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Respiratory 1 > Pathology 1 & 2 > Flashcards

Pathology 1 & 2 Flashcards

1
Q

Atelectasis:

A

incomplete expansion of lungs (neonatal) or collapse of previously inflated lung substance; usually reversible; hypoxia; predisposes to infection

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2
Q

types of atelectasis in adults:

A

1) resporption-
- follows complete airway obstruction
- excessive secretions
- mediastinal shift TOWARD atelectatic lung
2) compression-
- excessive air, fluid, blood or tumor in pleural space
- mediastinum shifts AWAY from affected lung
3) patchy
- loss of surfactant
- RDS
- postsurgical
4) contraction
- fibrosis around lung (cicatrization)

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3
Q

2 types of pulmonary edema:

A
  • hemodynamic disturbances (hydrodynamic or cardiogenic pulmonary edema)
  • edema caused by microvascular injury (dierct increases in capillary permeabiity 2ndary to microvascular injury)
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4
Q

hemodynamic pulmonary edema:

A
  • most commonly due to inc hydrostatis pressure (ex: Left sides CHF)
  • heavy WET lungs
  • HEART FAILURE CELLS
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5
Q

edema caused by microvascular injury:

A
  • mechanism: injury to capillaries of alevolar septa (vascular endothelium damage or damage to alveolar epithelial cells)
  • fliud and proteins leaked
  • LOCALIZED (Pneumonia & ALI) or diffuse (ARDS)
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6
Q

Obstructive pulmonary disease

A

-HARD TO GET AIR OUT

airway is obstructed=dyspnea

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7
Q

obstructive pulmonary diseases:

A
  • emphysema
  • Chronic bronchitis
  • asthma (reversible)
  • bronchiectasis
  • COPD = emphysema+chronic bronchitis
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8
Q

emphysema =

A

SMALL AIRWAYS - ACINUS

  • alveolar wall destruction
  • overinflation-airspace enlargement
  • DYSPNEA

smoking!

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9
Q

chronic bronchitis =

A
  • LARGE AIRWAYS-BRONCHUS
  • productive cough
  • airway inflammation
  • mucous gland hyperplasia, hypersection
  • smoking!
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10
Q

bronchiectasis

A
  • BRONCHUS
  • airway dilation and scarring

-peristent severe infections

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11
Q

asthma

A
  • Bronchus
  • smooth muscle hyperplasia
  • excess mucus
  • inflammation

immune mediated or undefined cause

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12
Q

small airway disease-bronchiolitis

A
  • Bronchiole
  • inflammatory/scarring
  • obliteration

-smoking!

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13
Q

COPD

A

RESERVE VOLUME INCREASED BC AIR IS TRAPPED IN LUNGS

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14
Q

Ratio FEV1/FVC in COPD

Ratio FEV1/FVC in restrictive disease?

A

DECREASES (BC FEV1 DECREASES more than FVC)

NORMAL OR INCREASED (TOTAL LUNG CAPACITY DECREASED)

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15
Q

Emphysema - obstructive:

A
  • more common and severe in males
  • associated with smoking and environmental pollutants
  • SYMPTOMS NOT APPARENT UNTIL 1/3 OF PULMONARY PARENCHYMA INCAPACITATED
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16
Q

Emphysema defined:

A

-irreversible enlargement of airspaces DISTAL to terminal bronchiole accompanied by destruction of airway walls but WITHOUT obvious fibrosis

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17
Q

2 types of emphysema??

A
  • alpha1 anti-trypsin

- smoking (pure chronic bronchitis)

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18
Q

factors associating smoking and emphysema

A
  • smokers have inc neutrophils in lun = neutro and macro accumulate in lung
  • smoking stimulates release of ELASTASE from neutro and macro
  • Macro elastase NOT inhibited by alpha1-antitrypsin
  • oxydants in cig soke and oxygen derived free radicals from neutrophils INHIBIT antiprotease = tissue damage via radicals
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19
Q

process to get emphysema: (protease antiprotease mechanism) (MOST POPULAR THEORY)

A

1) smoking=
a) dec alpha1-AT–antielastase
b) inc elastase secretion neutro and macro
==> ELASTIC DAMAGE
=====> emphysema

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20
Q

alpha1-antiprotease (antitrypsin)

genes:

A

-normal phenotype=PiMM (90%)
-deficiency phenotype = PiZZ most common
===> >80% of people with PiZZ develop symptomatic panacinar emphysema @ earlier age and inc severity if smoking

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21
Q

wHat does smoking do to alpha1 antiprotease?

