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Pathophysiology 1 > Test 3 > Flashcards

Test 3 Flashcards

1
Q

Air moving in and out of the lungs

A

Ventillation

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2
Q

Ventilation depends on three things:

A
  • Distensibility: the ease of which the lungs can inflate or distend
  • Resistance: Amount of force that the lungs have to work against
  • Elasticity: How well the lungs can recoil
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3
Q

Blood needs to flow to the lungs and provide oxygen. The air needs to be able to flow from the lungs into the blood stream. CO2 needs to be able to leave the blood stream and go to the lungs.

A

Perfusion

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4
Q

For every __L of air we inhale we need ___L of blood/min.

A

4L or air, 5L of blood/min

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5
Q

Clinical Manifestations of Respiratory Dysfunction

A 
Sneezing
Dysphagia
Dysphonia
Dyspnea
Abnormal Respiratory Rates
-Tachypnea
-Bradynea
Abnormal Respiratory Patterns
-Kussmaul
-Cheyne Stokes
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6
Q

Caused by Irritation in upper respiratory tract

A

Sneezing

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7
Q

difficulty swallowing

A

• Dysphagia

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8
Q

coarse voice

A

• Dysphonia

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9
Q

protective from irritants. Normal in healthy individuals. Must determine if ______ is productive or not. Persons with decreased _______ reflex have increase chances of infection

A

cough

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10
Q

coughing up blood

A

Hemoptysis

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11
Q

shortness of breath. (Can still have normal respiratory rate & be in severe respiratory distress)

A

• Dyspnea

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12
Q

positional. Person needs to sit up to breath – unable to lie flat & breathe properly

A

o Orthopnea

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13
Q

Wake up at night with extreme SOB, gasping for air

A

o Paroxysmal nocturnal dyspnea (PND)

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14
Q

slower than normal breathing

A

o Bradypnea

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15
Q

faster than normal breathing

A

o Tachypnea

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16
Q

Increase in depth of breathing. Increase in tidal volume. (can be normal after exercise, persons at rest should not have this pattern of breathing)

A

o Kussmaul

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17
Q

Progressive increase in the rate and depth of breathing followed by a period of apnea. Alternating periods of deep and rapid breathing.

A

o Cheyne Stokes

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18
Q

often seen in children. Not often seen in adults as the cartilage of the adult nose is harder than that of a child.

A

o Nasal flaring

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19
Q

Suprasternal, supraclavicular, substernal, subcostal, intercostal indrawing – seen in children, _____ _____ ______ ___at the subcostal area below the rib cage

A

chest wall caves in

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20
Q

snoring – indicates an obstruction usually in upper respiratory tract

A

o Sonorous breathing

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21
Q

Upper respiratory blockage, high pitched musical sound

A

o Stridor

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22
Q

Popping sound

A

o Crackles

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23
Q

Continuous musical quality

A

o Wheezes

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24
Q

Visceral pleura and parietal pleura rub against each other. Inflammation of pleura may cause this.

A

o Friction rub

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25
Q

usually from coughing. Cough so hard they strain muscles in the chest.

A

• Pain in chest

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26
Q

Respiratory pain is reproducible (act of coughing will elicit pain). Cardiac pain is described as a pressure and constant.

A

o Pleuritic

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27
Q

________poisoning is the exception person looks red

A

CO2

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28
Q

Sign of hypoxemia. Occurs in cystic fibrosis, COPD

A

• Clubbing of digits

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29
Q

early signs of hypoxemia. You will see this before changes in vitals occur

A

• Anxiety/Restlessness/Confusion

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30
Q

o Elevated carbon dioxide levels in the blood

o May also be referred to as hypercarbia

A

• Hypercapnia

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31
Q 
o	Decreased O2 concentration in the blood
o	Causes:
	Hypoventilation
	Diffusion abnormalities
	Ventilation-perfusion mismatch
A

