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Patho 2nd Semester > Respiratory Disorders > Flashcards

Respiratory Disorders Flashcards

1
Q

What kind of infection is influenza? Where does it occur? When?

A

Acute viral. URT. Seasonally

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2
Q

What types of influenza are there? Which is the most common?

A

A, B, C.

A

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3
Q

How long is the incubation period for influenza?

A

1-4 days

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4
Q

Who are most likely to contract influenza?

A

elderly, young, HC workers, chronically ill

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5
Q

Patho of influenza?

A

viral injury to cells in URT = cells lyse = inflammatory tissue damage

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6
Q

What will happen if influenza extends to the LRT?

A

bronchial and alveolar damage

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7
Q

Complicating sofà influenza?

A

Pneumonia and bronchitis

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8
Q

What can we do to prevent influenza prophylactically?

A

immunization

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9
Q

Amantidine treats what? Does what? what gen?

A

ANTIVIRAL

influenza, prevents unraveling of DNA, 1st gen

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10
Q

Relenza treats what? Does what? What gen/

A

ANTIVIRAL

influenza, inhibits replication of viral particles and prevents cell lysing, 2nd gen

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11
Q

Why do we give Abx to those with influenza?

A

Given prophylactically to prevent a secondary bacterial infection in the respiratory tract

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12
Q

Another name for pneumonia

A

Pneumonitis

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13
Q

What kind of infection is pneumonia?

A

Nosocomial

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14
Q

Where does the inflammation occur in pneumonia?

A

alveoli and bronchioles (terminal end)

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15
Q

What is an example of atypical pneumonia? Where does the activity occur?

A

Viral etiology. Within the cells of the lung wall

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16
Q

Example of typical pneumonia causes. Where does the activity occur

A

bacterial, toxic fumes. within the alveoli

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17
Q

Example of non infectious pneumonia

A

inhalation of toxins, aspiration

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18
Q

Pneumonia classified by what area of the lung affected is…

A

Lobar (one lobe)

Bronchopneumonia (diffuse)

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19
Q

What does pulmonary edema result in

A

Increased diffusion distance = impaired gas exhange

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20
Q

Patho pneumonia

A

impaired pulmonary defenses, so agent enters resp tract and gets into the lungs. there the agent causes inflammatory and tissue damage, leading to pulmonary edema (as exudate) leading to impaired gas exchange

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21
Q

What 6 manifestations pneumonia

A

fever, chills, dyspnea, sputum (mucus + exudate), headache, chest pain

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22
Q

What is inflamed in COPD?

A

airways, parenchyma, vasculature

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23
Q

What 2 disorders are included in COPD? What does COPD often coexist with?

A

chronic bronchitis and emphysema. asthma

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24
Q

Why is smoking an etiologic factor for COPD?

A

smoking contains irritants which increase mucus sections, induces coughing, and leads to inflammatory tissue damage of alveoli and BVs

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25
Q

4 Et COPD

A

smoking, recurrent respiratory infections, genetic defect of alpha 1 antitrypsin gene, aging

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26
Q

What is chronic bronchitis?

A

inflammation and obstruction of airways, usually due to smoking/chronic inf

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27
Q

Where do changes happen first in chronic bronchitis? What are they? Second? What are they?

A

large airways
hypertrophy of submucosal glads = hyper secretion
smaller airways
hyperplasia of goblet cells

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28
Q

What is the normal inspiration to expiration ratio?

A

1:2 or less

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29
Q

Why is there prolonged expiration in chronic bronchitis?

A

Air flow to and from the lung is impeded so it takes a longer time to exhale the air within the lungs

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30
Q

Patho of chronic bronchitis

A

excess mucus due to adaptive changes = mucociliary defenses are impacted. this allows infection to occur = inflammation = obstruction = AW collapse due to air being trapped in parts of lung

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31
Q

What happens in chronic bronchitis when the ventilation perfusion ratio is imbalanced?

A

Hypoxemia

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32
Q

Dx chronic bronchitis

A

productive cough for other 3 months per year in 2 consecutive years

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33
Q

Manifestations of chronic bronchitis and why

A 
hypoxemia and hypercapnia due to impaired resp fx
activity intolerance ( less o2 = less ATP production)
sputum, dyspnea, wheezing, crackles, prolonged expiration
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34
Q

What is emphysema

A

destruction of alveolar tissue and capillary beds

loss of compliance due to loss of elastic tissue

enlarged distal air spaces due to damage = loss of surface area

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35
Q

Et emphysema

A

smoking, genetic defect of alpha 1 antitrypsin

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36
Q

What is the connection between alpha 1 antitrypsin and emphysema

A

a1 AT inhibits proteases and elastases which break protein (tissue) in the lung down. Without the gene that codes for this protein, these enzymes cannot be regulated and tissue will be broken down in the lungs.