A

-functionally inactivates it == altered balance between proteases and anti-proteases = destruction of elastin and collagen

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22
Q

types of emphysema

-how defined?

A

-defined by anatomic distribution within lung lobule - related to acinus

  • 1) Centriacinar (centrilobular)
  • 2) panacinar (panlobular)
    3) Paraseptal (distal acinar)-adjacent to areas of fibrosis, scarring or atelectasis
    4) irregular (airspace enlargement with fibrosis)- associated with scarring- very common
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23
Q

centriacinar emphysema

A
  • most cases = heavy smokers
  • **-respiratory bronchioles affected and distal alveoli spared
  • greatest severity in APICAL segments of upper lobes!** –> MAJOR ROLE OF TOBACCO AND COAL
24
Q

panacinar emphysema

A
  • acini uniformly enlarged from respiratory bronchioles to terminal blind alveoli
  • associated with alpha1-AT deficiency
  • MOST COMMON IN BASILAR PORTIONS OF LUNG
  • often occurs TOGETHER with centriacinar
  • Histology/Gross- enlarged - tissue looks pulled apart- alveoli look huge
25
Q

Distal Acinar (paraseptal emphysema)

A
  • enlargement with destruction of distal portion of acinus - usually worse in upper lung zones
  • usually ADJACENT to pleura or to areas of scarring, fibrosis, or atelectasis
  • can form cyst like structures
  • Associated with SPONTANEOUS PNEUMOTHORAX & bullous disease of lung in young adults
  • NOT ASSOCIATED WITH SMOKING
26
Q

irregular emphysema (airspace enlargement with fibrosis)

A
  • acinus is IRREGULARLY involved
  • associated with SCARRING usually from inflammatory process
  • usually asymptomatic and insignificant
27
Q

bullous emphysema-

A

can give rise to pneumothorax and possibly death= dangerous

28
Q

death in emphysema

A
  • respiratory acidosis and coma
  • right sides heart failure (LATE)
  • massive collapse of lungs secondary to pneumothorax
29
Q

Emphysema tx:

A
  • bronchodilators
  • steroids
  • bullectomy
  • lung volume reduction surgery
  • lung transplants
  • substitution of a1-AT
30
Q

chronic bronhcitis and R sided HF?

A

-EARLIER EVENT

as opposed to emphysema where R sided HF is a late complication

31
Q

Pink puffers:

A
  • severe emphysema
  • over-ventilate and remain relatively well oxygenated
  • dec diffusion capacity
  • relatively normal blood gas values
  • not significant bronchitis
  • barrel cehst
  • DOE
  • PURSED LIP BREATHING
  • WL
32
Q

Blue bloaters

A
  • major component of chronic bronchitis
  • hypercapnia
  • abundant purulent sputum
  • severe hypoxemia (BLUE)
  • cor pulmonale and cardiac failure are resulting complications
33
Q

Chronic bronhcitis defined

A

CLINICAL DIAGNOSIS!

  • persistent cough with production of sputum for at least 3 months of year for at least 2 consecutive year
  • ma yhave dec airflow (dec FEV1)
34
Q

Chronic bronchitis

A

-chronic irritation by inhaled substances (SMOKING!!!!!, air pollution, grain, cotton, silica dust…)

35
Q

most common population affected by chronic bronchitis:

A

-middle-aged male smokers

36
Q

histology changes in chronic bronchitis:

A
  • chronic inflam (lymphs)
  • hypertrophy of submucosal glands of rachea and bronchi (REID INDEX)
  • goblet cell metaplasia
  • mucus hypersecretion with pluggin
  • bronchial epith may show squamous metaplasia and dysplasia
  • marked narrowing of bronchioles = possible BRONCHIOLITIS OBLITERANS (obliteration of lumen 2ndary to fibrosis)
37
Q

