Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

hemodynamic pulmonary edema:

A
  • most commonly due to inc hydrostatis pressure (ex: Left sides CHF)
  • heavy WET lungs
  • HEART FAILURE CELLS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Obstructive pulmonary disease

A

-HARD TO GET AIR OUT

airway is obstructed=dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

obstructive pulmonary diseases:

A
  • emphysema
  • Chronic bronchitis
  • asthma (reversible)
  • bronchiectasis
  • COPD = emphysema+chronic bronchitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

emphysema =

A

SMALL AIRWAYS - ACINUS

  • alveolar wall destruction
  • overinflation-airspace enlargement
  • DYSPNEA

smoking!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

chronic bronchitis =

A
  • LARGE AIRWAYS-BRONCHUS
  • productive cough
  • airway inflammation
  • mucous gland hyperplasia, hypersection
  • smoking!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

bronchiectasis

A
  • BRONCHUS
  • airway dilation and scarring

-peristent severe infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

asthma

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

immune mediated or undefined cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

small airway disease-bronchiolitis

A
  • Bronchiole
  • inflammatory/scarring
  • obliteration

-smoking!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

COPD

A

RESERVE VOLUME INCREASED BC AIR IS TRAPPED IN LUNGS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Emphysema defined:

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

2 types of emphysema??

A
  • alpha1 anti-trypsin

- smoking (pure chronic bronchitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Distal Acinar (paraseptal emphysema)
- 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
irregular emphysema (airspace enlargement with fibrosis)
- acinus is IRREGULARLY involved - associated with SCARRING usually from inflammatory process - usually asymptomatic and insignificant
27
bullous emphysema-
can give rise to pneumothorax and possibly death= dangerous
28
death in emphysema
- respiratory acidosis and coma - right sides heart failure (LATE) - massive collapse of lungs secondary to pneumothorax
29
Emphysema tx:
- bronchodilators - steroids - bullectomy - lung volume reduction surgery - lung transplants - substitution of a1-AT
30
chronic bronhcitis and R sided HF?
-EARLIER EVENT | as opposed to emphysema where R sided HF is a late complication
31
Pink puffers:
- 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
Blue bloaters
- major component of chronic bronchitis - hypercapnia - abundant purulent sputum - severe hypoxemia (BLUE) - cor pulmonale and cardiac failure are resulting complications
33
Chronic bronhcitis defined
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
Chronic bronchitis
-chronic irritation by inhaled substances (SMOKING!!!!!, air pollution, grain, cotton, silica dust...)
35
most common population affected by chronic bronchitis:
-middle-aged male smokers
36
histology changes in chronic bronchitis:
- 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
Reid index=
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
Chronic bronchitis | clinical picture:
- 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
Chronic bronchitis - usual bacterial and viral infection:
``` -bac= H influenza strep pneumo -viral= adenovirus RSV ```
40
How does smoking predispose chronic bronchitis patient to infection?
- interfering with ciliary action - direct damage to epith - inh the ability of bronchial and alveolar leukocytes to clear bacteria
41
review slide 48
review slide 48
42
Chronic bronchiolitis
- small airway disease - lumen filled with mucus - tall epithelium with goblet cell metaplasia - fibrous thickening of wall - INCREASED PROMINENCE OF SMOOTH MUSCLE
43
What is asthma:
- 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
Process of asthma:
- inflammation - hyperreactive airways - episodes of reversible bronchoconstriction
45
Rare potentially fatal asthma=
status asthmaticus (CO2 goes)
46
Atopic (extrinsic) asthma
-initiated by a type 1 hypersensitivity reaction after exposure to an extrinsic allergen
47
Non-atopic asthma
-initiated by diverse nonimmune mechanisms such as ingestion of aspirin, pulmonary infections, inhalants, and exercise
48
Allergic asthma (atopic)
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
Late phase allergic asthma how?
binding to left over IgE tiggers attack 4-8 hrs later
50
Asthma histology:
* *-curschmann spirals - whorls of shed epithelium * *-charcot-leyden crysals-crystalloids made of eosinophillic proteins - many eosinophils!!
51
bronchiectasis defined:
-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
***Two condition requsite for bronchiectasis?
- obstruction (tumors, foreign body, concretions, secretions) - chronic persistent infection
53
Assocaited conditions with bronchiectasis:
- obstructive - congenital or hereditary - necrotizing (suppurative) pneumonia aka Staph, kleb... - kartagener syndrome
54
Kartagener syndrome
- abnormal cilia - loss of radial spokes | - on histology have disordered radial spokes = cilia dont work
55
clinical featuers ofbronchiectasis
- 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions