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CardioPulmonary Vascular Disease > Pulmonary Diseases > Flashcards

Pulmonary Diseases Flashcards

1
Q

Describe the pathogenesis of CF?

A

Mutation on Ch. 7 of CFTR (epithelial Na/Cl transmembrane protein); most common type is absence of a phenylalanine group

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2
Q

What are the physiological consequences of CF?

A

impaired ability to clear mucous secretions increases risk of opportunistic infections; inability to remove salt & chlorine from the body causes endogenous dehydration

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3
Q

What congenital defect do male CF pts. have?

A

absence of vas deferens

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4
Q

What are GI indications of CF?

A

meconium ileus (first stool blocking small intestine due to thick mucus); steatorrhea (fatty stool)

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5
Q

What is the proposed pathophysiology for asthma?

A

increased ECM proteins & vascular hyperplasia leading to airway remodeling and decreased pulmonary function

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6
Q

Intermittent Asthma is clinically defined as what?

A

FEV1 > 80%; FEV1/FCV > 85%;; does not interfere w/ daily routine with daytime episodes <2d/wk & nightly episodes <2/month

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7
Q

What would be the treatment plan for intermittent asthma?

A

short-acting beta agonist once before bed time

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8
Q

Mild asthma is clinically defined how?

A

FEV1: > 80%; FEV1/FVC > 80%; minor limitation of activity; daytime episodes > 2d/wk and nightly episodes 3-4/mo

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9
Q

What would be the treatment plan for mild asthma?

A

Intermittent + low-dose inhaled corticosteroid

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10
Q

How is moderate asthma clinically defined?

A

FEV1: 60-80%; FEV1/FVC: 75-80%; daytime symptoms daily (1/day) & nightly episodes > 1/wk.; moderate limitation of activities

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11
Q

What would be the treatment plan for moderate asthma?

A

medium does ICS

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12
Q

How is severe asthma clinically defined?

A

FEV1 < 60%; FEV1/FVC < 75%; daytime symptoms daily and last all day long w/ nightly episodes every night; extremely limited activity

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13
Q

What would be the treatment plan for severe asthma?

A

refer to pulmonologist; medium does ICS + long-acting beta agonist

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14
Q

What are the clinical hallmarks of meconium aspiration syndrome?

A

foul-smelling amniotic fluid upon delivery; CXR: increased AP diameter & flattened diaphragms bilaterally; PHTN assoc. w/ increased PVR

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15
Q

What is the most common cause of bronchiolitis in neonates?

A

RSV

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16
Q

What is the preferred drug for treatment of neonatal bronchiolitis?

A

nirsevimab

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17
Q

What are PE findings indicative of pneumonia?

A

bronchophony in right lower lobe; dullness to percussion; prolonged expiratory phase assoc. w/ expiratory wheezing & crackles

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18
Q

dullness to percussion indicates what?

A

segmental infiltrates

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19
Q

what do the auscultatory findings indicate on PE of pneumonia?

A

consolidation

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20
Q

Neonates 1-3 months old are most susceptible to what RI?

A

RSV

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21
Q

Neonates within their first month of life are most susceptible to what RIs?

A

S. pneumoniae, strep B., E. coli; gram - bacilli

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21
Q

from 3 months - 5 yr of age, what RIs are these pts. most susceptible to?

A

RSV, S. pneumoniae, H. influenzae

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22
Q

ped pts. in age range 5-18 yrs are most susceptible to what RIs?

A

mycoplasma & S. pneumoniae

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23
Q

What are RIs that pts. >18 yrs. contract?

A

S. pneumoniae, M. pneumoniae, H. Influenzae, influenza, adenovirus

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24
Q

What are common Afebrile pathogens that cause RIs in neonates?

A

C. trachomatis, CMV, B. pertussis, M. hominis, U. urealyticum

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25
Q

What PE findings are indicative of epiglottitis?

A

high-pitched noise over trachea on inspiration w/o presence of wheezes or rales

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26
Q

What are the most common pathogens assoc. w/ epiglottitis?

A

Strep A. S. aureus. H. influenzae

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27
Q

What is the most common mutation of CF?

A

F508 deletion results in a misfolded CFTR protein being retained in the endoplasmic reticulum

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28
Q

What CF screening test is given for newborns?

A

elevated immunoreactive trypsinogen

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29
Q

What are common sinopulmonary symptoms of CF?

A

nasal polyposis, chronic cough, recurrent RIs, atelectasis, bronchiectasis

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30
Q

What are common GI manifestations of CF?

