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Unit 6: LGS > Week 6 > Flashcards

Week 6 Flashcards

1
Q

Four common types of obstructive pulmonary diseases

A

COPD
Asthma
OSA
Bronchiectasis

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2
Q

COPD

  • epi
  • risk factors
A
  • 4th leading cause of moridity/mortality

- Smoking, alpha-1-antitrypsin deficiency

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3
Q

Discuss factors that induce COPD

  • Oxidative stress
  • Inflammation
  • Anti-protease imbalance
A
  • ROS cause more cell damage and destruction -> more inflammation
  • Inflammatory cells, release of inflammatory mediators causing epithelial damage and release of more cytokines
  • anti-proteases stop proteses from breaking down a protein, and in case of COPD we want to stop elastase from breaking down elastin
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4
Q

NRF2 gene in COPD

  • what is it?
  • what happens if you knock it out
A
  • gene that codes for transcription factors that help with anti-oxidants; help fight oxidative stress
  • you remove someone’s ability to fight oxidation, they are more susceptible to emphysema and other lung diseases in general
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5
Q

Types of Emphysema

  • Centriacinar
  • Panacinar
  • Distal acinar
  • Irregular emphysema
A
  • More common; Basically the proximal portion of each acinus is involved
  • Panacinar: Does NOT mean all the acini are involved, Entire acinus of the involved acini is involved, Seen in pts with alpha-1 antitrypsin deficiency.
  • Distal acinar: believed to be involved in spontaneous pneumothorax, particularly in young people, b/c peripherally located, Associated with scarring
  • Irregular emphysema: Associated with scarring
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6
Q

Histo changes in emphysema

  • what is big change
  • mechanism
  • what does that cause?
A
  • Destroying walls of alveoli (acinar spaces) and you end up with big empty spaces
  • destroying alveolar walls and there is little fibrosis involved, so you end up with alveoli that are gone and large air spaces
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7
Q

Clinical definition of chronic bronchitis

A

cough productive of sputum for over three months’ duration during two consecutive years and the presence of airflow obstruction

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8
Q

What happens during chronic bronchitis

  • Mucus Hypersecretion; how does this happen? what happens over time? mechanism?
  • Inflammation
  • Infection
A
  • Associated with hypertrophy of submucosal glands in the trachea and bronchi, With time there is also a marked increase in goblet cells in small airways—small bronchi and bronchioles—leading to excessive mucus production that contributes to airway obstruction; You’re inhaling smoke/pollutants and your lungs are secreting mucus to try and clear this stuff out -> Under that stimulation of mucus hypersecretion, your body creates more mucus glands to try and keep up
  • Inflammation: Chronic inflammation –> can lead to fibrosis
  • Infection: Not really a cause but happens to be associated with it
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9
Q

Histo changes in chronic bronchitis

A

Goblet cell hyperplasia which increases thickness of mucosal gland layer; chronic inflammation and fibrosis

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10
Q

What is the reid index?

A
  • ratio of the thickness of the mucous gland layer to the thickness of the wall between the epithelium and the cartilage
  • the bigger it is the worst the bronchitis
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11
Q

Signs and symptoms of emphysema?

  • breathing- when? what does it do?
  • weight loss? why?
  • cough
A
  • Pursed lip breathing; late stages; creates positive pressure ventilation to open up the smaller airways
  • Fatigue
  • Cachexia if this a chronic issue; can be caused from energy expenditure with breathing
  • cough not as prominent b/c it’s deeper in the airways and you’re not trying to clear the mucus.
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12
Q

How can the kind of puff affect which disease the pt gets?

A
  • if it’s more of a shallow puff, then smoke may not be penetrating quite as deeply into the lungs. So they end up with a little bit more damage to the bronchi.
  • For people that are taking really deep puffs, the smoke may get deeper into the lungs, and so they present more with emphysema.
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13
Q

Signs and symptoms of chronic bronchitis?

