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PATH 3 > Lecture 6 - Respiratory Pathologies: Congenital, Parenchymal, Vascular, and Pleural Disorders > Flashcards

Lecture 6 - Respiratory Pathologies: Congenital, Parenchymal, Vascular, and Pleural Disorders Flashcards

1
Q

cystic fibrosis is a hereditary disorder affect what glands?

A

exocrine (decreased Na and Cl ion transport)

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2
Q

cystic fibrosis causes production of abnormally thick mucus which leads to blockages of the lumen of what 3 areas?

A

pancreatic ducts, intestines and bronchi (respiratory infections)

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3
Q

cystic fibrosis leads to what other condition?

A

COPD (and progressive loss of pulmonary function)

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4
Q

what is the most common autosomal-recessive (both parents are carriers) fatal disease?

A

cystic fibrosis

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5
Q

due to the blockage of the pancreatic duct, digestive enzymes are affected, resulting in malabsorption that leads to what?

A

retarded growth

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6
Q

what is the most important complication of cystic fibrosis?

A

viscous bronchial mucus plugs preventing normal breathing

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7
Q

what are complications of cystic fibrosis, besides viscous bronchial mucus plugs?

A 
mucus = bacterial growth
chronic bronchitis
recurent pneumonia
bronchiectasis
pulmonary fibrosis
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8
Q

define ‘atelectasis’

A

partial or complete collapse of lung

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9
Q

what is the primary cause of atelectasis, and why?

A

bronchial obstruction because air in the alveoli is absorbed into blood and alveoli collapse

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10
Q

what are other causes of atelectasis besides bronchial obstruction?

A 
failure to breath deep enough
insufficient surfactant (premature babies)
direct compression (pnuemothorax)
pleural effusion/inflammation
smoke inhalation
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11
Q

what are 6 acute clinical manifestations of atelectasis?

A 
dyspnea
tachypnea
cyanosis
fever
low BP
shock
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12
Q

what are 2 chronic clinical manifestations of atelectasis?

A

gradual onset of:
dyspnea and weakness
(possible to be asymptomatic)

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13
Q

define ‘pulmonary edema’

A

accumulation of excessive fluid in the interstitial tissue, alveoli or both

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14
Q

name 5 conditions that pulmonary edema is a common complication of:

A 
left sided heart failure
water retention conditions (kidney disease)
smoke inhalation
shock
acute respiratory distress syndrome
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15
Q

how does pulmonary edema manifest in initial stages?

A

possibly asymptomatic or could shows signs of restlessness, anxiety or feel-like developing a cold

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16
Q

how does pulmonary edema manifest as fluid builds up?

A 
progressive dyspnea
persistent cough with frothy sputum and hemoptysis
exercise intolerance
tachypnea
wheezing
hypoxia/cyanosis/hypercarpnia/acidosis
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17
Q

T or F: pulmonary edemas prognosis is often reversible, depending on the underlying condition?

A

true

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18
Q

with acute respiratory failure, lungs will show what?

A

DAD - diffuse alveolar damage

19
Q

what are 6 possible causes of acute respiratory distress syndrome?

A 
severe trauma
pulmonary infection/aspiration
prolonged cardiopulmonary bypass
shock
fat emboli
sepsis
20
Q

when does ARDS occur?

A

within 12-48 hours after initiating event

21
Q

what are 6 SSx of ARDS?

A 
shallow, rapid breathing
dyspnea
pulmonary edema
atelectasis
chest retractions
cyanosis
22
Q

what does MODS stand for?

A

multiple organs dysfunction syndrome

23
Q

what are 4 ways of treating ARDS?

A

treat underlying condition
CPAP machine
mechanical ventilation (PEEP)
sedations

24
Q

what does PEEP stand for?

A

positive end expiratory pressure

25
Q

what % of survivors from ARDS experience lung fibrosis?

A

40%

26
Q

what fraction of people die from ARDS within days?

A

1/3 - often from pneumonia

27
Q

define ‘sarcoidosis’

A

growth of tiny collections of inflammatory cells in different parts of lungs due to an unknown cause

28
Q

what organs can sarcoidosis affect?

A 
lungs (90%)
lymph nodes of thorax and neck
liver
lacrimal and salivary glands (1/3)
eyes
skin
29
Q

what is a theory for the cause of sarcoidosis?

A

maybe an immune response to an unknown substance, most likely inhaled from air

30
Q

is there a cure for sarcoidosis?

A

there is no cure, but most do well from modest treatment and it often goes away on its own (70% recover spontaneously within a year or 2, 20% persist and 10% lethal)

31
Q

define ‘pneumoconioses’

A

lung disease caused by inhalation of mineral dust, organic and inorganic particles (occupational disease - coal workers, silicosis, asbestosis)

32
Q

how do lungs present with coal-worker’s lung disease?

A

black, fibrotic and structurally abnormal

33
Q

what is the common name for antracosis?

A

coal-workers lung disease (develops in substandard work conditions)

34
Q

what condition does coal-workers lung disease predispose you to?

A

TB (not lung cancer)

35
Q

what is the most common lung disease caused by mineral particles from the environment?

A

silicosis

36
Q

what causes silicosis?

A

inhalation of small silica crystals from dust generated from - stone cutting, mining, sand blasting (develops 10-20 years after exposure)

37
Q

what cell does silica damage or kill?

A

macrophages

38
Q

what mechanism of silicosis causes massive fibrosis?

A

dead macrophages release free silica particles and fibrogenic factors that stimulates fibroblasts and produces collagen leading to formation of collagenous nodules, eventually causing silicotic nodules that destroy the parenchyma of the lungs leading to scaring/ fibrosis of lungs

39
Q

what is a common complication of silicosis?

A

TB (not lung cancer)

40
Q

what are 4 conditions linked to asbestos exposure?

A

pulmonary fibrosis
pleural fibrosis
lung cancer
mesothelioma

41
Q

true or false: asbestos kill macrophages?

A

false (macrophages release substances that result in extensive pulmonary fibrosis)

42
Q

how much more frequently do malignant tumors develop in fibrotic lungs?

A

5-6 times more frequently

43
Q

when smoking is combined with asbestosis how much higher is the risk of lung cancer?

A

50 times higher

44
Q

what pathology occurs almost exclusively in people exposed to asbestos?

A

mesothelioma

PATH 3 (12 decks)

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