• Hypoxemia

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32
Q

o Inadequate oxygen supply to the cells

A

• Hypoxia

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33
Q

End result of pulmonary disease

A

Respiratory Failure

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34
Q

Respiratory disease interferes with ______ _________or transport and can lead to ________ _______ as defined by either
o Arterial Blood O2 (PAO2) ___ mmhg/pH

A

Oxygen Intake, and can lead to respiratory failure

oArterial Blood O2 (PAO2) 45 mmhg/pH

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35
Q

Respiratory Failure May also result from

A

cardiac dysfunction, drugs, prolonged tachycardia in other disorders such as metabolic acidosis

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36
Q

Treatment of respiratory failure is based on the:

A

etiology of respiratory failure. Must treat whatever is causing the respiratory failure.

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37
Q

Tests to Evaluate Respiratory Function (6)

A
  • Chest Xray (CXR): easiest & least expensive. Won’t tell you everything.
  • Computed tomography (CT scan)
  • Blood gas analysis (ABG’s)
  • Pulmonary function tests (PFT)/spirometry
  • Sputum analysis (C&S, cytology – looking for cancer cells, Acid Fast Bacilli – TB test)
  • VQ scan (Ventilation/Perfusion Scan) – done in nuclear medicine. Measuring how well the lungs are being perfused with blood and oxygen
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38
Q

Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:

Resistance to air flow. Air has trouble getting in and out of the lungs. Diseases that block the flow of air in and out of the lungs are obstructive disorders

A

• Obstructive disorders

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39
Q

Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:

Air does not have trouble getting in and out of the lungs. The lungs have poor distensibility. Cannot fully expand

A

• Restrictive disorders

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40
Q

Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:

Caused by a pathogen (pneumonia, croup)

A

• Infectious disorders

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41
Q

Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:

Nothing wrong with lungs. There is a problem with blood flow to the lungs. (blood clot, pulmonary embolism)

A

• Disorders of Vascular Origin

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42
Q

Categories of Respiratory Disorders (Diseases)
Disorders affecting the respiratory system may be classified as:

Cancers

A

• Malignancies

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43
Q

OBSTRUCTIVE DISORDERS

10

A 
Croup
Epiglottitis
Bronchiolitis
Bronchitis
Asthma
COPD: Umbrella term for Chronic Bronchitis & Emphysema
Chronic Bronchitis
Emphysema
Bronchiectasis
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44
Q

• Caused by parainfluenza virus, influenza A or respiratory syncytial virus (RSV)
o Attacks upper respiratory structures
• Most commonly occurs in 6 months to 5 years age group.

A

Croup

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45
Q

Croup is characterized by ____________ extending from _____ _______to bronchial lumina

A

inflammation, vocal cords

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46
Q

Clinical Manifestation of Croup (6)

A 
o	catarrhal symptoms: sick looking eyes – red, runny eyes
o	rhinorrhea: runny nose
o	low-grade fever
o	barking cough
o	stridor
o	nasal flaring
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47
Q

Croup is not usually fatal; however, more serious in?

A

<6 months old.

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48
Q

• Causative organisms (not viral)
o Haemophilus influenzae type B – immunization helps prevent epiglottitis
o Streptococcus pneumoniae

A

Epiglottitis

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49
Q

Most common in ____ to _____ year age group, but may also affect adults

A

2 to 6

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50
Q

Epiglottitis Clinical manifestations: sudden onset

A

o sore throat, dysphagia, drooling, fever
o “sniffing position”, muffled voice, anxious
o stridor, respiratory distress

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51
Q

Epiglottitis Evaluation: based on symptoms:

A

o X-ray of soft tissues of neck.
o Characteristic “thumbprint”
o Do not attempt to examine pt’s throat. Depressing the tongue can cause laryngospasm – may not be able to be intubated after.

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52
Q

Epiglottitis can be _______________________

A

• Fatal: death may occur in a few hours

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53
Q

Epiglottitis treatment:

A

IV antibiotics quickly; may require rapid intubation.

