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pathophysiology > MOD 7 Respiratory system > Flashcards

MOD 7 Respiratory system Flashcards

1
Q

Organs involved in the airway

A

larynx, trachea, and large bronchus

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2
Q

organs involved in breathing

A

bronchioles and alveoli (gas exchange)

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3
Q

PaO2 normal levels

A

80-100

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4
Q

Hypercapnia

A

too much carbon dioxide in the BLOOD (caused by a problem with VENTILATION)

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5
Q

Hypoxemia

A

low oxygen in the BLOOD (which can lead to hypoxia)

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6
Q

Hypoxia

A

Low oxygen in the tissue (caused by a problem with perfusion)

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7
Q

INDICATORS OF SEVERE HYPOXIA

A

Tripod position
use of accessory muscles
(perioral) cyanosis

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8
Q

How are hypoxemia and hypoxia measured?

A

PaO2 levels
SaO2 levels

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9
Q

PaO2 measures what

A

Hypoxemia
oxygen in the blood (normal value 80-100)
Needle in the arterial artery to get an ABG
obtained from ABG
more accurate than oxygen saturation

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10
Q

SaO2 measures what

A

tissue perfusion - pulse oximeter reading >95%

measures Hypoxia

obtained from oxygen saturation measurement
uses a pulse oximeter

less accurate than ABG blood draw but painless and noninvasive

Sa (saturated, how well our tissues are saturated)

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11
Q

Ventilation/ perfusion abnormalities

A

Able to compensate for mismatches in ventilation

If ventilation is greater than perfusion the arterioles dilate and the bronchioles constrict (increasing perfusion and reducing ventilation)

If ventilation is less than perfusion the arterioles constrict while the bronchioles dilate to correct the imbalance

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12
Q

V/Q

A

ventilation/ perfusion
V/Q scans are done on the lungs to evaluate lung function after a pulmonary embolus

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13
Q

ventilation part of V/Q test

A

looks at the ability of air to reach all parts of the lungs

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14
Q

perfusion part of the V/Q test

A

test how well blood circulates within the lungs

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15
Q

Ventilation is what

A

AIR FLOW is disrupted it is a ventilation problem

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16
Q

Perfusion is what

A

BLOOD FLOW is disrupted it is a perfusion problem

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17
Q

ventilation mismatch

A

ventilation can be too fast (hyperventilation) for the exchange of gases to take place between the alveoli sac and the surrounding capillary

OR oxygen gets into the alveoli but CO2 cannot get out due to constricted airways as in asthma

OR Air gets into the alveoli but cannot get into the blood due to the buildup of fluid, mucous, and inflammation in the alveoli as in asthma, pneumonia, tumors, obstructions, etc.

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18
Q

Perfusion mismatches

A

1) blood clots impeding or stopping blood flow to the lung tissue
2) blood moving by the alveoli too fast for the exchange of gases to take place between the alveoli sac and capillary (tachycardia)
3) blood moving too slowly to oxygenate the lungs (bradycardia, heart blocks, heart failure, etc.)

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19
Q

First indicator of hypoxemia/ hypoxia

A

CHANGE IN LOC
-restlessness
-confusion
-anxiety
-personality changes etc.

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20
Q

Hypoxemia disturbs what organs first

A

Brain hence why change in LOC is the first indicator

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21
Q

The primary regulator of respiration is what

A

HIGH CO2 NOT LOW OXYGEN

Central Chemoreceptors in the brain are more sensitive to CO2 levels than to O2 levels

the brain makes changes in breathing rate and depth based on CO2 levels in the blood and CSF

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22
Q

Atelectasis

A

Air sac CANNOT EXPAND ( type of collapsed lung)
Caused by
-Blockage of the air passages (bronchus/ bronchioles
-pressure on the outside of the lung
-surfactant failure

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23
Q

RAT BED

A

Early symptoms
R: restlessness
A: Anxiety
T: Tachycardia/tachypnea

Late symptoms
B: bradycardia
E: Extreme restlessness
D: Dyspnea (severe)

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24
Q

Atelectasis common when

A

Soon after surgery or in patients who have limited mobility in the hospital (secretions build up in the lungs due to immobility)

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25
Q

What might develop after atelectasis

A

-pneumonia may develop quickly after atelectasis starts in the affected part of the lung

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26
Q

Ventilation/ perfusion is what two systems

A

Either a problem with the airway or the circulation
When assessing, find out whats not getting to the alveoli, is the blood not getting to the functional unit? perfusion.
Is O2 not getting to the functional unit? ventilation

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27
Q

Atelectasis is life-threatening when

A

atelectasis in an adult in a small area is usually not life-threatening

It is life-threatening when it is a larger area ESPECIALLY IN A BABY OR SMALL CHILD

