25

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

Answer 26

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)

Answer 27

CD: Type III or Type IV hypersentitivity reaction that produces granulomas PF:Chronic inflammation of the bronchioles, granulomas, and fibrosis

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

Usual Interstitial Pneumonia (UIP)

Answer 32

Sarcoidosis

Answer 33

Interstitial pneumonia

Answer 34

Follicular bronchiolitis

Answer 35

Hypersesntivity pneumonitis

Answer 36

Coal Workers’ Pneumoconiosis

Answer 37

* 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

Answer 38

* 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

Answer 39

* The Four Ts + Other: * Thymoma * Thyroid – goiters * Teratoma * Terrible Lymphoma * Congenital Diaphragmatic Hernia

Answer 40

* Cardiac/Great Vessels * Superior Vena Cava Syndrome

Answer 41

Patterns of Differentiation in Etiological Causes Tumor – will cause dilated veins of chest Trauma – will cause demarcated cyanosis of upper body

Answer 42

* Neurogenic tumors * Spine tumors * Descending aortic aneurysm/dissection * Bochdalek or hiatal hernias * Esophageal tumors

Answer 43

* 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

Answer 44

* 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

Answer 45

Pneumomediastinum

Answer 46

pancoast tumor

Answer 47

small vessel vasculitis excess of neutriphils in interstitial space

Answer 48

fibrinous pleuritis (right side) look at the extra fiberous layer - not normal