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54
Q

widespread infection of the bronchioles

A

Bronchiolitis

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55
Q

_______ ______ _____causes bronchiolitis (majority of cases)

A

respiratory syncytial virus (RSV)

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56
Q

True or False

Bronchiolitis not contagious?

A

False

It is highly contagious

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57
Q

Bronchiolitis is more prevalent is what age group and what time of year?

A

2 – 24 month age group, o November to February

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58
Q

Clinical manifestations of Bronchiolitis (7)

A

o Nasal congestion, mild conjunctivitis
o Inspiratory crackles, expiratory wheezes
o Use of accessory muscles, (such as intercostal indrawing), nasal flaring, increased work of breathing
o Tachypnea (with resp rate 50 – 60 per min. Can go up to 80)
o Tachycardia, poor feeding
o Pallor, cyanosis, hypoxemia
o Episodes of apnea

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59
Q

Pathogenesis of Bronchiolitis (4)

A

o Respiratory virus attacks lower bronchioles
o Bronchiole walls become very swollen & obstructed.
o Edema of submucosa, increase in mucus secretion
o Necrosis of bronchial epithelium
 Virus causes epithelial layers to slough off
 Clogs up bronchioles so air cannot get past them into the alveoli

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60
Q

Management of Bronchiolitis

A

o Humidity, fluids, rest

o Infection control precautions

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61
Q
  • Inflammation of the trachea and bronchi

* Acute or chronic

A

Bronchitis

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62
Q

Etiology of Bronchitis

A

influenza virus A or B, parainfluenza virus, respiratory syncytial virus (RSV); smoke or inhalation of chemical irritants

63
Q

Pathogenesis of Bronchitis (5)

A 
o	Bronchi become invaded by viruses 
o	Edema of mucous membranes
o	Increased mucous production
o	Loss of ciliary function 
o	Causing bronchiole irritation
64
Q

Manifestations of Bronchitis

A

o Expiratory wheezing, dyspnea, malaise
o Cough (productive or nonproductive) from increased mucus production
o Chest pain r/t persistent coughing

65
Q

• Treatment – Acute Bronchitis

A

o Increase fluids, smoking cessation, expectorants(thins out secretions)/antitussives(suppresses cough), antibiotics not routinely prescribed

66
Q

Chronic Bronchitis

A

permanent increase in thickness of the bronchi, and increase in the number of goblet cells. Which means increased mucus productions, increased cough, decreased cilia

67
Q

• Clinical Manifestations of Asthma (6)

A

o Dyspnea, with increased respiratory effort
o Wheezing (inspiratory and expiratory), SOB
o Prolonged expiration
o Cough – nonproductive during acute attack; productive with thick mucus as attack resolves
o Use of accessory muscles, respiratory distress with severe attacks
o May lead to respiratory failure

68
Q

treatment of asthma

A

o Acute attacks: inhaled bronchodilators, oral corticosteroids, oxygen prn
o Chronic management: avoidance of allergens and triggers, patient education, anti-inflammatories (ie. inhaled corticosteroids), antileukotrienes. Airway inflammation & fluid may be still be present in some individuals, even though they are asymptomatic

69
Q
  • Permanent damage
  • Cannot be cured
  • Person must live with symptoms
A

COPD: Umbrella term for Chronic Bronchitis & Emphysema

70
Q
  • Hypersecretion of mucus and chronic productive cough for 3 months a year for 2 consecutive years
  • Increase in the size and number of mucous glands and goblet cells
  • Airway obstruction caused by chronic infection and injury
A

Chronic Bronchitis

71
Q

• Clinical Manifestations of Chronic Bronchitis (4)

A

o increased mucus productions, increased cough
o At risk for recurrent pulmonary infections
o Peripheral & central edema
o Right sided heart failure (blue bloaters)
 Edemic, bloated, cyanotic

72
Q

• Loss of elastic recoil occurs from destruction of alveolar walls resulting in permanent enlargement of gas-exchange airways (Like a balloon that has been inflated too many times)

A

Emphysema

73
Q

In emphysema the _____big, boggy and stretched (ENLARGED)

A

o Alveoli

74
Q

_____ _ -______protects us from these enzymes that want to destroy our lungs tissue. Emphysema has a deficiency in this which is a primary cause.

