Unit 3 Pathophysiology - Chapter 36 Alterations of Pulmonary fx Flashcards

1
Q

Dyspnea

A
  • breathlessness
  • increased respiratory effort
  • often associated with respiratory and cardiac diseases
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2
Q

Orthopnea

A
  • recumbent position - dyspnea when lying down (l/t sitting position when individual leans slightly forward with arms propped in front)
  • associated with heart failure
  • SOB
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3
Q

Paroxysmal nocturnal dyspnea

A
  • occurs after sleeping 1-2 hrs at night requiring person to sit or stand for relief
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4
Q

Coughing

A

protective reflex that expels secretions and irritants from lower airways; mediated by vagus nerve

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5
Q

Abnormal sputum

A
  • altered amount, consistency, color, and odor
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6
Q

Hemopytsis

A
  • blood mucus d/t bronchitis, TB, abscess, neoplasms (abnormal mass), or other ways that damage vessels
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7
Q

Abnormal breathing patterns

A
  1. Kussmaul (form of hyperventilation, rapid, deep breahing at a consistent pace)
  2. obstructed breathing (prolonged expiration d/t narrowed airways and increased airway resistance)
  3. restricted breathing (difficulty breathing, breathlessness, or feeling suffocation)
  4. gasping (agonal respiration)
  5. Cheyne-Stokes respirations (origin - heart failure or stroke, too much carbon dioxide in body, rhythm fluctuates between fast & slow breathing, or causing breathing to stop)
  6. sighing (uncomfortable awareness of feeling unable to take a deep, satisfying breath, often while sighing or yawning)
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8
Q

Hypoventilation

A

Decreased alveolar ventilation

caused by
* airway obstruction
* chest wall restriction
* altered neurologic control of breathing
* L/t increased PaCO2

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9
Q

Hyperventilation

A

Increased alveolar ventilation

caused by
* anxiety
* head injury
* severe hypoxemia
* L/t decreased PaCO2

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10
Q

Cyanosis

A

Blue discoloration

caused by
* desaturation of hemoglobin
* polcythemia (blood disorder w/ too many RBC => cause blood to increase in volume and thicken)
* peripheral vasoconstriction

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11
Q

Clubbing

A
  • d/t disease that mess w/ normal pulmonary circulation or cause chronic hypoxemia
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12
Q

Chest pain in pulmonary sense

A
  • inflamed pleurae, trachea, bronchi, or respiratory muscles
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13
Q

Hypoxemia

A

caused by
* decreased o2 content in inspired gas
* hypoventilation
* diffusion abnormaility
* ventilation-perfusion mismatch
* shunting

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14
Q

Acute respiratory failure

A

caused by inadequate gas exchange or ventilation
* PaO2 <50 mmHg
* or PaCO2 >50 mmHg and pH >7.25

Low oxygen levels in your blood can cause:

  • Difficulty with routine activities such as dressing, taking a shower, and climbing stairs, due to extreme tiredness
  • Shortness of breath or feeling like you cannot get enough air (called air hunger)
  • Drowsiness
  • A bluish color on your fingers, toes, and lips

High carbon dioxide levels in your blood can cause:

  • Blurred vision
  • Confusion
  • Headaches
  • Rapid breathing

It is often caused by a disease or injury that affects your breathing, such as pneumonia, opioid overdose, stroke, or a lung or spinal cord injury

While slow development => chronic respiratory failure

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15
Q

What happens if chest wall is deformed, traumatized, immobilized, or become heavy with fat?

A
  • work of breathing increased
  • ventilation compromised => decrease in tidal volume d/t compression of lungs or impaired chest wall muscle function
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16
Q

Flail chest

A

chest in which sections of broken ribs are isolated from, and interfering with, normal chest movements. That means the chest cannot expand properly and cannot properly draw air into the lungs. This is why stabilization after blunt trauma is important.

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17
Q

Pneumothorax

A

accumulation of air in pleural space d/t spontaneous rupture of weakened area of pleura or 2ndary to pleural damage caused by disease, trauma, or mechanical ventilation

there’s a defect in the pleura that allows air to leak into the pleural space, causing the partial or total collapse of the affected lung. The air trapped does not, however, continue accumulating, and some of the air is also able to escape during expiration. As a result, the intrapleural pressure does not keep increasing, which allows the affected lung to partially expand and fill with oxygen during inspiration.

