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HEENT Patho > deck_541931 > Flashcards

deck_541931 Flashcards

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2
Q

Which side of the lungs is a FB more likely to get stuck in?

A

Right

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3
Q

Where are Goblet cells and submucosal glands located in the respiratory tree?

A

Walls of trachea and bronchi. Not bronchioles.

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4
Q

What do neuroendocrine cells secrete in the respiratory tree?

A

Serotonin, Calcitonin

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5
Q

What are type 1 alveolar pneumocytes?

A

cover 95% of alveolar surface

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6
Q

What are type 2 alveolar pneumocytes?

A

they are rounded cells that secrete surfactin and cover 5% of alveolar surface. They give rise to type 1 cells.

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7
Q

What are Pores of Kohn?

A

connect alveoli to alveoli

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8
Q

Does hypoplasia lung defect usually affect 1 or both lungs?

A

both

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9
Q

What is agenesis?

A

congenital defect where 1 or 2 lobes are missing.

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10
Q

What is tracheal atresia?

A

condition of abnormally closed or absent trachea.

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11
Q

At which point is a tracheal/ bronchial stenosis a clinical manifestation?

A

When it is less than 50% of its size

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12
Q

What can happen with esophageal atresia and distal fistula?

A

Food/drink intake will induce vomiting

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13
Q

What can happen with no esoophageal atresia but “H” fistula”?

A

Fluid can pass from esophagus into trachea.

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14
Q

What is eupnic respirations

A

“normal” breathing. 8-16bpm, 400-800 tidal volume.

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15
Q

What are Kussmaul Respiration?

A

inc vent rate and tidal volume

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16
Q

Characteristics of restricted breathing?

A

small TV, rapid rate, rapid expiration

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17
Q

What are Cheyne Stokes Respiration?

A

Alternating periods of deep and shallow breathing. Brainstem breathing pattern.

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18
Q

What could cause Kussmaul Respirations?

A

metabolic problem. DKA

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19
Q

What can hyperventilation cause?

A

hypocapnia= 1)tingling in fingers/lips 2)dec resp drive= fainting

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20
Q

What causes cyanosis?

A

saturated hemoglobin of 5gm or more

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21
Q

What are signs of central cyanosis?

A

blue buccal mucosa and lips

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22
Q

What are signs of peripheral cyanosis?

A

blue nail beds

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23
Q

What is clubbing associated with?

A

chronic hypoxia= inc vascular growth

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24
Q

What is important to consider about location of irritant receptors in the airway?

A

few receptors in distal bronchi and alveoli so it is possible for secretions to accumulate distally w/o cough.

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25
Q

what is the effectiveness of cough dependent on?