A

Alpha1-antitripsin

75
Q

Secondary cause to emphysema

A

injury to lungs from inhaled toxins

o Cigarette smoke – toxins within cigarettes destroys alpha1-antitripsin

76
Q

• Clinical manifestations of emphysema (4)

A

o Barrel chest (anterior-posterior diameter of chest is larger than it should be because the lungs are always in a state of hyperinflation)
o Pursed lip breathing – they have to make the extra effort to exhale. It isn’t natural for them, they have to force air out of lungs.
o Sit in tripod position – most comfortable way they can breath
o Weight loss – thin, emaciated appearance

77
Q

People with emphysema are at High risk for pneumonia as they cannot _____________ ___________

A

effectively expectorate

78
Q
  • Dilation of the bronchi

* Pocket forms on side of bronchi and they have different shapes

A

Bronchiectasis

79
Q

Bronchiectasis can develop _________ ____________ _____________

A

abscess, infection, burst

80
Q

Bronchiectasis Occurs as a result of __________ of muscle and elastic fibers of bronchial wall

A

weakening

81
Q

RESTRICTIVE DISORDERS (2)

A

Pneumonia

Atelectasis

82
Q

Pneumonia

• Etiology (3)

A

o Begins with Inhalation of pathogens. Pathogens then establish themselves inside the lungs
o Aspiration – vomiting and inhaling gastric contents. Burns the bronchi and respiratory passages
o Endogenous – infection that occurs somewhere else in the body. Travels to the lungs and establishes infection there

83
Q

Pneumonia

• Pathogenesis

A

o Set off inflammatory reaction
o Alveoli fill with exudate (drainage)
o Consolidation

84
Q

Pneumonia

• Clinical manifestations may vary with cause, age and severity of illness (3)

A

o Fever, chills
o Cough (may or may not be productive)
o Dyspnea, crackles over affected lobe

85
Q

collapse of lung tissue

A

Atelectasis

86
Q

Atelectasis two types:

A

o Obstruction

o Compression by external mass

87
Q

Atelectasis • Pathogenesis (3)

A

o Airless alveoli shrivel due to elasticity – because they are not receiving air
o Interferes with blood flow through lungs (decreased gas exchange & oxygenation)
o Client will become hypoxemic very quickly

88
Q

Atelectasis • Risk factors (2)

A

o Immobility – secretions pool in lungs and clog small bronchioles. And alveoli that are passed the area of obstruction do not receive air and shrivel. Inhibits blood vessels. If oxygen isn’t restored the tissue becomes necrotic and dies.
o Surgery

89
Q

Atelectasis • Clinical manifestations (9)

A 
o	Dyspnea
o	Cough
o	Fever
o	Leukocytosis
o	Tachypnea
o	Focal decreased breath sounds
o	Increased crackles at lung bases
o	Hypoxemia
o	Decreased depth of respiratory excursions
90
Q

Chest Wall Structural Abnormalities – prevent lungs from expanding

Hunched back. Elderly with osteoporosis. Inhibits chest expansion

A

• Kyphosis

91
Q

Chest Wall Structural Abnormalities – prevent lungs from expanding

(chest excavation) Sternum is displaced backwards

A

• Pectus excavatum

92
Q

Chest Wall Structural Abnormalities – prevent lungs from expanding

Sternum is protruding forward. Bird chest.

A

• Pectus carinatum

93
Q

Chest Wall Structural Abnormalities – prevent lungs from expanding

spine is ‘S’ shaped. Interferes with movement of ribs and inhibits movement of chest wall.

