Resp Conditions Flashcards

1
Q

Conducting airways

A

Trachea (Rings of cartilage)
Bronchi - trachea to lungs
- as bronchi approach lungs they become narrower and break off into branches known as bronchioles

Aveolar ducts
- connection to aveoli

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2
Q

Where does gas exchange occcur in the lungs

A

Aveoli

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3
Q

Aveloar acapillerly membrane

A

Less than 5 cm thick
Site of gas exchage
If filled with fluid, gas exchange is impaired

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4
Q

Functional components of the respirotary system

A

Neurochemical control
Mechanics of breathing
Gas transpoprt
Control of Pulmonary Circulation
Respiratory Defense mechanisms

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5
Q

Peripheral ChemorecepotORS

A

Located in clusters composing the aortic body and carotid bodies, in similar locations to baroreceptors

These recepotrs sense changes in O2, and CO2 levels as the rate of perfusion into and out of their cells changes from the capilleries since they get high levels of blood flow, the perfusion rate of O2 in and CO2 out is an accurate measure of the level in the body. And since CO2 and O2 together compose Bicarbonate and Hydrogen - the major players in acid base balance, chemorecepotrs also measure this.

If there is an upset in levels, the chemoreceptors releases neurotranspmitters to a cranial nerve nearby to stimulate compensatory mechanisms

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6
Q

Which nerves are associated with chemoreceptors

A

Vagus nerve and glossopharyngeal (10 and 9)

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7
Q

Where do the cranial nerves associated with chemoreceptors travel to?

A

to themedulla oblongataand theponsin the brainstem. Several responses are then coordinated which aim to restore pO2.

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8
Q

What response would the brainstem stimulate if there was low pO2

A

Therespiratory rateandtidal volumeare increased to allow more oxygen to enter the lungs and subsequently diffuse into the blood
Blood flowis directed towards the kidneys and the brain (as these organs are the most sensitive to hypoxia)
Cardiac Outputis increased to maintain blood flow, and therefore oxygen supply to the body’s tissues

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9
Q

Central chemorecptors

A

Central chemoreceptors are located in the medulla oblongata of the brainstem. They detect changes in the arterial partial pressure of carbon dioxide (pCO2). When changes are detected, the receptors send impulses to the respiratory centers in the brainstem that initiate changes in ventilation to restore normal pCO2.

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10
Q

Response to high levels of pCO2 in blood

A

Detection of an increase in pCO2 leads to an increase in ventilation. More CO2 is exhaled, the pCO2 decreases and returns to normal.

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11
Q

Response to low levels of CO2 in blood

A

Detection of a decrease in pCO2 leads to a decrease in ventilation. Less CO2 is retained in the lungs, the pCO2 increases and returns to normal.

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12
Q

What is different about the mechanism of pCO2 in central chemoreceptors

A

The mechanism behind how central chemoreceptors detect changes in arterial pCO2 is more complex, and is related to changes in the pH of the Cerebral Spinal Fluid (CSF).

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13
Q

What do central chemoreceptors respond to

A

High CO2 levels
Low pH

NOT O2 levels

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14
Q

Muscels of inspiration

A

Diaphragm

External interscostal muscels

Accessory muscle
- (sternalcremastoid)
- Scalene

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15
Q

What is compliance in relation to lung elasticity

A

The ability of the lung to stretch and expand

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16
Q

Airway ressistiance

A

Normally low

Edema, obstruction, and bronchospasm can increase airway ressitsnce
- Causing breathing to becom more difficult

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17
Q

Aveolar surface tension

A

Surfactant a lipoprotein reduces the surface reducing the amount of pressure needed for the alveoli to inflate and decreases their tendency to collapse.

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18
Q

Work of breathing

A

Detereined by musclular effort required for ventilation

Normally low but increased by certain dx

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19
Q

Gas transport of O2

A

Ventilation of lungs
Diffusion of O2 from alveoli into capillary blood
Perfusion of systemic capillaries with oxygenated blood
Diffusion of O2 from systemic capillaries into cells

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20
Q

Gas transport of CO2 (Removal)

A

Diffusion of CO2 from cells into systemic capillaries
Perfusion of pulmonary capillary bed by venous blood
Diffusion of CO2 into alveoli
Removal of CO2 from lungs by ventilation

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21
Q

How does oxygenated blood reach the body?

A

Oxygenated blood travels from the lungs through the pulmonary veins and into the left side of the heart, which pumps the blood to the rest of the body.

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21
Q

How does O2 deficient blood (CO2 rich) reach the lungs?

