Week 4/5 Flashcards
1
Q
Atelectasis - what is it? - common causes of resorption atelectasis
A
- 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
2
Q
Types of Atelectasis and mediastinal shift - resorption - compression - contraction
A
- 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
3
Q
Pulmonary edema - discuss how pt with CHF develop pulm edema - How to develop Pulmonary edema that is non-cardiogenic - Specifics of pneumonia - explain ARDS
A
- 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
4
Q
Acute Lung Injury - also known as? - sxs - four most common causes
A
- noncardiogenic pulmonary edema - abrupt onset of significant hypoxemia and bilateral pulmonary infiltrates w/ absence of cardiac failure - infection, trauma, inhaled/chemical injury - hematologic
5
Q
How can sepsis or head injuries damage the alveoli?
A
- sepsis: bacterial endotoxins can cause a defect in permeability - head injuries: increase in microvascular permeability and/or pulmonary vasoconstriction ad left ventricular dysfunction
6
Q
Discuss how clinical presentation of acute lung injury is related pathologically to ARDS - sxs - pathway of dx
A
- 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
7
Q
Why does mechanical ventilation often not work in patients with acute lung injury?
A
- 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
8
Q
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
A
- 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
9
Q
Pleural Effusion - what is it?
A
- excess accumumlation of fluid between pleural layers causes restricted lung expansion during inspiration
10
Q
What is the mechanism and physiology behind nephrotic syndrome
A
- 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
11
Q
What is the mechanism and physiology behind carcinomatosis
A
- decreased lymph drainage - multiple tumors –> block lymph drainage –> buildup of lymph fluid –> rupture of lymph ducts –> pleural effusion
12
Q
What is the mechanism and physiology behind atelectasis
A
- 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
13
Q
What is the mechanism and physiology behind pneumonia
A
- increased vascular permeability - lung infection –> pneumonia –> inflamm mediators –> increased vascular permeability –> pleural effusion
14
Q
What is the mechanism and physiology behind congestive heart failure
A
- increased hydrostatic pressure - CHF -> pasive congestion in pulmonary circulation -> increased hydrostatic pressure in lungs -> increased fluid into interstitial spaces -> pleural effusion
15
Q
- What is this?
- where are the bronchi? how many?
- structure of bronchi
- epithlium in lumen
- types of cells (4)
- type of cartilage
A
- 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
16
Q
- What is this?
- what is found in the lamina propria/submucosa?
- type of cartilae found here
- smooth muscle cells?
A
- lung tissue
- seromucous glands, cartilage, smooth muscle
- bronchial (hyaline)
- yes
17
Q
- what is the difference between a bronchi and bronchiole?\
- what is a pulmonary lobule?
- what is a pulmonary acinus?
A
- 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
18
Q
What is this?
- what is difference between the 2?
- waht are the non-ciliated secretory cells called?
A
- 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
20
Q
What is this?
- describe histo
- function
A
- club cell
- non ciliates, non mucous secreting
- secretes surfactant, antimicrobial peptides, SER enxyes, and repairs airway damage
21
Q
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
A
- 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
22
Q
Alveoli Structure and Function
- what is priduced by II alveolar cells? How do they make it and store it?
A
- surfactant; lamellar bodies
23
Q
What is this?
- types of cells indicated by arrow? function?
A
- Visceral pleura
- Meothelial cells -> secrete pleural serous fluid
24
Q
Imaging modality anf view depicted?
- how was the patient positioned?
A
PA and Lateral chest xray
- patient is standing, back is to x-ray machine and front is to plate
25
Q
What are the imaging modaloty and view depicted?
- How was patient poisitioned
A
- AP/ Frontal CXR
- Patient supine, x-ray machine to chest, the board on the back
26
Q
- Imaging modality, body part, orientation, and window?
- Identify the major airway structures
- whay can’t you see the heart?
A
- ST chest, coronal. lung window
- becase it is a lung window and the heart has a higher density thatn the lungs allowing them to be separated
27
Q
- imaging modality, and view?
- age of patient? how?
- abonrmalities in the lungs?
- how many support devices are there?
- are all support devices properly placed?
A
- AP, fronatl CXR
- infacnt because you can see the thymus, the ribs are mor horizontal, the ribcage has a trapezoid shape and there are ossification areas
- R: hypertranslucent= hyperinflation; L: pneumothroax
- Endotracheal tube, nasogastric tube, ECG leads
- No, the ETT is in the right main bronchus
28
Q
- Imaging modality and views
- dx? why?
A
- Frontal and lateral chest xray in an infant
- Foreign body in esophagus because in lateral x-ray you can see the strip of air in front of esophagus meaning that the trachea is clear
29
Q
What are the imaging modality, boday part, orientation and window depicted?
- which lung is this?
- name the fissure(s)
A
- CT chest, sagittal, lung window
- right lung
- horizontal on left and oblique on right
30
Q
imaging modality, body part, orientation and window?
- describe the abnormalities?
A
- CT chest/ axial. lung window
- Large right pneumothroax
31
Q
- imaging modality and views depicted?
- relative age and sex of patient? Explain.
- Major abnormalities? Explain.
A
- PA and lateral CXR
- Elderly female because there is degenerative changes in the spine and breast tissue
- Sever pulmonary hyperinflation because there is diaphragmatic flattening on both the PA and lateral views; increased AP dimension of the ches as well as increased retrosternal clear spacr on the lateral view
32
Q
- 52 year old previously healthy woman comes into clinic complainging of fatigue, cough, and left sided chest pain. Temp of 101.7 and diminished breath sounds in left base anteriorly.
- What imaging do you order and why?
- describe the abnormality
- dx?
A
- 2 view chest x-ray because she has chest pain and diminished breath sounds; also is is relatively inexpensive and readily availabke making it a good screening test
- airspace infiltrates in the lingula
- Lingular pneumonia
33
Q
22 year old previously healthy woman comes into clinic with recent onset of shortness of breath and left sided chest pain. BP of 88/54 and diminished breath sounds in left side of chest diffusely.
- what imaging do you order and why?
- what in the imaging modality and view depicted? why?
- abnormality? explain.
- emergency?
A
- CXR, because of shortness of beath and dimnished breath sounds
- AP upright CX becuase of the patient instability
- large left pneumothorax; lung of chest wall injury allows air into pleural space but not out, so air accumulate and compresses the lung
- yes