A

• Scoliosis

94
Q

Painful interferes with lung expansions. Leading to pneumonia or atelectasis

A

• Rib fractures

95
Q

o Usually 2 fractures per rib in consecutive ribs or fracture of sternum plus consecutive ribs.
o Results in paradoxical breathing
o Treatment: pain control and management of underlying pulmonary and/or cardiac injury (Chest tubes, mechanical ventilation)
o Can cause pneumothorax

A

• Flail chest (multiple rib fractures)

96
Q

• An accumulation of air in the pleural space
o Causes atelectasis (greater amount of air = more severe atelectasis)
• May result from underlying disease (such as COPD) or from chest trauma (rib fractures)

A

Pneumothorax

97
Q

• Types of pneumothorax

A 
o	Spontaneous
	Primary
	Secondary 
o	Open 
o	Tension
98
Q

Pneumothorax: Spontaneous

• Primary

A

o Spontaneous rupture of blebs (air blister) on visceral pleura. May occur during rest, exercise, or sleep.
o Usually occurs in men between 20 – 40 yrs

99
Q

Pneumothorax: Spontaneous

• Secondary

A

o Resulting from trauma or spontaneous rupture of bleb on visceral pleura secondary to pre-existing pulmonary disease

100
Q

• Opening in chest wall secondary to trauma such as stab wounds, bullet wounds. (CHEST INJURY)
• Air is drawn through the wound into the pleural space during inspiration and forced back out during expiration. Wound in the chest wall appears to be “sucking air” and is visibly bubbling; therefore referred to as “sucking wound”
o Leads to atelectasis
• Pressure in pleural space equals atmospheric pressure

A

Pneumothorax: Open

101
Q

As person inhales, air is entering through chest wall. The issue is a flap will develop. Air cannot escape bc of flap. Every time they inhale more and more air get into the pleural space. Increases pressure inside thoracic cavity.

A

Pneumothorax: Tension (WORST PNEUMOTHORAX)

102
Q

• Air enters the pleural space during inspiration; on expiration, opening is sealed and air becomes trapped, increasing the pressure within the thoracic cavity

A

Pneumothorax: Tension (WORST PNEUMOTHORAX)

103
Q

manifestations of tension pneumothorax

A

o Initially: Chest pain, dyspnea, tachycardia, decreased breath sounds on affected side,
o As pneumothorax progresses: absent breath sounds on affected side, hypoxemia, laboured breathing, jugular venous distension, hypotension, contralateral tracheal shift.

104
Q
  • Accumulation of excessive fluid in the pleural space

* Fluid is heavy and sits at bottom of pleural space

A

Pleural Effusion – same principle as pneumothorax but instead of air it is fluid in the pleural space

105
Q

blood in pleural space usually associated with trauma

A

o Hemothorax

106
Q

watery drainage in pleural space, low protein count (seen in pneumonia)

A

o Transudate

107
Q

watery but has high protein count (seen in tumors – lung cancer)

A

Exudate

108
Q

pus in pleural space (seen in lung abscesses)

A

Empyema

109
Q

lymphatic fluid leaking into pleural space

A

Chylous pleural effusion

110
Q

• Clinical manifestations are associated with the extent of atelectasis (amount of drainage) Symptoms worsen as drainage increases (3)

A

o Dyspnea, tachypnea, tachycardia, decreased breath sounds on affected side
o Fever associated with infection (empyema)
o Hypoxemia, laboured breathing, hypotension, contralateral tracheal shift

111
Q

• Form of respiratory failure
• Causes
o Direct – pneumonia, smoke inhalation, chemical inhalation, inhalation of toxic fumes, near drowning
o Indirect – caused by other diseases such as pancreatitis, drug overdose

A

Acute Respiratory Distress Syndrome (ARDS)

112
Q

 Fibroblast cells deposit protein along walls of alveoli occur with the increased inflammation. This increases the thickness of the alveoli and decreases gas exchange.
 Prominent fibrosis (thickening)

A

o Fibroproliferative phase

113
Q

• Pathogenesis of ARDS

A

o Acute phase
 Inflammatory mediators damage structure of alveoli
 At the same time we have an increase in coagulation factors
 Lots of inflammation at site
 Alveolar membrane becomes damage as a result of inflammation & edema
 Increase in coagulation factors causes increase in blood clotting inside the lungs
 Can recover from this phase If damage isn’t too severe