A

Inspiratory volume

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26
what is chronic cough defined as?
persistent cough for > 3 weeks
27
What is typical with hemoptysis?
blood from airwaybright redalkalinemixed with frothy sputum
28
What is typical with hematemesis?
blood from GI tractDarkAcidicFood particles may be present
29
What is type 1 resp failure?
hypoxia w/o hypercapniaPa02 less than or equal 50mmHg
30
What is type 2 resp failure?
hypoxia with hypercapniaPa02 less than or equal 50mmHg and PaC02 greater than or equal 50 with pH less than or equal 7.25
31
What is neonatal atelectasis?
incomplete expansion of the lungs
32
What is Acquired atelectasis?
collapse of previously inflated lung
33
Where does the mediastinum shift in Resorption atelectasis?
toward the affected side due to dec pressure
34
Where does the mediastinum shift in compression atelectasis?
away from the affected side.
35
What is bronchiectasis?
permanent dilation of bronchi and cronchioles
36
What causes bronchiectasis?
Caused by destruction of muscle & elastic tissue, resulting from or associated with chronic necrotizing infections.
37
What conditions can be associated with Bronchiectasis?
Congenital conditions: CFPost-infectious conditions: TB, bact, virusBronchial obstruction: tumors, FB, mucusOther conditions: RA, systemic Lupus, IBD
38
What is characteristic of lungs with Bronchiectasis?
Infection: InflammationNecrosisFibrosisDilation of airways
39
What is Bronchiolitis?
Inflammatory obstruction of the small airways or bronchioles
40
What is Bronchiolitis obliterans?
fibrotic process occluding airways and causes permanent scarring of the lungs Common after lung transplantation.
41
What are characteristics of Bronchiolitis?
Most commonly in children: Due to RSVIn adults: accompanies chronic bronchitisUsually diffuse
42
What causes pulm edema with inc hydrostatic pressure and normal oncotic pressure?
Left Heart failure, Mitral stenosis
43
What causes Pulm edema with normal hydrostatic pressure and dec oncotic pressure?
nephrotic syndrome, liver Dz
44
What causes pulm edema with normal hydrostatic pressure and normal oncotic pressure?
Microvascular Injury...-Infections- Aspiration- Drugs- Radiation
45
What drug can cause pulm edema due to microvascular inj?
penicillin (after 10 days)
46
Which part of the lungs is most affected by pulm edema?
lower lobes
47
What are "heart failure cells?"
hemosiderin laden macrophages from pulm edema
48
What occurs in the lungs with pulm edema?
Hemosiderin laden macrophages abundantFibrosisThickening of alveolar walls results in lungs becoming firm and brown “brown induration”
49
What is the 2012 criteria for ARDS?
Respiratory symptoms must have started within one week of a known clinical insultBilateral opacities on chest radiograph or CT scanRespiratory failure must not be fully explained by cardiac failure or fluid overload (consider echocardiograph to rule out)Hypoxemia must be present on minimal ventilator settings
50
What is mild ARDS?
PaO2/FiO2 >200mmHg but ≤300mmHg
51
What is moderate ARDS?
PaO2/FiO2 >100mmHg but ≤ 200mmHg
52
What is severe ARDS?
PaO2/FiO2≤100mmHg
53
What are the majority of ARDS cases caused by?
SepsisDiffuse pulmonary infectionsGastric AspirationMechanical Trauma
54
What type of bacteria usually cause ARDS form sepsis?
gram negative which activates the complement system
55
What is the pathogenesis of ARDS?
Imbalance between pro-inflammatory mediators and inflammatory mediators leading to accumulation of neutrophils releasing oxidants, PAF, LKs which damage albeolar epithelium.
56
What does IL-8 do?
chemotaxic factor for neutrophils
57
What does IL-1 and TNF do?
activation of endothelial cells and neutrophils
58
Which transcription factor shifts the balance to a pro-inflammatory state?
Kappa Beta
59
What is involved after macrophage activation?
cytokine production, IL-1 & TNF effect on endothelial cells
60
What is involved after Neutrophil activation?
free radicals, PAF, LKTs, proteases
61
What are the 3 main phases of ARDS?
1)Exudative: diffuse alveolar damage2)Fibroproliferative: fibrosis and laying down of hyaline cartilage3)Recover/chronic
62
Which cells are affected first in exudative phase of ARDS?
Type 1 alveolar pneumocytes
63
What are the consequences of damage to alveolar pneumocytes?
SwellingBleb formationNecrosis
64
What cells other than pneumocytes are damaged in the exudative phase of ARDS and what is the implication of this?
Capillary endothelial cells are damaged causing microthrombi. This is indicated by presence of vWF.
65
What is the implication of diffuse alveolar damage during exudative phase of ARDS?
inc vascular permeablility
66
What is the implication of basement membrane thickening during exudative phase of ARDS?
dec diffusion of O2= vent-perfusion mismatch
67
What occurs in the fibroproliferative phase of ARDS?
Persistent hypoxemia: Development of hypercarbiaFibrosing alveolitisFurther decrease in pulmonary compliancePulmonary hypertensionSurfactant dysfunction
68
1st tests to order for ARDS?
CXRABGCVPCBCSputum/blood CultureUALipase
69
What tests would you order to rule out cardiogenic pulmonary edema in a ARDS workup?
BNP: BNP < 100 pg/mL bilateral infiltrates & hypoxemia suggests ARDS/ALI Echocardiogram normal in ARDSPulmonary artery catheterizatioin
70
What is Lung Injury Prediction Score(LIPS)?
Identifies who is unlikely to develop ALI/ARDS based on a point system grading the predisposing conditionsAlerts clinicians to implement prevention strategies for those at riskUnder further investigation and current studies are being done to improve the prediction scoring system

HEENT Patho (3 decks)

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