Reid index=

A

ratio of distance from BM to cartillage compared to distance of mucous gland
(mucus gland/normal bronchial wall)
- should be less and 0.4
-just pathology after death –> only have clinical diagnosis

38
Q

Chronic bronchitis

clinical picture:

A
  • persistent cough and sputum production
  • lead to COPD with outflow obstruction, hypercapnia (high CO2), hypoxemia, possible cyanosis
  • pulmonary HTN
  • HF
  • recurrent infections
  • resp failure
  • may cause squamous metaplasia and dysplasia of bronchial epithelium –> potential for cancer
39
Q

Chronic bronchitis - usual bacterial and viral infection:

A 
-bac=
H influenza
strep pneumo
-viral=
adenovirus
RSV
40
Q

How does smoking predispose chronic bronchitis patient to infection?

A
  • interfering with ciliary action
  • direct damage to epith
  • inh the ability of bronchial and alveolar leukocytes to clear bacteria
41
Q

review slide 48

A

review slide 48

42
Q

Chronic bronchiolitis

A
  • small airway disease
  • lumen filled with mucus
  • tall epithelium with goblet cell metaplasia
  • fibrous thickening of wall
  • INCREASED PROMINENCE OF SMOOTH MUSCLE
43
Q

What is asthma:

A
  • chronic inflammatory disorder fo airways
  • recurrent episodes of wheezing, breathlessness, chest tightness, coughing at night or early morning usually
  • WIDESPREAD BUT VARIABLE BRONCHOCONSTRICTION = airflow limitation

-REVERSIBLE!

44
Q

Process of asthma:

A
  • inflammation
  • hyperreactive airways
  • episodes of reversible bronchoconstriction
45
Q

Rare potentially fatal asthma=

A

status asthmaticus (CO2 goes)

46
Q

Atopic (extrinsic) asthma

A

-initiated by a type 1 hypersensitivity reaction after exposure to an extrinsic allergen

47
Q

Non-atopic asthma

A

-initiated by diverse nonimmune mechanisms such as ingestion of aspirin, pulmonary infections, inhalants, and exercise

48
Q

Allergic asthma (atopic)

A

1) initial sensitization to inhaled antigens stimulaet induction of CD4 cells of TH2 type**
2) **TH2 cells release cytokines (IL4 & IL5)
- production of IgE by B-cells (IL4)
- growth of mast cells (IL4
- growth and activation of eosinoph (IL5)
3) subsequent IgE mediated reaction to inhaled antigens –> acute response and late phase reaction

49
Q

Late phase allergic asthma how?

A

binding to left over IgE tiggers attack 4-8 hrs later

50
Q

Asthma histology:

A
  • *-curschmann spirals - whorls of shed epithelium
  • *-charcot-leyden crysals-crystalloids made of eosinophillic proteins
  • many eosinophils!!
51
Q

bronchiectasis defined:

A

-permanent dilation of bronchi and bronchioles caused by destruction of muscle and elastic supporting tissue, resulting from or associated with chronic necrotizing infections

IRREVERSIBLE

52
Q

***Two condition requsite for bronchiectasis?

A
  • obstruction (tumors, foreign body, concretions, secretions)
  • chronic persistent infection
53
Q

Assocaited conditions with bronchiectasis:

A
  • obstructive
  • congenital or hereditary
  • necrotizing (suppurative) pneumonia aka Staph, kleb…
  • kartagener syndrome
54
Q

Kartagener syndrome

A
  • abnormal cilia - loss of radial spokes

- on histology have disordered radial spokes = cilia dont work

55
Q

clinical featuers ofbronchiectasis

A
  • chronic productive cough
  • hemoptysis
  • fould sputum
  • blood sputum
  • SYSTEMIC=fever WL weakness
  • COMPLICATIONG=pulm HTN, brain abscess, rare cor pulmonale, LUNG ABSCESS!

Respiratory 1 (9 decks)

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