114
Q

• Clinical manifestations of ARDS

A

o Dyspnea, tachypnea, tachycardia, increased respiratory effort.
o Hypoxemia unresponsive to increasing fractions of inspired oxygen (Fi02), poor lung compliance
o Can result in respiratory failure and if not reversed – death
o Restlessness, exhaustion, decreased mental status

115
Q

Inherited disease. Genetic abnormality. Respiratory, pancreatic, and GI tract ducts become clogged with a very thick mucus. Normally, we have a little bit of mucus in secretions. In cystic fibrosis, the mucus is so thick it plugs the ducts.

A

Cystic Fibrosis (cystic = duct)

116
Q

• CF gene located on chromosome __

A

7

117
Q

• CFTR (cystic fibrosis transmembrane regulator)

A

Abnormal expression of protein

118
Q

• Characterized by ______ _________ __ ____ _______and concentrated sweat, often causing obstruction of GI and respiratory tracts

A

excessive secretion of thick mucus

119
Q

CF Respiratory effects (blocks ducts in respiratory tract)

A 
o	Cough, wheeze, recurrent pneumonia
o	Barrel chest, clubbing bc of hypoxemia
o	Bronchospasm
o	Mucus in lung
o	Causes hypoxemia
120
Q

CF Gastrointestinal effects (mucus prevents liver and pancreas from secreting enzymes)

A

o Failure to thrive, malabsorption

o Diabetes, pancreatitis, hepatic failure

121
Q

No tx for CF only Manage symptoms by supplementing digestive enzymes

A

 Cotezyme

122
Q

• As the client with cystic fribrosis ages they can develop:

A

o Pancreatitis
o Liver failure
o Diabetes
o Respiratory problems bc lungs begin to fail, become hypoxemic
 Can go into respiratory failure
 Usually need lung transplant eventually

123
Q

Etiology – Lung disease caused by chronic exposure to industrial products

A

Pneumoconiosis

124
Q

fine particle silica(dust) inhalation

A

• Silicosis

125
Q

in buildings in 50s as fire retardant

A

• Asbestosis

126
Q

coal miner’s lung, accumulation of soot, fine particle dust

A

• Anthracosis

127
Q

pesticides, fine hay particles

A

• farmer’s lung

128
Q

• Macrophages (WBCs) secrete____________which destroy alveolar walls

A

lysozymes

129
Q

• Causative organism: Bordetella pertussis

A

Pertussis – whooping cough

130
Q

• Droplet infection of Pertussis – whooping cough

A

highly contagious

131
Q

Pertussis – whooping cough Pathogenesis

A

o Attached to cilia in respiratory tract produces a toxin which initiates an inflammatory response
 Incubation Period 5 – 21 days
 Prodrome: 1 – 2 wks; Rhinorrhea (runny nose), fever, malaise (resembles bad cold)
 Paroxysm : 1 – 6 wks; Paroxysmal coughing spasm (associated with vomiting)
 Convalescence: wks – months
 Can be dangerous in infants and babies bc of coughing spams – cause vomiting. This causes increased risk for aspiration.

132
Q

Pertussis – whooping cough Clinical Manifestations

A
  • Bruising around eyes

* Broken blood vessels in eye from coughing

133
Q

Pertussis – whooping cough • Complication:

A

o Risk of aspiration in infants ( 1 – 3 infants deaths per year in Canada)
o Petechiae, bruising, fractured ribs, pneumonia

134
Q

Tuberculosis • Mode of transmission

A

caused by inhalation of bacterium

o aerosolized droplet

135
Q

Tuberculosis • Populations at risk (large populations living in small areas)

A 
o	Elderly
o	HIV
o	Homeless
o	Refugee camps
o	Travelers
136
Q

TB Clinical Manifestations:

A

• Primary infection may be asymptomatic
• Active disease:
o Fever, fatigue, malaise, weight loss, night sweats, cough (may be productive, may cough up blood), sputum production, hemoptysis

137
Q

• A severe form of pneumonia caused by:

A

SARS associated coronavirus (SARS-CoV).