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18
Q

Open pneumothorax

A
  • air builds up in pleural cavity caused by a hole in chest
  • puts pressure on lung can l/t lung collapse
  • pleual cavity is equal to atmospheric pressure (mainly lung affected)

causes:
* trauma (blunt or penetrating)
* Iatrogenic pneumothorax (medical examination or tx) - transtracheal aspiration (inserting needle into lung tissue), lung biopsy (portion of tissue removed), or tube thoracostomy (chest tube into plueral space or mediastinum to remove air, excess, fluid, blood)

treatment:
* three-way dressing
* chest tube
* surgical repair

sx:
* sudden chest pain
* SOB
* rapid and shallow breathing
* elevated HR
* hypoxia

diagnosis
* hyperresonant (high pitched?) sounds
* absence of breath sounds in individual’s back indicate air or fluid in pleural space

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19
Q

closed pneumothorax

A
  • air that enters pleural cavity from lungs themselves
  • defect of or damage to pulmonary parechyma (portions of lungs involved in gas exchange, including alveoli, alveolar ducts, and respiratory bronchioles)
  • other causes can potentially be COPD, cystic fibrosis, lung cancer, or pneumonia

Cystic fibrosis affects the cells that produce mucus, sweat, and digestive juices. It causes these fluids to become thick and sticky. They then plug up tubes, ducts, and passageways.

sx
* sudden chest pain
* SOB
* rapid and shallow breathing
* elevated HR
* hypoxia

can be a spontaneous pneumothorax (spontaneous meaning without UNDERLYING lung disease) or… secondary (w/ underlying lung disease)

pleural cavity pressure is lesser than atomspheric pressure (mainly lung affected)

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20
Q

tension pneumothorax

A

layering order 1) parietal pleura 2) pleural space 3) visceral pleura

  • air enters pleural space
  • in TENSION - air cannot leave (cause pleural cavity pressure to be greater than atmospheric pressure)
  • pressure on lung, trachea, heart, and other structures
  • pleural injury

causes:
* spontaneous (primary - w/o underlying lung disease)
* secondary (simple - w/ underlying disease)
* traumatic (any kind - chest injury or mechanical ventilation)

sx:
* SOB
* acute chest pain
* low blood pressure
* low blood O2
* Increasec HR

tx: needle decompression

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21
Q

Pleural effusion

A
  • accumulation of fluid in pleural space
    result from d/o
  • transudate (occurs d/t increased hydrostatic pressure or low plasma oncotic pressure)
  • Exudate (occurs d/t iflammation and increased capillary permeability - includes proteins flowing through)
  • can occassionally result from blockage or injury that causes lymphatic vessels to drain into pleural space
22
Q

Empyema

A
  • infected pleural effusion
  • or presence of pus in pleural space
  • usually d/t lymphatic drainage from sites of bacterial pneumonia
23
Q

Aspiration

A
  • passage of fluid and solid particles into lung
  • d/t impaired swallowing and coughing
  • RESULTS in pneumonitis (noninfectious cause of lung inflammation) and pulmonary infection
24
Q

Atelectasis

A

collapse of alveoli d/t
* lung tissue compression
* absorption of gas from obstructured alveoli
* impairment of surfactant

25
Q

Bronchietasis

A
  • abnormal dilation of bronchi usually secondary to another pulmonary disease
  • usually infection or chronic inflammation
26
Q

Bronchiolitis

A
  • inflammatory obstruction of small airways
  • common in children
27
Q

Brochiolitis obliterans

A
  • can organize pneumonia in which alveoli and bronchioles become filled with plugs of connective tissue
  • popcorn lungs (d/t workers inhaling diacetyl chemical)
  • worsens overtime
  • sx: shortness of breath, dry cough and sometimes wheezing and fatigue in the absence of a cold or asthma. Symptoms will normally develop over a few weeks or months and can flare up while exercising or doing manual labor.
  • WHILE bronchiolitis obliterans syndrome is d/t lung transplantation complication
28
Q

Pulmonary fibrosis

A
  • excess connective tissue in lungs
  • diminishes lung compliance, decrased O2 diffusion and hypoxemia
  • d/t idiopathic or disease

sx
* Shortness of breath, particularly during exercise.
* Dry, hacking cough.
* Fast, shallow breathing.
* Gradual unintended weight loss.
* Tiredness.
* Aching joints and muscles.
* Clubbing (widening and rounding) of the tips of the fingers or toes.