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28
Q

S/S of atelectasis

A

Dyspnea, chest pain, or cough

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29
Q

TX of atelectasis

A

Pulmonary Hygiene: Incentive spirometry and TCDB (have patient Turn, Cough, and Deep Breath frequently)
those actions keep the alveoli open and prevent further lung collapse

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30
Q

Risk factors for developing atelectasis

A

-Anesthesia
-foreign object in the airway
-lung disease
-mucus that plugs the airway
-prolonged bed rest
-shallow breathing
-pressure on the lungs caused by pleural effusion
-tumors that block an airway

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31
Q

Airway vs breathing problems

A

airway is the flow of things (CPAP)
breathing is the exchanging of CO2 and O2 (smoking)

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32
Q

Absorption atelectasis

A

ALVEOLI CANNOT EXPAND BECAUSE THE AIRWAYS ARE BLOCKED AND AIR CAN NOT GET INTO THE AIR SAC OR THERE IS NO NITROGEN IN THE AIR SAC TO KEEP IT OPEN ex: Post-Op atelectasis

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33
Q

the main cause of atelectasis

A

POST OP atelectasis (general anesthesia)

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34
Q

what is post-op atelectasis

A
  1. oxygen (given in general anesthesia) pushes CO2 and nitrogen gases out of the alveoli
  2. oxygen then leaves the alveoli too as it gets absorbed into the capillaries
  3. no gas is left in the alveoli to keep it open
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35
Q

Compression atelectasis

A

caused by outside pressure pushing on the alveoli and collapsing them such as a space-occupying tumor, or pleural effusion

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36
Q

Pneumothorax

A

Air escapes from the lung
the air escapes from the lung and filled in the pleural space, between the lung and chest wall, this build up puts pressure on the lung so it cannot expand as much.

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37
Q

pneumothorax caused by

A

injury to the lung
such as gun shot or knife
wound to the chest, rib fracture, or certain medical procedures

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38
Q

Collapsed lung caused by air blisters

A

air blisters break open, sending air into the space around the lung.

can result from a MECHANICAL VENTILATOR IS SET TOO HIGH OR WITHOUT WARNING PEOPLE WITH WEAKENED ALVEOLI (COPD patients) TALL THIN PEOPLE AND SMOKERS.

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39
Q

A collapsed lung that occurs without any cause

A

Spontaneous pneumothorax

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40
Q

lung diseases that increase the chance of getting a collapsed lung

A

Asthma
COPD
Tuberculosis
cystic fibrosis
whooping cough

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41
Q

Pleuritis/ Pleurisy

A

Inflammation of the lining of the lungs and chest (the pleura) causes chest pain when taking a breath or coughing. The normally smooth surfaces lining the lung become rough. They rub together with each breath resulting in a rough, grating sound called a FRICTION RUB.

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42
Q

Pulmonary Embolism

A

arteries in the lungs become blocked by a blood clot
restricts blood flow to the portion of the lung resulting in a PERFUSION MISMATCH and ultimately that portion of the lung can die

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43
Q

A pulmonary embolism caused by blood clots from where

A

DVT, they travel from the legs

44
Q

High risk for a P.E.

A

Use of birth control pills (causes hypercoagulation)
Large bone fractures (releases fatty emboli- causing fat embolism syndrome)
Smoking (vasoconstriction slows blood flow leading to clot formation)
Atrial fibrillation (clots form in atria of the heart)
Post operatively (3-10 days after)

45
Q

Symptoms of P.E.

A

Shortness of breath S.O.B. , chest pain, s/s of hypoxia and cough

46
Q

DX: for P.E.

A

V/Q scan and blood test (D-Dimer) and platelet count

47
Q

Pleural effusion

A

build-up of fluid between ribs and lungs in the pleural space fluid can be: serous fluid, pus (empyema), lymph fluid, or blood (hemothorax).

48
Q

how to remove pleural effusion

A

It can be aspirated with a needle because it is in a cavity of the body. if large enough a pleural effusion can cause a compression atelectasis

49
Q

Pulmonary Edema

A

build-up of fluid in the interstitial tissue of the lung. Pulmonary edema occurs when the alveoli fill up with excess fluid seeped out of the blood vessels in the lung instead of air

50
Q

Pulmonary edema is commonly caused by what

A

Left-sided heart failure** (backup of fluid in the lungs)
kidney failure (kidney doesn’t remove excess body fluid)
sepsis (see below ARDS)
any lung damage

51
Q

Difference between Effusion and Edema

A

Pleural effusion: fluid in the pleural cavity which CAN BE DRAINED OUT via THORACENTESIS

Pulmonary edema: swelling of the interstitial lung tissue CANNOT BE DRAINED OUT

52
Q

ARDS

A

acute (adult) respiratory distress syndrome

53
Q

ARDS starts with what

A

Acute lung injury/ insult of some type ( infection/ sepsis, trauma, hypoxic event, aspiration of gastric juices/ vomit, pulmonary embolism, blood transfusion, reaction, etc.)

