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Pathology II > Exam 1 Part 1 > Flashcards

Exam 1 Part 1 Flashcards

1
Q

what 3 factors are involved in maintaining adequate respiration?

A
  • adequate intake of air
  • rapid diffusion
  • adequate perfusion
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2
Q

where is the blood air interface?

A

between type I pneumocytes & endothelium

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3
Q

what are the 4 classical classifications of pulmonary pathology?

A
  1. degenerative
  2. inflammatory
  3. pleural
  4. neoplasm
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4
Q

what are congenital pulmonary abnormalities? what can they cause?

A
  • agenesis
  • hypoplasia
  • tracheal/bronchial anomalies
  • all can cause NRDS
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5
Q

what is pulmonary hypoplasia often secondary to?

A
  • IUGR

- congenital diaphragmatic hernia

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6
Q

what TE fistula is the most common?

A

esophageal atresia + distal TE fistula

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7
Q

what causes NRDS? what is it also known as?

A
  • lack of surfactant
  • born <28 wks
  • hyaline membrane disease (membranes form as result of loss of surfactant)
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8
Q

what are some other causes of NRDS (besides congenital)?

A
  • over sedation of mom
  • head trauma during birth
  • aspiration of blood or amniotic fluid
  • intra-uterine hypoxemia
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9
Q

is atelectasis a disease itself?

A

NO it is an anatomic/physiologic/geometric CONCEPT seen in many disease states

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10
Q

what are the 3 forms of atelectasis?

A
  1. resorption, tumor
  2. compression, pleural effusion
  3. contraction, diffuse lung fibrotic process
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11
Q

what is PEd? what are causes of PEd?

A
  • accumulation of fluid in lungs= impaired gas exchange= possible respiratory failure
    1. failure of heart to remove fluid from lung circ
    2. direct injury to parenchyma
    3. fluid overload
    4. hypoalbuminemia
    5. lymphatic obstruction
    6. “strange things”
    7. infection
    8. liquid or gas or chemical aspiration
    9. chemotherapeutic agents
    10. high altitude sickness
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12
Q

what are the 4 main pathologic mechanisms which lead to PEd?

A
  • increased venous pressure
  • increased oncotic pressure
  • lymphatic obstruction
  • alveolar injury
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13
Q

how does acute PEd present? chronic PEd?

A

ACUTE: rapid, pain, potentially life threatening, usu due to left ventricular failure
CHRONIC: pain or maybe not

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14
Q

what are sxs of acute PEd?

A
  • tachypnea
  • extreme dyspnea (SOB)
  • restlessness & anxiety (sense of suffocation)
  • marked bronchospasm & wheezing (cardiac asthma)
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15
Q

what can alveolar fluid act as in chronic PEd? how are the alveolar walls? what else appears in the alveoli?

A
  • culture medium for bac
  • walls become fibrotic
  • micro-hemorrhages phagocytized by MOs= heart failure cells
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16
Q

is ARDS NCPE or CPE? what does this lead to accumulating in the alveoli?

A
  • ARDS is NCPE

- leads to exudate (proteins) in the alveoli

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17
Q

what does ARDS lead to?

A
  • low blood O2
  • increased permeability of pulmonary bvs
  • fluid accumulation in lungs
  • death of lung cells
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18
Q

what is ARDS commonly due to? what if it is idiopathic?

A
  • sepsis
  • widespread lung infections
  • gastric aspiration
  • mechanical trauma
  • multi-organ failure
  • burns, inhaled gases & chemicals
  • about 20% no identified risk factor= INTERSTITIAL PNEUMONIA
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19
Q

what is damaged in ARDS? what does this lead to?

A
  • endo and/or type 1 epithelial cells, possibly type 2 epis
  • damage to endo & type 1 leads to increased permeability of capillaries, flooding of fluid, loss of gas exchange
  • damage to type 2 leads to less surfactant
  • form microscopic clots= decreased blood flow & O2
  • hyaline membranes (protein-rich fluid & dead alveolar epithelial cells)
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20
Q

what immune cell causes the most damage in ARDS and how?

A
  • neutrophils
  • produce oxidants, proteases, PAF, leukotrienes
  • normally balanced by antioxidants, anti-proteases, anti-inflammatory cytokines
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21
Q

SSxs of ARDS?

A
  • tachypnea
  • dyspnea
  • cyanosis
  • respiratory failure & possible acidosis
  • bilateral fluid seen on CXRs
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22
Q

what is the prognosis of ARDS? what does it often progress to? how does resolution happen?

A
  • prognosis: 30-70% mortality rate, increases with age, usu due to sepsis
  • often progresses to multi-system organ failure and death
  • resolution includes resorption of fluids & debris, replacing epi & endothelial cells
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23
Q

what are the characteristics of obstructive lung diseases?

A
  • small airway expiratory disease

- hyperexpansion on CXR

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24
Q

what are the characteristics of a restrictive lung disease?

A
  • large airway inspiratory disease
  • lacking compliance
  • infiltrative
  • reduced lung volume, dyspnea, cyanosis
  • reduced gas transfer
  • ground glass on CXR
25
Q

on a CXR with obstruction how will the lucency and density be? for restriction?

A

obstruction: more lucency, less density
restriction: less lucency (more opacity), more density

26
Q

how is restrictive airway disease’s capacity and flow rate?

A

capacity decreased, flow rate normal

27
Q

what are the two classes of restrictive disorders?

A
  • chest well disorders w/normal lungs

- acute or chronic interstitial & infiltrative diseases

28
Q

in restrictive how is lung capacity? FVC? examples?

A

decreased total lung capacity, decreased FVC

examples: asbestos, ARDS, chest wall disorders

29
Q

in obstructive how is flow rate? FEV? examples?