A

Oxygen-deficient, carbon dioxide-rich blood returns to the right side of the heart through two large veins, the superior vena cava and the inferior vena cava. Then the blood is pumped through the pulmonary artery to the lungs, where it picks up oxygen and releases carbon dioxide.

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22
Q

How is pulmonary circulation controlled?

A

Inside diameter (Caliber) of pulmonary artery lumina decreases as smooth muscle in arterial walls contracts
Contraction increases pulmonary artery pressure

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23
Q

Most inportatn cause of pulmonary arterey constriction

A

Low PaO2

Low O2 in the blood - alveolar hypoxia - hypoxic vasoconstriction

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24
What can Aveolar hypoxia affect
Can affect only one part of lung or entire lung If only one part of lung, arterioles to that segment constrict, shunting blood to other, well-ventilated portions of lung to better match ventilation & perfusion If all lung segments affected  pulmonary hypertension Chronic alveolar hypoxia can result in permanent pulmonary artery hypertension  leads to cor pulmonale & heart failure
25
Pulmonary heart dx
Core Pulmonelli Enlargemennt and strain on right side of heart (Right ventricle) Pulmonary HTN COPD Leading causes Can lead to HF
25
Defense mechs of respiratory system
Filtration of air by nasopharynx - Hairs trap dust and bacteria to protect the lungs Mucociliary Clearance system Cough reflex Reflex bronchoconstriction Alveolar macrophages
26
Mucociliary Clearance system
Invovles Mucous and IgA protection (antibodies) Cilia move mucous towards mouth Cystic fibrosis COPD Can decrease the functionality of this system
27
Bronchosconstriction benefit
Prevents entrance of infectants into lungs
28
Ventilation perfusion scan
Diagnosis of PE IV radiostop. injected into vein, pictures are taken of vein to identfy PE Ventilation portion - Client inhale radioactive gas, outlines aveoli, this is photographed - diminished or absent radioactivity suggests lack of perfusion/airflow
29
X-ray diagnostic for resp infections
Enlarged airways & check for pneumonia
30
Pulmonary funtion test
Forced spirometry: Measures amount of air exhaledin one forced breath Lung volume tests-This test measures the amount of air you can hold in your lungs and the amount of air that remains after you exhale (breathe out) as much as you can. Peak flow meter- measure how fast you can blow air from your lungs
31
PaO2
Amount of O2 in bloodstream free of hemoglobin Normal range is 80-100mmhg
32
Atelectasis
Collapse of aveoli or lung
33
Atelectasis Common after
Sx
34
Pneumonia
Acute inflammation of lunch parenchyma caused by microbioal agent
35
Risk factros for pneumonia
Altered LOC, immunocompromised/ suppressants, chronic dx, age, Tube feed, aspiration risk, smokers/noxious inhalation
36
Lobar type of pneumonia
Consolidation of one lobe of one lung
37
Lobular or Bronchopneumonia
Patchy consolidation throughout lungs
38
Risk factors for atelectasis
Post ope, age, obesity, bed ridden
39
Primary goals for nurse for pt with atelectasis
A primary nursing goal is getting them moving (deep breathing), position changes, pain meds Caution with narcotics bc decreased resp
40
Types of pneumonia
Community acquired Hospital Acquired Fungal (Rare) Aspiration Opportunistic
41
For studying, focus on NURSING CARE, not on PATHO
42
White stuff in the lungs on an x-ray is
Consolidation
43
Most common manifestation of pneumonia
Chest Pain Fever Chills Sweats Fatigued Cough (with sputum) Dyspnea
44
Older adults manifestations of pneumonia
Confusion Dry cough Extra pulmonary manifestations (i.e. muscle aches)
45
What provides definite diagnosis for pneumonia
Sputum C&S Chest x-ray
46
Objective data for Pnuemonia
SPO2, cough production, accessory muscle use etc.
47
Subj data for pneumonia
Hx of smoking, lung dx, exposure, length of symptoms, types of s/s,
48
Labs for infection
WBC (high) CRP (Marker of inflammation) ABGs - ON exam
49
Nursing diagnoses for pneumonia
Ineffective breathing pattern Ineffective airway clearance Acute pain Imbalanced nutrition: less than body requirements Activity intolerance
50
Tx for pneumonia
Acetaminophen for fever Tx of infection (sweats/chills) Encourage doable activity Sit them up in bed Turning/repositioning (for lung expansion) Small frequent meals AT LEAST 3 fluid (potential IV)
51
Pleurisy
