Week 4/5 Flashcards
(45 cards)
Atelectasis - what is it? - common causes of resorption atelectasis
- incomplete expansion of the lungs or collapse of previously inflated lung, producing areas of relatively airless pulmonary parenchyma - bronchial asthma, chronic bronchitis, bronchiectasis, and post op states; foregin body aspiration; bronchial tumors
Types of Atelectasis and mediastinal shift - resorption - compression - contraction
- complete obstruction of an airway because of excessive excretions -> air resorbed from dependent alveoli –> collapse; mediastinal goes towards the impingement - significant volumes of fluid (transudate, exudate, or blood), tumor, or air accumulate within the pleural cavity; medistinal shift is away from liquid - focal/ generalized pulmonary or pleural fibrosis prevents full lung expansion
Pulmonary edema - discuss how pt with CHF develop pulm edema - How to develop Pulmonary edema that is non-cardiogenic - Specifics of pneumonia - explain ARDS
- hemodynamic pulm edema: due to increase hydrostatic pressure on venule side of capillary; fluid accumulates initially in basal regions of lower lobes because hydrostatic pressure is greatest in these sites - due to injury in alveolar septa; primary injury to vascular endothelium or damage to alveolar epithelial cells which produces inflammatory exudate that leaks into the interstitial space and alveoli - edema remains localized - when diffuse alveolar edema is an important contributor to acute respiratory distress syndrome
Acute Lung Injury - also known as? - sxs - four most common causes
- noncardiogenic pulmonary edema - abrupt onset of significant hypoxemia and bilateral pulmonary infiltrates w/ absence of cardiac failure - infection, trauma, inhaled/chemical injury - hematologic
How can sepsis or head injuries damage the alveoli?
- sepsis: bacterial endotoxins can cause a defect in permeability - head injuries: increase in microvascular permeability and/or pulmonary vasoconstriction ad left ventricular dysfunction
Discuss how clinical presentation of acute lung injury is related pathologically to ARDS - sxs - pathway of dx
- tachypnea, dyspnea, cyanosis - pneumocyte injury -> endothelial activation (alveolar macrophages, TNF, inflamm mediators) -> adhesion and extravasion of neutrophils -> increased recruitment and adhesion of leukocytes -> more endothelial injury and local thrombosis -> accumulation of intra-alveolar fluid into hyaline membranes -> diffuse alveolar damage
Why does mechanical ventilation often not work in patients with acute lung injury?
- ventilation/perfucion mismatch occurs because the functional abnormaltiies are not evenly distributed throughout the lung - Some areas are collapsed and others have normal levels of ventilation - Poorly aerated regions continue to be perfuse -> V/Q mismatch and hypoxemia
20 year old male with w/ hemoptysis, hematuria, and elevated serum creatine compatible with acute renal failure…. - syndrome - targets - how does this manifest? - prognosis if untreated? - iron stain - IgG - Treatment
- Good pasture syndrome: encironmental insult unmasks normally hidden epitopes that form ani-collagen antibodies - non-collagenous domain of the alpha 3 chain of collagen IV in basement membranes of kidney glomeruli and lung alveoli - rapidly progressive glomerulonephritis –> renal failure and hematuria; necrotizing hemorrhagic interstitial pneumonitis –> hemoptysis and focal pulmonary consolidations on CXR - uremia (elevated level of urea in blood) is cause of death - positive in lung; supports dx of goodpastures by confirming presence of hemosiderin-laden macrophages in alveoli - linear IgG deposition along pulmonary capillary basement membrane is virtually diagnostic of good pastures - intensive plasmapharesis bc it removes circulating Anti-GB< antibodies and chemical mediators of immunologic injury
Pleural Effusion - what is it?
- excess accumumlation of fluid between pleural layers causes restricted lung expansion during inspiration
What is the mechanism and physiology behind nephrotic syndrome
- M: decreased oncotic pressure - damage to the glomerulus –> loss of plasma protein –> loss beyond synthetic capacity of liver –> hypoalbuminemia –> decreased intravascular colloid osmotic pressure –> increased fluid into interstitial spaces –> pleural effusion
What is the mechanism and physiology behind carcinomatosis
- decreased lymph drainage - multiple tumors –> block lymph drainage –> buildup of lymph fluid –> rupture of lymph ducts –> pleural effusion
What is the mechanism and physiology behind atelectasis
- increased negative intrapleural pressure - pleural effucion –> increase pressure on lung –> decrease lung volume to less than resting –> loss of contact between visceral and parietal pleura –> atelectasis
What is the mechanism and physiology behind pneumonia
- increased vascular permeability - lung infection –> pneumonia –> inflamm mediators –> increased vascular permeability –> pleural effusion
What is the mechanism and physiology behind congestive heart failure
- increased hydrostatic pressure - CHF -> pasive congestion in pulmonary circulation -> increased hydrostatic pressure in lungs -> increased fluid into interstitial spaces -> pleural effusion
- What is this?
- where are the bronchi? how many?
- structure of bronchi
- epithlium in lumen
- types of cells (4)
- type of cartilage

- Lung tissue
- black boxes; 3
- large lumen, lined by respiratory epi and rich hyaline cartilage
- respiratory epithelium; psuedostratified ciliated columnar epi with goblet cells
- goblet cells, epithelia, smooth muscles, neuroendocrine cells
- hylaine cartilage
- What is this?
- what is found in the lamina propria/submucosa?
- type of cartilae found here
- smooth muscle cells?

- lung tissue
- seromucous glands, cartilage, smooth muscle
- bronchial (hyaline)
- yes
- what is the difference between a bronchi and bronchiole?\
- what is a pulmonary lobule?
- what is a pulmonary acinus?

- bronchi: columnar epi with many goblet cells and removes FB’s; bronchioles: cuboidal epi with few goblet cells, cartilage plates and muscous glands absent
- terminal bronchiole
- starts at the respiratory bronchiols, includes alveolar ducts and sacs also
What is this?
- what is difference between the 2?
- waht are the non-ciliated secretory cells called?

- terminal bronchial on left and respiratory bronchiole on right
- more smooth muscle at the terminal bronchiole and it goes into a respiratory bronchiole but respiratory bronchiole is the beginnig of where there is air exchange
- club cells
Trace the path of air flow from terminal bronchiole to the alveoli
- waht happens to epi from bronchioles to alveoli
- terminal bronchiole -> respiratory bronchiole -> alveolar duct -> alveolar sac -> alveoli
- simple cuboidal -> Type I and II alveolar cells
What is this?
- describe histo
- function

- club cell
- non ciliates, non mucous secreting
- secretes surfactant, antimicrobial peptides, SER enxyes, and repairs airway damage
What is this?
- functions of Type I alveolar cells, Type II alveolar cells, Alveolar macrophages, Dendritic cells, Stromal cells
- What type of connective tissue do stromal cells produce?
- what happens in emphysema

- alveolar cells
- Type I alveolar cells: gas exchange
- Type II alveolar cells: surfactant
- Alveolar macrophages: phagocytosis
- Dendritic cells: APC
- Stromal cells: support
- Elastic and Reticular fibers
- elastic and reticular fibers decrease which allows for compliance to increase and elasticity to decrease
Alveoli Structure and Function
- what is priduced by II alveolar cells? How do they make it and store it?

- surfactant; lamellar bodies

What is this?
- types of cells indicated by arrow? function?

- Visceral pleura
- Meothelial cells -> secrete pleural serous fluid
Imaging modality anf view depicted?
- how was the patient positioned?

PA and Lateral chest xray
- patient is standing, back is to x-ray machine and front is to plate