29
Q

Risks of inhalation of noxious gases or prolonged exposure to high o2 concentrations?

A
  • damage bronchial mucosa
  • alveolocapilllary membrane damage
  • inflammation or acute respiratory failure
30
Q

Pneumoconiosis

A

inhalation of dust particles in workplace
* coal dust (anthracosis)
* silica (silicosis)
* abestos

causes
* chronic inflammation
* pulmonary fibrosis
* susceptibile to lower airway infection and tumor formation

31
Q

Hypersensitivity pneumonitis

A
  • or extrinsic allergic alveolitis
  • allergic or hypersensitivity rxn to many allergens
32
Q

Pulmonary edema

A
  • excess water in lung d/t disturbance of capillary hydrostatic pressure, oncotic pressure, or capillary permeability
  • common cause => left sided heart failure, increasing hydrostatic pressure in pulmonary circulation

Transudate – increased hydrostatic pressure (CHF, venous outflow obstruction) causes fluid leakage or decreased colloid osmotic pressure (decreased protein synthesis [liver disease] or increased protein loss [kidney disease) leads to fluid leakage too

Exudate – fluid and protein leakge d/t stasis and vasodilation + increased interendothelial spaces from inflammation

33
Q

acute lung injury (ALI) and acute respiratory distress syndrome (ARDS)

A
  • acute, diffuse inflammatory injury to alveolocapillary membrane and decreased surfactant production
  • causing increased membrane permeability + pulmonary edema + atelectasis (Atelectasis is a condition where alveoli in your lung or a part of your lung deflates, causing a partial or complete collapsed lung.)
  • Blood clots. Lying still in the hospital while you’re on a ventilator can increase your risk of developing blood clots, particularly in the deep veins in your legs. If a clot forms in your leg, a portion of it can break off and travel to one or both of your lungs (pulmonary embolism) — where it blocks blood flow.
  • Collapsed lung (pneumothorax). In most ARDS cases, a breathing machine called a ventilator is used to increase oxygen in the body and force fluid out of the lungs. However, the pressure and air volume of the ventilator can force gas to go through a small hole in the very outside of a lung and cause that lung to collapse.
  • Infections. Because the ventilator is attached directly to a tube inserted in your windpipe, this makes it much easier for germs to infect and further injure your lungs.
  • Scarring (pulmonary fibrosis). Scarring and thickening of the tissue between the air sacs can occur within a few weeks of the onset of ARDS. This stiffens your lungs, making it even more difficult for oxygen to flow from the air sacs into your bloodstream.

sx:
* severe shortness of breath
* Labored and unusually rapid breathing
* Low blood pressure
* Confusion and extreme tiredness

34
Q

Obstructive pulmonary disease

A
  • characterized by airway obstruction that causes difficult expiration
  • can be acute or chronic
  • includes asthma, chronic bronchitis and emphysema
35
Q

Asthma

A
  • chronic inflammatory disorder (bronchial mucosa) l/t
  • hyperresponsiveness
  • mucosal edema
  • airway constriction
  • variable obstruction to airflow that is reversible

potential obstruction caused by episodic airway epithelial expsoure to antigen causing
* bronchospasm (muscles that line bronchi tighten => airways narrow)
* bronchial inflammation
* mucosal edema
* increased mucus production

36
Q

COPD

A
  • coexistence of two phenotypes (chronic bronchitis and emphysema); frequently overlap
  • there is a asthma-COPD overlap syndrome (clinical sx of asthma and COPD)