A

recurrent pancreatitis due to pancreatic insufficiency; hepatic dysfunctions including fibrosis, cholethiasis, & cirrhosis

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31
Q

What physiologic insult arises due to perfuse excretion of NaCl for CF pts.?

A

salt-loss syndrome: chronic metabolic alkalosis

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31
Q

If both parents are carriers for CF, what is the probability of passing the gene onto offspring?

A

25%

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32
Q

If one parent is affected and the other a carrier for CF, what is the probability of offspring that will become affected?

A

50% chance

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33
Q

If both parents are affected w/ CF, what is the probability of it being passed down to offspring?

A

100%

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34
Q

What is the pathogenesis of genetic acquired AAT deficiency?

A

mutations of the SERPINA1 genes

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35
Q

What is the function of alpha-1-antitrypsin in the lungs?

A

anti-inflammatory protease inhibitor that inhibits neutrophil elastase from damaging the lungs

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36
Q

What long-term complications can arise due to AAT deficiency?

A

emphysematous COPD

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37
Q

AAT deficiency can cause what other extra pulmonary symptoms?

A

panniculitis, vasculitis, glomerulonephritis, & hepatitis/cirrhosis

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38
Q

Why should AAT serum levels not be tested if pt. has HPI of acute illness?

A

b/c AAT is an acute phase reactant will be naturally elevated during the acute phase of infection

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39
Q

What is the qualitative definition of atelectasis?

A

incomplete/reduced expansion of the lungs or collapse

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40
Q

What are clinical hallmarks of atelectasis?

A

pain on affected side assoc. w/ dyspnea; dullness to percussion on involved side; absent breath sounds, absent chest excursion; tracheal deviation towards affected side

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41
Q

What is the definition of obstructive atelectasis?

A

mucus plugs, exudates in bronchi, aspiration of foreign bodies; intrabronchial tumors

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42
Q

What are the physiological consequences of resorption atelectasis?

A

gas absorption from the alveoli promotes retraction of the lung & an airless state within affected regions of the alveoli leading to arterial hypoxemia ; the unaffected lung distends and displaces the surrounding structures resulting in a mediastinal shift towards the atelectatic area

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43
Q

How is compression atelectasis defined clincally?

A

accumulation of fluid within the pleural cavity

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44
Q

What are PE findings of compression atelectasis?

A

mediastinum and trachea deviation away from affected side & hyperresonance

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45
Q

how is contraction atelectasis clinically defined?

A

reduction of lung volume subsequent to severe parenchymal scarring

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46
Q

What are examples of contraction atelectasis?

A

fibrosis of narrowed bronchial lumen; granulomatous lung disease (TB) or necrotizing pneumonia

47
Q

RSD is a special form of atelectasis that is caused by what?

A

loss of surfactant

48
Q

For babies that have to be delivered prematurely, what can the mother be given to reduce development of RDS?

A

glucocorticoids

49
Q

What is the clinical definition of pulmonary edema?

A

accumulation of excess fluid in the alveoli

50
Q

describe the pathogenesis of hemodynamic edema.

A

caused by increased left ventricular & atrial filling pressures; this subsequently raises pulmonary venous pressure leading to decreased cardiac output which will activate RAAS which will lead to pulmonary edema

51
Q

What diseases can potentially cause hemodynamic induced pulmonary edema?

A

liver failure, nephrotic syndrome

52
Q

what are causes of pulmonary edema assoc. w/ microvascular injury?

A

RDS, pneumonia, radiation, lung trauma, high altitudes, opioid overdoes

53
Q

Why does edema accumulate in the basal pulmonary regions first?

A

b/c hydrostatic pressure is greatest in these regions

54
Q

what are the histological findings of hemodynamic pulmonary edema?

A

diffuse alveolar spaces flooded w/ fluid; dilated alveolar capillaries, microhemorrhages; hemosiderin-laden macrophages (commonly asscoc. w/ HF)

55
Q

What is the pathogenesis of microvascular injury assoc. pulmonary edema?

A

primary injury to the vascular endothelium and alveolar epithelial cells; this produces an inflammatory exudate into the interstitial space and alveoli

56
Q

What metabolic insult results from ARDS?

A

respiratory acidosis

57
Q

describe the exudative phase of ARDS?

A

immune-mediated destruction of epithelial-interstitial-endothelial barrier which allows fluid to flow into the interstitium and airspaces

58
Q

describe the proliferative phase of ARDS?

A

recovery of destroyed alveolar barrier

59
Q

describe the fibrotic phase of ARDS?

A

impaired removal of alveolar collagen limits functional recovery

60
Q

What casues surfactant to be reduced in ARDS?