A

flow rate decreased, FEV decreased

examples: emphysema, chronic bronchitis, asthma

30
Q

what is emphysema known as? what does it have?

A

COPD or end-stage lung disease

  • progressive air trapping, wheezing
  • bullae
31
Q

what are the 2 forms?

A

centrilobular: more common, central parts of respiratory bronchioles affected, more severe in upper lobes, occurs in heavy smokers
panacinar: enlarged from respiratory bronchiole to terminal alveoli, more severe in lower lobes, anterior aspect, alpha 1 antitrypsin deficiency

32
Q

what does emphysema include in terms of dz?

A

emphysema, chronic bronchitis, (asthma, bronchiectasis, cystic fibrosis)

33
Q

what are there increased numbers of in emphysema? what do they release?

A

-MOs, t lymphs, neutrophils which release leukotriene, IL-8, TNF

34
Q

what is alpha 1 antitrypsin normally good for? what inhibits it?

A
  • inhibits proteases

- inhibited by oxidants and free radicals

35
Q

smoking enhances what two products of MOs (and neutrophils)?

A
  • elastase from MOs
  • matrix metaloproteinase from MOs and neutrophils
  • both destroy lung tissue
36
Q

what are the two antioxidants which normally balance oxidants?

A
  • glutathione

- super oxide dismutase

37
Q

what are the gross morphological aspects of emphysema? when does it manifest?

A
  • voluminous lungs
  • apical blebs or bullae
  • enlarged acini
  • loss of elastic recoil (=restrictive disease aspect)
  • manifests after 1/3 of functioning lung lost
  • progressive dyspnea
  • some complain of cough or wheezing
38
Q

how do pts with emphysema look? how is their pulse ox? what do they develop overtime? what are causes of death?

A
  • weight loss common
  • pt sits hunched, barrel chested
  • PINK PUFFER
  • pursed lips
  • expiratory airflow limitation
  • PULSE OX OFTEN NORMAL
  • overtime develop cor pulmonale and CHF
  • death often due to respiratory acidosis and coma or R heart failure
39
Q

what is the definition of chronic bronchitis?

A
  • persistent cough w/sputum production for at least 3 mos for 2 consecutive years in absence of any other identifiable cause
  • related to cigs and smog
40
Q

what is the morphology?

A
  • excess mucus in large airways
  • similar to emphysema
  • cigs predispose to emphysema (loss of ciliary fxn, damage to epi, increased mucus production, inhibition of MOs)
41
Q

histology of bronchitis?

A
  • increased mucous gland layer
  • increased goblet cells w/in bronchi
  • reduced number of ciliated cells
42
Q

is chronic bronchitis defined clinically or pathologically?

A

CLINICALLY

43
Q

what do pts w/chronic bronchitis look like? what may they develop? cause of death sometimes?

A
  • persistent cough w/sputum
  • DOE
  • hypercapnia
  • hypoxemia
  • BLUE BLOATER
  • may develop cor pulmonale, CHF
  • death may be due to superimposed acute infxns
44
Q

what is asthma? is it reversible?

A
  • chronic inflammatory disorder of airways
  • recurrent episodes of wheezing, breathlessness, chest tightness, cough
  • partly reversible with tx or spontaneously sometimes
45
Q

what are the 4 classical histological findings in asthma?

A
  1. inflammation
  2. bronchial narrowing
  3. increased mucous
  4. SM hyperplasia (hypertrophy)
46
Q

what are the hallmarks of asthma?

A
  • wheezing
  • strong allergic role (IgE, eosinophils)
  • chronic small airway obstruction (obstructive component) & infection
47
Q

when does asthma often start?

A

childhood

48
Q

what are the two forms of asthma?

A

atopic (allergic) or non-atopic (infection)

49
Q

how do you diagnose asthma?

A
  • increased airflow obstruction
  • difficult prolonged expiration/wheezing
  • elevated eosinophil count in peripheral blood
50
Q

what is status asthmaticus?

A

unremitting attacks, often increasingly resistant to tx

51
Q

classification or causes of asthma?

A
  • atopic
  • non-atopic
  • drug induced
  • occupational
  • exercise-induced
  • asthmatic bronchitis
  • respiratory infections
  • environmental exposures
52
Q

how common is atopic asthma amongs all the types? what Ig? when does it being & what is it triggered by?

A
  • most common
  • type IgE mediated hypersensitivity
  • begins in childhood
  • triggered by dust,mold, pollens, roach or animal dander, foods
53
Q

what are common triggers of non-atopic & drug induced asthma? what is sampter’s triad?

A
  • viral respiratory infections triggers, air pollutants

- aspirin: asthma, rhinitis & nasal polyps, hives (inhibition of COX not LOX= bronchioconstriction)

54
Q

what are possible causes of occupational asthma?

A

-fumes, organic & chemical dusts, gases & other chemicals

55
Q

who experiences exercise induced asthma? what is it possibly due to?

A
  • ppl who don’t experience asthma under any other circumstance
  • possibly due to air not being warmed and humidified before entering lungs
56
Q

what are the phases of asthma?

A

early: bronchoconstriction, more mucus, vasodilation/increased permeability
late: inflammation, eosinophils, neutrophils, T cells (recruited by mast cells, epis, T cells)

57
Q

what is eotaxin of late phase of asthma?

A

-produced by airway epi, moves eosinophils to site

58
Q

what is MBP?

A

major basic protein: causes epi damage and airway constriction

59
Q

is there airway remodeling in asthma?

A
  • yes asthma changes structure of bronchial wall
  • hypertrophy & plasia of muscle layer
  • epi injury
  • increased vascularity
  • hypertrophy & plasia of mucus glands
  • deposition of subepithelial collagen

Pathology II (6 decks)

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