Chornic bronchitis (long term inflammation of bronchi causing airway obsturcting d/t bronchial smooth muscle hypertrophy, increase in size + number of epithelial mucous glands/goblet cells, and increased production of thick, tenacious mucus)

Emphysema (destruction of elastin in alveolar septa [seperates each individual alveolus - the elastin provides stretch, recoil, and elasticity to skin]) and loss of passive elastic recoil
— causing —
* airway collapse, obstruction to gas flow during expiration & air trapping
* * In emphysema, the alveoli become inflamed and rupture, creating air pockets within the lungs. These air pockets decrease the surface area of the lungs, making the lungs less efficient at exchanging gases.

septal deterioration in emphysema can be d/t a1-antitryipsin deficiency (AAT is a protein that protects lungs and liver from damage => can l/t COPD and cirrhosis) or old age tends to be panacinar or panlobular ( Commonly resides in the lower half of the lungs [usually affect all] and destroys the tissue of the air sacs, causing a distinctive, uniform enlargement of air spaces. It is associated with a genetic disease (homozygous alpha-1 antitrypsin deficiency)

  • smoking can result in septal deterioration too => centriacinar or centrilobular (primarily the upper lobes. Occurs with loss of the respiratory bronchioles in the proximal portion of the acinus, with sparing of distal alveoli)
37
Q

Paraseptal emphysema

A
  • large bullae formation [fluid-filled saces form on organ’s surface]
  • outermost area of lungs [outer regions]
38
Q

Upper respiratory tract infections

A
  • short term disabiilty
  • rhinitis (common cold), pharyngitis (inflammation of the pharynx, causing a sore throat) and laryngitis – inflammation of the larynx (voice box)
39
Q

Lower (serious) respiratory tract infection

A
  • pneumonia
  • tuberculosis
40
Q

Acute bronchitis

A
  • acute infection or inflammation of large airways or bronchi; self limiting and caused by viruses
41
Q

Pneumonia

A
  • lower respiratory tract
  • CAP (community acquired)
  • HCAP (healthcare-associated)
  • HAP (hospital-acquired)
  • VAP (ventilator-associated)

Pneumococcal pneumonia
* caused by pneumococcus
=======can cause following =========
* Blood infection (bacteremia).
* Brain and spinal cord membrane (lining) infection (bacterial meningitis).
* Lung infection (pneumonia).
* Bone infection (osteomyelitis).
* Joint infection (septic arthritis).
* Widespread inflammation of tissues and organs (sepsis), as a reaction to septicemia (bacteria in the blood).

(4) phases
1) consolidation (pulmonary air space filled with fluid, such as pus [in this case], fluid [pulmonary edmea], blood or neoplastic cells) —- first 24 hours vascular engorgement => alveolar walls congested and infection spread to pleura
In the lobar consolidation, an entire lobe is involved. The alveolar space is filled with inflammatory exudate made up of WBC, bacteria, plasma and debris.

2) red hepatization (2-3 days after) lasts for 2-4 days. Immune cells, white blood cells, and red blood cells enter the lung tissue to try and fight off the infection. As a result of this inflammatory response, you may experience increasing productive cough, shortness of breath, extreme fatigue, muscle aches, fever, and chills. [reminiscent of firm like liver]

3) Gray hepatization — This stage occurs on days 4-6 and lasts for 4-8 days. The red blood cells disintegrate, leaving the lungs looking gray. Symptoms usually persist during this stage.

4) Stage of resolution, some secretions can be in the airway. The interstitium and architecture of the lung remain intact and complete recovery occurs. Productive cough.
* swelling, lung abscess, scar tissue, or pleural adhesion remain l/t chronic lung disease

sx:

  • Chest pain.
  • Cough.
  • Difficulty breathing.
  • Fever or chills.
    **meningitis **
  • Fever
  • Headache.
  • Low appetite, poor drinking or vomiting in babies.
  • Sensitivity to light.
    bacteremia
  • Chills
  • Fever
  • Confusion

or l/t sepsis..