54
Q

Acute lung injury causes (in the cases of ARDS)

A

SEVERE LUNG INFLAMMATION also referred to as SIRS (systemic inflammatory response syndrome)

55
Q

in response to lung injury, the body releases what

A

chemical mediators, clotting factors, vasodilating agents, etc.

56
Q

After ARDS

A

the lungs stop producing surfactant which leads to atelectasis

57
Q

First stage of ARDS

A

respiratory alkalosis
lungs initially try to compensate for hypoxia by breathing faster (tachypnea) causing Hyperventilation.
Results in respiratory alkalosis

58
Q

intermediate stage (2) of ARDS

A

Acidosis (respiratory and metabolic)
as hypoxia worsens the lungs won’t be able to maintain the fast rate of breathing and respiratory acidosis will develop as CO2 builds up. Metabolic acidosis will also develop as the acid from CO2 and the breakdown of cells increase. Lack of O2 also leads to anabolic respiration which leads to more acid

59
Q

Intermediate stage 3 of ARDS

A

Pulmonary edema
combination of hypoxia and acidosis causes damage to the epithelial wall between the alveoli and the adjacent capillaries that forms the blood/air barrier. The damage to that barrier leads to fluid from the blood leaking into the air sacs and drown the patient slowly.

60
Q

Intermediate stage 4 of ARDS

A

Blood Clotting
Platelets respond to the inflammation and tissue damage by making MICRO CLOTS THROUGHOUT THE LUNG TISSUE. this adds to the problem by blocking perfusion which in turn leads to worsening hypoxia

61
Q

Late stage of ARDS

A

Respiratory failure
the continued acidosis and tissue death ultimately cause further hypoxia, decreased cardiac output, hypotension, and death. (about 40% of the people who develop ARDS will die from complications)

62
Q

Long-term effects of ARDS

A

if patients survive they will have PERMANENT LUNG DAMAGE as well as PSYCHOLOGICAL and COGNITIVE impairment due to the brain being deprived of adequate oxygen

63
Q

COPD

A

chronic obstructive pulmonary disease
a group of lung diseases that block airflow and make breathing difficult

64
Q

types of COPD (the most common)

A

emphysema and chronic bronchitis

65
Q

Symptoms of COPD

A

symptoms often do not appear until significant lung damage has occurred and will usually worsen over time

66
Q

The leading cause of COPD

A

smoking

67
Q

Causes of airflow being impaired COPD

A

-the airways and air sacs lose their elastic quality
-the walls between many of the air sacs are destroyed
-the walls of the airways become thick and inflamed
-the airways make more mucus than usual, which can clog them

68
Q

Asthma

A

reactive airway disease
chronic inflammatory disorder of the airway due to hyper-responsiveness of the airway to ANY NUMBER OF AIRBORNE IRRITANTS (pollen, perfume, exercise, infections, pollution, etc.)

69
Q

What causes inflammation physiologically in asthma

A

products of inflammation (chemical mediators) go into mass production and overwhelm the lungs. resulting in inflammation. leading to wheezing!

The airways tend to react strongly to certain inhaled substances

70
Q

Emphysema

A

PERMANENT damage to the lung as a result of the inflammatory process. Abnormal and permanent enlargement of the airways accompanied by destruction of alveolar walls without obvious fibrosis. The lungs lose their ability to recoil after each respiration

71
Q

Characteristic sign of emphysema

A

anatomical change in the PATIENT’S CHEST FROM OVAL TO ROUND. Result of the body trying to adjust for the extra work of breathing

72
Q

Patients with COPD don’t react to high PCO2 why

A

patients with COPD live with high levels of CO2 so high PCO2 don’t stimulate respiration

73
Q

What stimulates respirations for COPD patients

A

they breathe only in response to low O2 levels. If too much O2 is given to a patient with COPD it removes their respiratory drive and causes respiratory arrest

74
Q

Bronchitis

A

mucus membrane in the lungs (bronchial passages) becomes inflamed. It swells and grows thicker, narrows or shuts off tiny airways in the lungs. Leading to coughing spells that may be accompanied by phlegm and breathlessness

75
Q

Two types of bronchitis

A

Acute 1-3 weeks
Chronic lasting at least 3 months of the year COPD that can be treated

76
Q

Acute bronchitis

A

NOT A COPD
causes hacking cough and phlegm production that sometimes accompanies an upper respiratory infection.
usually viral origin
should return to normal after resolution of infection

77
Q

Chronic Bronchitis

A

Is a COPD
hyper-secretion of thick mucus (thicker than normal)
last 3 months of the year and for at least 2 consecutive years
Caused by irritants that increase mucus production and size and number of mucous glands along with damage to cilia
vulnerable to viral and bacterial infections