Inflammation of pleurisy
52
Pleural effusion
Fluid in the pleural space
53
Atelectasis
Collapsed alveoli
54
Delyaed resolution
Long healing
55
Lung abcess
Abscess in lung
56
Empyema
Purulent exudate in pleural cavity
57
Pericarditis/endocarditis
Inflammation of endocardium/pleura
58
Bacteremia
Bacterial infection in the blood
59
Meningitis
Infection of the meniges/SC
60
Pneumothorax
Collapsed lung
61
Pulmonary embolism
Blockage of pulmonary arteries by a thrombus, fat embolus, air embolus, bacterial vegetations, tumour tissue, etc.
62
Most PE develop from
DVT (clot) which originates in deep calf, femoral, popliteal, or iliac veins Thrombus breaks free & travels as embolus until it lodges in pulmonary vasculature
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Clinical manifestations
Chest pain Anxious Acute dyspnea Tachycardia Foamy blood tinged sputum cough, pleuritic chest pain, hemoptysis, crackles, fever, sudden change in mental status
64
Difference bw pneumonia and PE in diagnossi
PE is sudden onset
65
D-dimer test
Senses blood clots in blood
66
Tests for PE
V/Q scan, D-dimer, lunmg scan, pulmonary angiography, ABG
67
Conservative therapy for PE
Prevent or treat atelectasis Narcotics for pain
68
How to stabilize cardiopulmonary system in PE
Intubation and mech ventilation FLudis to increase preload for HOTN
69
TB
Usually involves lungs Can also occur in larynx, kidneys, bones, adrenal glands, lymph nodes & meninges or be disseminated throughout body `
70
What dx Kills more people worldwide than any other infectious disease
TB
71
Why is TB still a major problrm
Poor adherence to drug therapy - multi-drug resisstant strains COntinued exposure to populations in which TB is more prevalent Presence of pools of high-risk groups - indigenous, homelessness etc.`
72
TB spread by
Airborne droplets Not spread by hands, books, glasses, dishes, or other fomites Can remain airborne for minutes to hours Not highly infectious; usually requires close, frequent, or prolonged exposure
73
Diagnostic test for TB
Sputum test for acid-fast bacilli Gastric washings (from stomach), CSF, pus from abscess
74
Chronic bronchitis
Chronic productive cough lasting at least 3 months a year for 2 consecutive years
74
Emphysema
Abnormal & permanent enlargement of alveoli due to rupture and damage reducing the surface area for gas exchange.
75
Who can present with pboth emphysema and chronci bronchitis
COPD
76
COPD - Chronic Obstructive Pulmonary Disease characterized by
COPD is a respiratory disorder caused largely by smoking and characterized by progressive, partially reversible airway obstruction, systemic manifestations, and increasing frequency and severity of exacerbations
77
Causes of COPD
Smoking Infections Heritdity Occupational air quality Age
78
What is the patho of COPD
Chronic inflammation found in airways & lung parenchyma (respiratory bronchioles & alveoli) Airflow limitations during forced exhalation caused by loss of elastic recoil; not fully reversible, structural changes in lungs Airflow obstruction caused by mucus hypersecretion, mucosal edema & bronchospasm
79
Abnormal gas exchange in COPD caused by
Hypoxemia & hypercapnia Bullae & blebs
79
Pulmonary HTN
Those with COPD are at risk of this Vasoconstriction because of hypoxemia leads to thickening of vascular smooth muscle in alveoli and surrounding capillaries causing pressure in pulmonary circulation to increase this mild to moderate pulmonary hypertension; may lead to hypertrophy of right ventricle or cor pulmonale
80
Systemic effects of COPD
Cachexia Weakness, exercise intolerance & deconditioning Osteoporosis Chronic anemia Also anxiety and depression
80
Clinical manifestations of COPD
1. Cough 2. Sputum Production 3. Dsypnea 4. Increased WOB 5. Barrel Chest 6. Prolonged exp, wheezes, decreased breath sounds - tripoding 7. Wt loss and anorexia 8.Fatigue 9 Blueish red colour to skin
81
Collaborative care for COPD
Smoking cessation Improve ventilation (Bronchodilators Long term O2 Therapy Remove bronchial secretions - nebulized bronchodialators Reduce complications DVT prophylaxis, influenza and pneumococcal vaccines Surgical therapy - lung volume reduction, lung transplant
81
Diagnosis of COPD
Consider COPD when person experiences symptoms of cough, sputum production , or dyspnea; history of smoking or exposure to risk factors; or both Diagnosis confirmed by spirometry FEV1/FVC ratio < 70% Classified as mild, moderate, severe, and very severe
82