A

protein rich edema interacts w/ alveolar surfactants during exudative phase which decreases pulmonary compliance and promotes formation of hyaline membranes

61
Q

how long does the exudative phase last?

A

first 1-7 days after insult

62
Q

How do the lungs compensate for The loss of type 1 pneumocytes during exudative phase in the proliferative phase?

A

Type II pneumocytes differential into type 1 pneumocytes; Type II pneumocytes also drain alveolar edema during this phase as well and promote proliferation of myofibroblasts and endothelial vascular proliferation

63
Q

the proliferative phase takes place how long after the initial insult?

A

1-3 weeks

64
Q

When does the fibrotic phase start to manifest and what can be expected to find histologically?

A

3 weeks after initial insult; telangiectasia w/ collagenous fibrosis and refractory rigidity of alveoli due to architectural remodeling

65
Q

What would a pulmonary function test reveal for a case of obstructive lung disease?

A

increased RV & TLC; decreased FEV1, FVC, & FEV1/FVC (<0.7)

66
Q

centriacinar emphysema is most commonly assoc. w/ what risk factor?

A

cigarette smoking

67
Q

Panacinar emphysema is commonly assoc. w/ what deficiency?

A

AAT

68
Q

describe the pathogenesis of AAT-deficiency induced panacinar emphysema?

A

genetic deficiency on Ch. 14

69
Q

what bronchioles are affected in centriacinar emphysema?

A

central and or proximal parts w/ distant alveoli spared; affected area mostly localized to upper lobes

70
Q

what bronchioles are affected in panacinar emphysema?

A

ALL are uniformly enlarged from apex to base w/ most severe damage done to the lower lobes

71
Q

Describe the pathogenesis of emphysema?

A

damage to respiratory epithelium resulting in parenchymal destruction: this can be caused by inflammatory mediators, oxidative stress, and infections

72
Q

How does chronic use of tobacco products casue emphysema?

A

substances from tobacco smoke cause oxidative stress on lung tissue which can promote inflammation and endothelial dysfunction leading to permanent tissue damage; Also, it is important to note that ROS inactivate antiproteases like AAT

73
Q

What physiological consequences result form emphysema?

A

increased lung compliance w/ decreased elasticity and obstructive air trapping; during exhalation, terminal bronchioles collapses due to radial traction which traps air distally where elastic tissue has been lost

74
Q

What are the histological features of emphysema?

A

abnormally large alveoli separated by thin septa w/ focal centriacinar fibrosis

75
Q

What are clinical hallmarks of emphysema?

A

barrel-chest, pt. must sit in forward-hunched pos. to breath with expiration being prolonged; weight loss is also common

76
Q

What is the qualitative definition for DLCO and is it reduced or increased in the case of emphysema?

A

ability of lung ot transfer gas from inhaled air into the blood stream; decreased in emphysema: serves as an indicator for extent of lung damage

77
Q

What would an ABG indicate for suspected emphysema?

A

low PaO2 (ooo shocker there); decreased PaCO2 assoc. w/ respiratory alkalosis

78
Q

What CXR findings are indicative of emphysema?

A

hyperlucency ( bigger area of dark space due to more air being trapped in the lungs); increased AP diameter; heart displaced more vertically and flattened diaphragm

79
Q

What would you expect to find for paraseptal emphysema?

A

proximal bronchioles intact; distal ones affected

80
Q

what is the main cause of paraseptal emphysema?

A

spontaneous pneumothorax

81
Q

If there are irregularities in the uniformity of affected bronchioles, what is the emphysema classified as?

A

irregular emphysema

82
Q

What is the clinical criteria for chronic bronchitis?

A

persistent cough w/ sputum production for at least 3 months in at least 2 consecutive years

83
Q

describe the pathogenesis of chronic bronchitis?

A

Must have an initiating factor such as exposure to noxious stimuli activating secretion of inflammatory mediators; these mediators then cause mucus hypersecretion and hypertrophy of submucosal glands; excessive mucus production eventually leads to airway obstruction and increased number of goblet cells

84
Q

how does tobacco smoke lead to chronic bronchitis?

A

damage of airway lining leads to chronic inflammation which can interfere with ciliary action to clear mucus and debris from the airway

85
Q

In addition to the histological characteristics of inflammation, the bronchial epithelium may also show what else?

A

squamous metaplasia: Lungs’ response to adaptation of consistent airway irritation

86
Q

What physiological insults arise from chronic bronchitis?

A

hypercapnia & hypoxemia leading to cyanosis and PHTN

87
Q

Would you expect the lung elasticity to be lower or normal for chronic bronchitis?

