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Pathology A > resp diseases > Flashcards

resp diseases Flashcards

1
Q

name some of the chemicals that contribute to toxicity in cigs and where they are deposited in the body

A

formaldehyde, ammonia, hydrogen cyanide, acetone, carbon monoxide

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2
Q

what are the organ systems that are are effected by smoking

A

nicotine - ns
carcinogens - cancers
ROS - cardiovasc, strokes
volatilised hydrocarbons - widespread damage

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3
Q

what is anthracosis

A

black pigments = macrophages that are phagocytosing carbon pigments, but die

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4
Q

what are the specific effects of smoking on neurological system

A 
ntsm release - stimulus and relaxant
dopamine = addiction 
serotonin = calming 
aCH = memory 
aCH + norepinephrine - sharpness
beta-endorphins - decrease anxiety
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5
Q

effcts of smoking on cardiovascular effects

A

inc HR, blood pressure
widespread vessel-damage, causes vasoconstriction
accelerated atherosclerosis through endothelial injury

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6
Q

smoking impact on lung defence mechanisms

A

paralyses cilia = smokers cough to remove toxins
affected alveolar macrophages phag ability
reduced immune response = widespread inflammation
inc mucus secretions = inc infection risk egflu, pneumonia

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7
Q

what is COPD

A

Chronic bronchitis + emphysema
obstruction os airflow in pulmonary (bronchial tree)
progressive + inflammation

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8
Q

what are the risk factors for COPD

A

smoking, hereditary deficiecy of a1-antitrypsin, asthma, airway hyper-responsiveness

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9
Q

dscribe both chronic bronchitis and emphysema

A 
CB = inc musuc + obstruction of small airways 
emphysema = enlarged air space + destruction of lung tissue
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10
Q

how is COPD diagnosed

A

forced expiratroy V in 1 second FEV1 = decrased bc of:

  • inc resistance bc narrowed airway (CB)
  • dec outflow pressure = loss of elastic recoil (emphysema)
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11
Q

what are the 5 elements of pathogenesis in copd and what do they cause

A
  1. infalmmation + fibrosis bronchial wall
  2. hypetrophy of submucosal glands
  3. hypersecretion mucus (1+2+3 = obstruct airway = mismatch between ventilation + perfusion)
  4. loss elastic lung fibre = impairs exp flow => air trapped + ariway collapse
  5. loss alveoli = loss SA
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12
Q

what clinical features impact copd

A

time of day (worse morning)
severity day
relative contributions of CB and emphysema

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13
Q

what are the early clinical features of COPD

A

insidiious-onset with progressive decline
fatigue, exercise intolerance, cough, dysponea, sputum production
rhonchi = prolonged low-frequency gurgles

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14
Q

late clinical copd paitents

A

hypoxaemia + hypercania
= vasoconstrict pulmonary arteries, pulmonary artery hypertension, RHS heart failre + pulmonary oedema
cyanosis bc vent/perf imbalance

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15
Q

describe copd treatmnet

A

DEPENDS ON STAGE
stop smoking
early diagnosis can halt progression
o2 therapy maintain 90% perfusion
immunisation against flu and pneumoccoal disease
bronchodilators = b2 adrenergic agonist
removal of distented lung tissue/lung transplant

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16
Q

what is emphysema

A

abnormal permanenet enlargement of teh airspace distal to terminal bronchioles
destruction of alveolar walls without fibrosis
inc airspace = hyperinfaltion, inc lung capacity, impaired ventilation
pathogenesis = protease/antiprotease theory (inherited deficiency)

17
Q

dscribe protease/anti-protease theory

A

normallyl balanced prod + destruction
a2-antitrypsin = anti-protease protects lungs
in emphysema = toxins => ROS => dec a1-antitrypsin (or hereditary)
neut + alveolar macs release protease/elastase to destruct elastin/proteins
overall = dec anti-protease activity, destruction elastin = dec outflow pressure

18
Q

clinical features of emphysema

A 
pink puffers 
60 yrs older 
dyspnear on exertion 
use accessory muscles like pursed lips
lungs overinflated (barrel chest)
weight loss 
minimal productive cough 
lack cyanosis
19
Q

what is the definitino of chronic bronchitis

A

persistent cough with sputum prod for at least 3 months in 2 consecutive years

20
Q

describe CB pathogenesis

A

cig damage = squamous metaplasia
airway obstruction = mucus plus
hypersecretion mucus in large airways from hypertrophy of submucosal glands
hypersecretion of mucus in small airways bc inc in goblet cells
acute +chronic inflam => fibrosis (further obstruction)
more predisposed to infections from pathogens

21
Q

CB clinical presentation

A 
blue bloaters 
cyanosis + oedema 
persistent cough + sputum 
hypoxia, hypercapnia
dyspnea on exertion
22
Q

what is the main type of malignant primary tumour and its characteristics and where it arises

A

bronchogenic carcinoma
poor 5yr survival
aggressive, highly metastatic
from bronchi epithelium
pale appearnace bc chronic inflam healing response
arise in/around lung (squamous cell carcinoma) or in peripphery = alveolar septal cells/ terminal bronchioles

23
Q

what is the pattern of spready of lung cancer

A

penetrate bronchus wall
fungate into bronchioles
extend to pleural surface
spread to tracheal, bronchial + mediastinal nodes
metastasise => adrenal, liver, brain, bone

24
Q

symptoms of lung cancers

A 
non-specific = cough, weight loss, chest pain, dyspnea
later = bronchial obstruction, pleural invasial and effusion, chest wall invasion + rib destruction, pericardial involvement -> pericarditis + cardiac tamponade
25
Q

what are the 4 main types of small cell carcinoma

A
  1. small cell carcinoma = only smokers
  2. non-small cell: adenocarcinoma = common women + non-smokers
  3. non-small cell : squamous cell carcinoma = common men + smokers
  4. non-small cell: large cell carcinoma = highly anaplastic = poorly differentiated
26
Q

describe microscopically small cell carcinoma

A

only smokers
highly malignant; ectopic hormone production
from neuroendocrine cells of bronchial epithelium
large number of cells, small in size little cytoplasm, lack structure

27
Q

describe microscopically adenocarcinoma

A

women + nonsmokers
abnormal glandular appearance
dark nuclear appearance (dividing cells)
(looks like disorganised glands)

28
Q

describe microscopically squamous cell carcinomas

A 
common men + smokers 
areas of squamous metaplasa 
highly variable, slow growing, resectable
keratin accumulation/pearls 
ark nuclei = dividing cells
keratin pearls
29
Q

describe microscopically large cell carcinoas

A

poor differ

29
Q

describe microscopically large cell carcinoas

A

poor differentiation, unrecognisable combo of squamous and adenocarcinoma
anaplastic tumours with large polygonal cells with pleomorphic nuclei
may contain IC mucus
may be giant cells
may have clear/spindle shaped cells

Pathology A (26 decks)

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