A
  • persistent cough
  • productive sputum
  • dyspnea
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14
Q

Blood gas level in COPD

A
  • Increased CO2: hypercapnia

- Decreased O2: hypoxemia

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15
Q

Spirometry and COPD

  • FEV1
  • FVC
  • Ratio
  • TLC and RV
A
  • FEV1: decrease -> She has difficulty exhaling, and collapsed alveoli
  • FVC: might not be quite as affected first, but a little later on will see it go down
  • Ratio: decreased; FEV1 decreases disproportionately compared to FBC. Both values go down, but FEV1 goes down more
  • TLC and RV: Increased due to air trapping
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16
Q

Flow volume curve with obstructive

A
  • in later stages of obstruction, we get that air trapping, and not as much volume coming out.
  • the overall volume and residual volume goes up, but it’s stuck in the lungs.
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17
Q

Imaging in COPD

  • what imagining technique would you use?
  • results?
A
  • x-ray

- hyper-inflated lungs, vasulature is shown

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18
Q

Treatment of COPD exacerbations

  • what happens if SABA is not working?
  • What happens if those both aren’t working?
A
  • oxygen, albuterol, IV corticosteroids
  • add a SAMA -> triotropium
  • corticosteroid
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19
Q

Beta 2 agonist signaling at beta adrenergic receptors

A

it’s a multimeric protein, GalphaS subunit. If we agonize that, we are prolonging the cascade so we keep generating cAMP, upregulate PKA and then cause an increase K+ channel activation, downregulate PLC IP3, and increase the Na+/Ca+ATPase

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20
Q

Why would we need antibiotics to treat COPD?

- why would this happen

A

an infection will cause exacerbation and trapping in there. So we need to eliminate the infectious process to get them over that up
- Steroids increase the risk for infection; and there is not effective clearing of mucus secretions which can block the ciliated cells which would stop the functioning of the muco-ciliary elevator and lesses the defenses of the airway which raises increase in risk of infections with COPD.

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21
Q

theophylline’ MOA

A
  • It blocks the degradation of cAMP, increases PKA activity for the relaxation
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22
Q

Different types of asthma

  • atopic
  • non-atopic
  • drug induced
  • occupational
A
  • IgE mediated hypersensitivty triggered by allergens; smoking
  • inflammatory reaction triggered by viruses or inhaled air pollutants; URI
  • aspirin -> inhibits PGE2
  • triggered by fumes, organic and chemical dusts, gases, or other chemicals
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23
Q

Pathogenesis of Asthma

  • genes
  • airway inflammation
  • early reaction
  • late phase reastion
A
  • genetic pre-disposition –> TH2/IgE response to allergens
  • potent inflammatory mediators remodeling of airway wall
  • bronchoconstriction (caused by leukotrienes) , increase mucus production, variable degree of vasodilation, and increased vascular permeability
  • leukocytes (eosinophils, neutrophhils, and more T cells)
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24
Q

Signs and symptoms of asthma

- when do sxs occur?

A
  • recurrent episodes of wheezing, dyspnea, and chest tightness
  • at night or in the morning
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25
Q

Big difference between asthma and COPD

A

asthma is reversible and COPD is not.

26
Q

Confirmatory tests for Asthma

A
  • Pre and post bronchodilator spirometry because we want to see how responsive they are to beta agonism.
27
Q

Treatment for Asthma

  • integrative
  • bronchodilation…. which is better?
  • Why are ICS combined with LABAs
A
  • avoid environmental triggers w./ online trackers, use of HPA filters, cold water fish and colorful fish and veggies
  • beta agonist or anti-muscarinic; anti-muscarinic is a better controller medication but only some patients respond
  • Bronchodilators don’t tx actually cause of disease process whereas the CS do treat the actual inflammatory process that is causing the presentation.
28
Q

under what conditions might anti muscarinic drugs be preferable over beta 2 agonists?

A
  • Someone w/ persistent sx who is not doing well with their current therapy.
  • Also Pt’s with severe cardiac dz that cannot tolerate AE of beta 2 agonists.
29
Q

What is beta receptor desensitization?