78
Q

Cystic Fibrosis

A

an inherited disorder that affects the exocrine or mucus-producing glands. The exocrine or mucus-producing glands secrete abnormally thick mucus.
Thick secretions obstruct the bronchioles

79
Q

C.F pathophys

A

impaired chloride sodium reabsorption. Chloride movements alters vascular osmolarity and trigger sodium shift.
SODIUM LEAVING THE TISSUE WATER FOLLOWS WHICH LEADS TO DEHYDRATION OF THE TISSUE

80
Q

s/s of C.F

A

salty-tasting skin, at risk for infection, inability to gain weight, greasy/ fatty stools

81
Q

Pneumonia

A

inflammation of the parenchymal structures of the lung, such as the alveoli and bronchioles.

82
Q

Tuberculosis risk populations

A

-people from developing countries
-high-density living conditions
-immunocompromised
-children

83
Q

TB

A

airborne transmission
Active TB (infected, symptomatic and contagious)
Latent TB (infected but not symptomatic and not contagious can develop into active)

84
Q

Etiology of Pneumonia

A

Infectious (pathogen- caused by bacteria, viruses, fungus, etc.)
Noninfections (i.e. inhalations, toxic gases, aspirations of foreign body)

85
Q

S/S of TB

A

coughing, with or without blood, and chest pain
fever, night sweats, weight loss, and tiredness

86
Q

TB test

A

Skin test - test if exposed to TB
Tb blood test - Test if exposed to TB
chest x-ray - test if contagious
sputum sample - test if contagious

87
Q

Transporting a TB patient outside of their hospital room who wears the mask?

A

The patient should wear a standard surgical or medical mask. not an N95 because we don’t want them to have a harder time breathing

88
Q

Lung cancer is top

A

top cause of cancer deaths in both men and female

89
Q

Bronchogenic carcinoma

A

is cancer that originates in the lining of the bronchi about 90% of lung cancers are bronchogenic the other 10 percent begin in bronchioles, alveoli, or trachea

90
Q

Tuberculosis can be treated by

A

6-9 months on treatment of antibiotics

91
Q

Cause of Lung cancer

A

heavy smokers have 20 times greater chance
nonsmokers who reside with a smoker have a 24% increase in risk of developing cancer

92
Q

Symptoms of lung cancer

A

Lung cancer does not produce S/s until well advanced (has metastasized to distant parts of the body) making it more difficult to treat
unaccountable weight loss (cachexia)
diagnosis is confirmed through a tissue biopsy

93
Q

Treatment of lung cancer

A

surgery, chemotherapy, and or radiation

94
Q

Lung cancer categories

A

Non-small cell lung cancers
small-cell lung cancer

95
Q

non-small cell lung cancers

A

the most common type of lung cancer (about 85%) squamous cell carcinoma adenocarcinoma and large cell carcinoma are all subtypes

96
Q

small cell lung cancer

A

Also called oat cancer (about 10-15%) of lung cancers highly malignant an brain metastasis is common, poor prognosis. chemotherapy is usually the main treatment for small cell lung cancer

97
Q

due to the proximity of the meningies lung cancer

A

travels up the spinal cord and to the brain

98
Q

Manifestations of lung cancer

A

-changes in organ function, lung damage, inflammation, and organ failure
-**local effects of tumors- compression of nerves or veins, gastrointestinal obstruction **
-hormones secreted by tumor cells - can cause low blood sodium levels or high calcium levels
-nonspecific signs of tissue breakdown- muscle waisting bone break down pathological fracture

99
Q

Causes of Hemoptysis

A

Most common is TB
Left sided heart failure
lung cancer
pneumonia
bronchitis
bronchiectasis

100
Q

Tuberculosis and hemoptysis

A

results is usually mild to moderate and may be associated with other symptoms, including unexplained weight loss, cough, purulent sputum, (thick, opaque, yellowish white discharge)

101
Q

Acute bronchitis or chronic and hemoptysis

A

very common cause of hemoptysis, usually mild

102
Q

bronchiectasis hemoptysis

A

chronic dilation and consequent infection
cystic fibrosis is an example of a disease that leads to bronchiectasis

103
Q

Lung cancer and hemoptysis

A

initially diagnosed because of hemoptysis

104
Q

lung cancer and hemoptysis: bleeding results from what

A
  1. necrosis of the tumor (death of the ell that makes up the tumor)
  2. the rupture of small blood vessels in the area
  3. a tumor invading one of the pulmonary blood vessels leads to major hemorrhage
105
Q

Pneumonia and hemoptysis

A

as the lung tries to protect itself the lungs fill with liquid, blood, and pus. in addition to hemoptysis, other symptoms include a high fever, cough, and chest pain

pathophysiology (14 decks)

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