A

normal

88
Q

Describe the pathogenesis of atopic asthma?

A

allergen sensitization; Th2 and IgE mediated Type 1 Hypersensitivity rxn.

89
Q

what are common causes of non-atopic asthma?

A

viral RIs, inhaled air pollutants

90
Q

What drug is assoc. w/ drug-induced asthma?

A

aspirin via inhibition of COX pathway and decreased PGE2 production

91
Q

IL-5 plays what role in the pathogenesis of asthma?

A

activates eosinophils

92
Q

IL-13 plays what role in the pathogenesis of asthma?

A

stimulates mucus secretion from submucosal glands

93
Q

What role does IgE play in the pathogenesis of asthma?

A

binds to Fc receptors on submucosal mast cells; mast cells release granule contents and produce and recruit more inflammatory mediators

94
Q

Describe what happens during the early phase reaction assoc. w/ asthma?

A

bronchoconstriction triggered by direct stimulation of subepithelial vagal receptors

95
Q

What happens during the late-phase rxn. assoc. w/ asthma?

A

recruitment of leukocytes (eosinophils and neutrophils)

96
Q

leukotrienes C4, C5, & E4 promote what?

A

prolonged bronchoconstriction, increased vascular permeability, and increased mucous secretion

97
Q

What role does acetylcholine play in the pathogenesis of asthma?

A

causes airway smooth muscle constriction via direct stimulation of M3 receptors

98
Q

Eosinophiles release what substance and what is the clinical significance of this?

A

galectin-10 forms charcot-leyden crystals: strong induces of inflammation and mucus production

99
Q

histamine also plays a role in the pathogenesis of asthma; what does it do in this context?

A

promotes bronchoconstriction

100
Q

susceptibility locus for asthma is located on which chromosome?

A

Ch. 5q

101
Q

what HLA class is linked to production of IgE antibodies against antigens like ragweed pollen?

A

Class II HLA alleles

102
Q

Variations of the gene that encodes for IL-33 lead to what consequences?

A

IL-33 and its receptor ST2 induces production of Th2 cytokines

103
Q

Variants of the gene encoding for TSLP, is released by what cells and thought to have a role in initiating allergic rxns.

A

cytokines produced by epithelium

104
Q

What are some of the histological characteristics of asthma?

A

hypertrophy & hyperplasia of bronchial smooth muscle; epithelial injury; increased airway vascularity; hyperplasia of goblet cells; hypertrophy of subepithelial mucous gland; subepithelial fibrosis w/ type I type III collagens; thickening of airway wall

105
Q

curschmann spirals result from what?

A

extrusion of mucus plugs from subepithelial mucous gland ducts

106
Q

what would labs of suspected asthma reveal for acute and chronic cases?

A

respiratory alkalosis for acute; respiratory acidosis for chronic

107
Q

what is the qualitative definition for brochiectasis?

A

destruction of smooth muscle and elastic tissue by inflammation from persistent or severe infections

108
Q

what are some long-term consequences of bronchiectasis?

A

permanent dilation of bronchi and bronchioles; chronic necrotizing infections

109
Q

What are the most common congenital and hereditary conditions assoc. w/ bronchiectasis?

A

CF; primary ciliary dyskinesia; kartagener

110
Q

How does CF cause bronchiectasis?

A

chronic bacterial infections due to thick mucus build up causes widespread damage to airway epithelium

111
Q

How does primary ciliary dyskinesia result in bronchiectasis?

A

mutations of ciliary proteins ( such as dynein) can lead to ciliary dysfunction and impair mucociliary clearance opening a floodgate for recurrent infection

112
Q

Kartagener is a type of primary ciliary dyskinesia; describe its pathogenesis.

A

assoc. w/ ciliary dysfunction during embryogenesis leading to congenital malrotation of organs; assoc. w/ situs inversus and male infertility due to sperm dysmotility

113
Q

What immune disorders are assoc. w/ bronchiectasis?

A

RA, SLE, IBD, post-transplant

114
Q

What are the gross features of bronchiectasis?

A

bilateral lower lobe pathology w/ dilated airways that appear cystic and filled with mucopurulent secretions; permanent dilation w/ secondary infection

115
Q

What are some of the histological features of bronchiectasis?

A

inflammatory exudate; desquamation of epithelial lining; squamous metaplasia; necrotizing ulceration; bronchial fibrosis

116
Q

What are some of the clinical hallmarks assoc. w/ bronchiectasis

A

severe, persistent cough w/ foul smelling hemoptysis in sputums; orthopnea

CardioPulmonary Vascular Disease (7 decks)

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