A
  • when beta arrestin comes on and does not allow for the G proteins to cause signal transduction there is a loss of response.
  • when someone who has a lot of asthma attacks going on in a week, they might be using their rescue inhaler multiple times a day, multiple times a week which will cause desensitization
  • beta arrestin make receptors go into the lysosome for degradation and not returning them to the cell surface, so now the drug can no longer have its receptor to bind. You have downregulation and decrease in receptor density at the cell surface
30
Q

Obstructive sleep apnea risk factors

A
  • larger tongues, longer soft palates, and greater neck circumference
31
Q

Patho mech for OSA

A
  • sympathetic nervous system surges due to apnea, hypoxia, hypercapnia, and arousal -> increases peripheral resistance and cardiac stiulation -> post-apneic increases BP and heart rate
  • intermittent hypoxia -> reactive oxygen species -> impairs endothelially mediated vasodilation
32
Q

Signs and Sxs of OSA

A
  • loud snoring
  • gasping, choking, nocturnal diaporesis and restlessness related to airway obstruction
  • nocturia
  • excessive daytime sleepiness
33
Q

Studies for OSA

A
  • sleep study; n calculate their AHI- apnea hypopnea index. If it’s elevated- that’s >15/h so that’s 1 every 4 minutes that they stop breathing, then that’s considered enough to require tx for sure. If they have <15 then you see how bad their sx are.
34
Q

Treatment for OSA

Treatment for pulmonary HTN

A
  • continuous positive airway pressure and intr-oral devices

- diuretics, O2, anti-coagulation and vasodilators. (CCB-> NO and PDE-5 inhibitors)

35
Q

Apnea vs hypopnea

A

see how often they stop breathing entirely, for several seconds which is called an apnea. If they stop breathing for a little bit, we call that a hypopnea which isn’t as bad as an apnea.

36
Q

Bronchiectasis

  • what is it?
  • what does it cause?
A
  • destruction of smooth muscle and elastic tissue by chronic necrotizing infection
  • permanent dilation of bronchi and bronchioles in lung segment
37
Q

2 types of restrictive lung dx

A
  • interstitial

- extra-stitial

38
Q

Subtypes of restrictive lung dx

  • interstitial fibrosing
  • interstitial granulomatous
  • extrs-stitial
A
  • UIP and NSIP
  • Hypersensitivty pneumonitis, sarcoidosis
  • Chest wall, neuromuscular
39
Q

Interstitial lung dx risk factors

  • organic
  • inorganic
A
  • wheat weevils, spores to bacteria, fungi, animal proteins, bacterial products
  • coal dust, silica particles, asbestos, heavy metals
40
Q

Interstitial lung dx patho

  • fibroblasts
  • what happens proximal to alveoli?
A
  • fibroblasts lay down collagen and there is so much fibrosis that it cuts off the end of the distal alveoli, and scarring over it, so you’re not getting effective gas exchange when you cut your alveoli in half
  • bronchiolar epithelium metaplasia
41
Q

Patho concepts of interstial lung dx

  • Fibroblastic foci
  • Mature fibrosis
  • Honeycombing
  • Masson bodies
A
  • Immature fibroblast proliferation in a small area
    (interstitial fibrosis)
  • lots of collagen, scarring, pink.
  • Fibrosis between cystic spaces, looks like swiss cheese
  • bronchiolar and alveolar plugs of connective tissue
42
Q

Difference between fibroblastic foci and mature fibrosis

A

Immature fibroblasts lay down immature collagen, fibrogenesis is going on right now, and that’s different from mature interstitia

43
Q

Difference between idiopathic pulmonary fibrosis and usual interstital pneumonia

A
  • IPF is clinical dx while UIP is the name pathologists use to explain the pattern of tissue seen in IPF
44
Q

Distribution of UIP/IPF

A

in the lower lung fields between the septa

45
Q

Maturity of fibrotic lesions in UIP?

A

temporally heterogeneous which means not all of the fibrosis is at the same stage

46
Q

How do people get IPF/UIP?

A
  • Pathogenesis of IPF/UIP includes environmental exposure, genetically susceptible individuals, and aberrant repair.
  • a lot of people are exposed to harmful substance that they breath in but they do not get lung dx so even though this is important there must be something genetically wrong especially for the fibroblasts to inappropriately be responding to cytokines
47
Q

What is the UIP pattern?