138
Q

SARS quickly leads to ___________ ____________

A

respiratory failure

139
Q

SARS Pathogenesis

A

o Incubation period 2 to 7 days
o Onset: fever, chills, myalgia, headache
o Nonproductive cough; progresses to pneumonia
o May develop hypoxemia
o Period of communicability:
 when pt symptomatic.
 CDC recommends isolation for 10 days post symptoms

140
Q

• Mode of transmission for SARS

A

airborne (CDC) – highly contagious

141
Q

• WHO guidelines: SARS may be suspected in a patient with

A

o Fever of 38°C and
o History of
 travel to high risk areas OR
 Contact with someone with a diagnosis of SARS

142
Q

Influenza – respiratory illness. Can have gastro symptoms comes from the

A

• Orthomyomyxoviridae – family that influenza comes from…. Awe  (comes from birds)

143
Q

• Influenza A
• Influenza B
• Influenza C
Which is the most serious

A

Influenza A – most serious

144
Q

Influenza – respiratory illness Complications

A

o Croup, viral pneumonia, secondary bacterial infections
o Cardiac complications
o Reye’s syndrome (encephalopathy – brain damage, secondary to infection)
o Guillain-Barre syndrome

145
Q

Blood clots have developed in lungs or develop elsewhere in the body. An embolus (piece of blood clot) breaks off and travels to lungs

A

Pulmonary Embolism – blood clot to lungs

146
Q

often caused by DVT Prolonged immobility

A

o Venous stasis (sluggish blood flow)

147
Q

 often caused by DVT
Polycythemia vera (increase coagulability)
 Medications (birth control)

A

o Hypercoagulability (promote blood clotting)

148
Q

 often caused by DVT
Hyperglycemia can inflame blood vessel
 When we start an IV (venipuncture)
 Smoking

A

o Inflammation of blood vessel

149
Q

Pulmonary Embolism – blood clot to lungs Pathogenesis

A

o Initially a blood clot (thrombus) forms within the deep veins. The clot becomes embolus, by becoming dislodged from its original site and travels through the systemic circulation and into the pulmonary circulation. The clot eventually travels into a branch of the pulmonary circulation. It can either occlude a small vessel causing temporary symptoms until the fibrinolytic system destroys it. It may manifest as multiple small emboli, or it may be large enough to block the flow of blood distal to the obstruction, creating death of pulmonary tissue (an infarction).
o Can have multiple small emboli or one large one

150
Q

Pulmonary Embolism – blood clot to lungs

• Clinical Manifestations varies with severity

A

o Initially – anxiety, restlessness
o Dyspnea, tachypnea, chest pain, tachycardia
o As it worsens – May experience hemoptysis
o Hypoxia/cyanosis
o Massive occlusion from poor blood flow to tissue – profound shock

151
Q

Lung Cancer

• Small cell

A 
o	Rapid growing
o	Unresponsive to treatment
o	Grows in central bronchi region
o	Grows from the outside of lung inside
o	Doubles in size in 33 days
o	Usually isn’t found until it has spread considerable
o	Has poorest outcome
152
Q

Lung Cancer

• Non-small cell

A

o Squamous cell
 grows centrally
 easily found
 grows slowly

o	Adenocarcinoma
	Slow growing cancer
	Grows peripherally
	Grows more quickly than squamous cell
o	Large cell carcinoma
	Grows in cluster
	Grows peripherally
	Slow growing
	Fairly easy to find & indentify
o	If found early there may be success in treating them
153
Q

Lung Cancer what is the first sign

A

Persistent nagging cough

154
Q

Lung Cancer effects

A

o Obstruction of airflow
o Inflammation
o Pleural effusion, hemothorax, pneumothorax
o Paraneoplastic syndrome (SIADH) – tumors manufactures and secretes ADH
 Swelling
 Hyponatremia

Pathophysiology 1 (3 decks)

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