  • Confusion.
  • Difficulty breathing or shortness of breath (dyspnea).
  • Extreme discomfort or pain.
  • Fever or chills.
  • Rapid heart rate.
  • Sweating.
  • Death if not treated quickly.
42
Q

Viral pneumonia

A

acute self limiting lung infection cause by influenza virus

43
Q

TB

A
  • M tuberculosis (tubercle bacillus){
  • can invade other ograns
  • can survive within macrophages // resist lysosomal killing // multiply within cell // transit into dormant stage making itself resistant to host defense + drugs
  • Bacilli may remain dormant within tubercles (small tissue masses caused by bacteria => breathing impairment, coughing, and release of sputum)
  • if immune system is compromised => recurrence of active disease
44
Q

Aspiration pneumonia

A
  • destruction of lung parenchyma (l/t circumscribed areas of abcesses – accumulation of pus w/ suppuration or discharging of pus from wound, sore, etc)
45
Q

Pulmonary embolism

A

occlusion of portion of pulmonary vascular bed d/t
* thormbus (most common)
* tissue fragment
* air bubble
D/t size and location the embolus can cause:
* hypoxic vasoconstriction
* pulmonary edema
* atelectasis
* pulmonary hypertension
* shock
* DEATH

46
Q

Pulmonary artery HTN

A
  • pulmonary artery pressure
  • defined as MAP greater than 25 mmHg at rest
    CAUSED BY
  • elevated left ventricular pressure
  • increased blood flow through pulmonary circulation
  • obliteration or obsturction of vascular bed
  • active constriction of vascular bed produced by hypoxemia or acidosis
47
Q

Cor pulmonale

A

right ventricular enlargement d/t chronic pulmonary HTN
* this can proceed to right ventricular failure if pulmonary HTN is not reversed

48
Q

Laryngeal cancer

A
  • mainly men (less than 1% of cancers)
  • squamous cell carcinoma of true vocal cords most common
  • progressive hoarseness
49
Q

Lung cancer

A
  • smokoing of cigarettes or tobacco
  • leading cause
50
Q

Non-small cell lung cancer types

A
  • squamous cell carcinoma
    1) mainly smoking and COPD
    2) near hila or lung roots and project into bronchi (central location)
    3) penumonia and atelectasis; chest pain late sx d/t large tumors (well localized, metastazie later)
    4) 30%
  • adenocarcinoma
    1) women, non smokers, Asians
    2) EGFR (epidermal growth factor receptor mutation and ALK (anaplastic lymphoma kinases - target for therapy
    3) peripheral regions of pulmonary parenchyma
    4) asymptomatic => routine chest xray // pleuritic chest pain and SOB
    5) 35-40%
  • large cell undifferentiated carcinoma
    1) 10-15%
    2) centrally and grow to distort trachea and widening of carina (where windpipe divided into two bronchi)
    3) neither radiation or chemotherapy or surgery can increase survival
51
Q

Neuroendocrine tumors

A
  • SCLSs or small cell lung carcinomas
    1) central part
    2) tobacco smoking (strongest correlation)
    3) neuroendocrine cells that contain granules exist throughout tracheobronchial tree
    4) Tumor-derived hormone production
    5) Paraneoplastic syndromes (e.g - hyponatremia [antidiuretic hormone, cushing synhdrome [adrenocorticotropic hormone], hypocalcemia [calitonin], gynecomastia (gonadotropins), carcinoid syndrome [serotonin], and lambert-eaton myasthenic syndrome [d/o of neurmuscular junction where nerve and muscle meet to active muscle])
    6) rapid growing

Paraneoplastic syndromes are a group of rare disorders that occur when the immune system has a reaction to a cancerous tumor known as a “neoplasm.”

  • Bronchial carcinoid tumors
    1) slow growing and low potential to metastaize
    2) logcal surigcal resection is curative (bronchoscopic resection)
52
Q

Other tumors

A
  • small cell carcinoma or oat cell
  • bronchial adenoma
  • adenocystic tumors (cylindromas) — rare bronchial gland tumors (trachea or large airways and cause obstruction) // some able to surive to 10-15 years
  • mucoepidermoid carcinomas (bronchial tumors)
  • mesothelioma (abestos exposure up to 40 years prior to diagnosis // dypanea and chest pain d/t tumor-derived pleural fluid and invasion of chest wall)