A

normal lung, immature ongoing fibrosis, and mature fibrosis following the septae

48
Q

Non specific interstitial pneumonia

  • associations
  • phases
  • histo changes
  • prognosis and management
A
  • idiopathic or associated with connective tissue disease
  • cellular (early, inflammatory) or fibrotic (late)
  • interstital inflammation predominates, with diffuse temporarily homogeneous interstitial fibrosis w/o fibroblasti foci, granulomas, honeycombing, or hyaine memebranes
  • responds to steroids and is favorable prognosis
49
Q

Histologically compare and contrast early and late NSIP

A
  • cellular: lots of blue nuclei with thickened alveolar sepatae
  • fibrosing: pink, collagen indicative of scarring; the gradual thickening of the septae are all the same age
50
Q

Cryptogenic Organizing Pneumonia (BOOP)

  • cause
  • distribution
  • histo
  • treatment and prognosis
A
  • unknown
  • subpleural and peribronchial consolidation
  • loose organizing tissue in the alevoli not the interstitum
  • steroid responsive, good prognosis
51
Q

Interstital Lung Dx signs and symptoms

A
  • dyspnea, ocugh, wheezinf, fatigue, weight loss, night sweats, substernal/pleuritic chest pain
52
Q

Studies for Dx of UIP/IPF

A
  • spirometry; all lung volumes are decreased -> but FEV1/FVC ratio is normal because volume decreases proportionally
  • CXR: distribution in lower lung fields, net like opacities (fibrosis is septa rather than clumped in air space), diaphragm raised on edges
  • CT: honey comb opacities
53
Q

Whar is tension bronchiectasis?

A

scar tissue/fibrosis of the lung tissue will decrease lung elasticity, resulting in pulling-up of the diaphragm edges.

54
Q

Tx for interstitial lung dx

- UIP/ IPF

A
  • supportive car w/ O2 to improve sat; transplant
55
Q

Restrictive chest wall risk factor

A

obesity

56
Q

restrictive chest wall pathogen

  • upper airway
  • lower airway
  • diaphragm
  • accessory muscles
  • ventilatory drive
  • mixed component
A

obesity changes the strx of the upper airways -> bigger soft palate, larger tongue, increase neck thickness -> causes upper airway obstruction

  • in lower airway the adipose tissue on top of lungs is compressing them
  • flattened it out
  • unable to compensate because of weight
  • blunted central hypercapnic and hypoxis vent drive –> due to leptin resistance (leptin normally stimulates ventillation)
  • pt would most likely also have sleep apnea; so would have obstructive and restrictive
57
Q

restrictive chest wall signs and sxs

A
  • snoring
  • witnessed apnea/hypopneas
  • cognitive impairment
  • unrestful sleep
  • excessive daytime sleepiness
  • dyspnea
  • hypoxemia
  • prominent pulmonia component of second heart sound
  • JVD
58
Q

Is the pulmonary hypertension caused by low oxygen & vasoconstriction or by the sleep apnea, reactive oxygen species destruction or combination of both?

A
  • Combination of both
  • When you’re not getting adequate oxygen then you have incomplete mitochondrial respiration so you’re going to end up w/those ROS, those free radicals
  • When you have increased oxidation somewhere that tends to trigger inflammation, all the inflammatory cytokines & other cells that come in tend to do damage in the area including damage btwn the pulmonary vascular interface.
  • That will end up impairing gas exchange, eventually you’ll have hypoxemia
59
Q

How do you get right sided heart failure with restrictive chest wall

A
  • The damage to the blood vessels of the lungs eventually will put additional stress on the heart, & you’ll eventually get to R sided heart failure.
  • It doesn’t take long bc the R side of the heart can’t compensate quite as easily as the L side, so it won’t be long once you have R sided that it starts to impact & back up over to the L side as well.
60
Q

How to dx restrictive chest wall with studies

  • ABG
  • EKG
A
  • hypercapnia on ABG; HCO3 level <27 excludes dx

- EKG: S1 Q3 T changes

Unit 6: LGS (10 decks)

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