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37
Q

How does one get an alpha 1 antitrypsin problem?

A

smoking or inherited

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38
Q

How does smoking effect A1AT?

A

inhibits A1AT

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39
Q

What role does smoking play in emphysema’s pathology?

A

smoking inhibits A1AT and attracts inflammatory cells, causing tissue damage. With increased proteases, alveolar walls are destroys, alveoli merge and surface area is lost.

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40
Q

How would one describe the airspaces in emphysema?

A

permanently distended

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41
Q

How does dead space develop in emphysema?

A

alveoli walls are damaged, so air moves out of alveoli and gets trapped between alveoli

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42
Q

What is dead space? An example of normal area this is?

A

area within respiratory tract when no gas exchange

trachea

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43
Q

Dead space in emphysema ultimately results in

A

impaired work of breathing

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44
Q

Why is there impaired perfusion in emphysema?

A

Capillary walls have been destroyed

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45
Q

Bullai? Blebs?

A

air trapped pushing against pleural membrane and form bubbles. blebs are smaller as above

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46
Q

Which accessory muscles are used in emphysema?

A

Trapezius, sternocleidomastoid

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47
Q

Why does a barrel chest occur? What diameter changes?

A

Increased WOB and use of accessory muscles in breathing. Traverse diameter gets closer to anterior posterior diameter and decreases

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48
Q

What other breathing manifestations would one see with emphysema?

A

Pursed lip breathing, nasal flaring, dyspnea

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49
Q

Centriacinar emphysema

A

Destruction in terminal and respiratory bronchioles

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50
Q

Panacinar emphysema

A

destruction of alveoli, terminal bronchioles, and respiratory bronchioles

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51
Q

How do we limit profession of emphysema

A

smoking cessation, avoid airway irritants

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52
Q

What are the staged based drug regimes for emphysema?

A

short acting beta agonists and anticholinergics (bronchodilators)

add inhaled steroids

inhaled steroid and long acting beta agents

theophylline (bronchodilator)

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53
Q

What bacteria causes TB

A

Mycobacterium tuberculosis

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54
Q

How can one get TB

A

drinking milk (Bowvine form) airborne, inhaled (human TB)

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55
Q

What happens when a person inhales TB for the first time?

A

TB => alveoli
macrophages engulf TB but cannot kill, bring to T cells, T cells stimulates MFs to increase their concentration of lytic enzymes
++ lytic enzymes => destruction of surrounding lung tissue

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56
Q

What is the Ghon focus? What is in it?

A

The primary lesion in TB. Contains tubercle bacilli, immune cells and modified macrophages

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57
Q

When does the Ghon focus under go necrosis?

A

When the numbers of orangisms increases, and therefor the hypersensitivity reaction increases too

58
Q

What forms the Ghon complex?

A

The primary lesion and granulomas

59
Q

How can someone develop secondary TB?

A

inhalation of TB again, or reactivation of previously healed primary lesion… HS reaction begins

60
Q

Manifestations of primary TB

A

night sweats, fever, weight loss, fatigue

61
Q

Manifestations of secondary TB

A

low grade fever, night sweats, anorexia, dyspnea, orthopnea

62
Q

What 2 screening tests are done for TB

A

skin test and CXR

63
Q

What 2 diagnostic tests are done for TB and why they are done

A

culture from DNA for active TB

Genotyping to identify strains

64
Q

What tx for TB

A

drugs (INH, streptomycin, rifampin)
chemotherapy
BCG vaccine prophylaxis

65
Q

What kind of infection is the common cold?

A

Viral infection of the URT

66
Q

What 5 viruses can cause the common cold?

A

rhinovirus, parainfluenza virus, respiratory syncytial virus, coronavirus, adenovirus

67
Q

How long is the incubation period for the common cold?

A

~5 days

68
Q

How long does the common cold lasT?

A

7-10 days

69
Q

Manifestations of common cold

A

dry/stuffy nasopharynx
excessive production of nasal and eye secretions
mucus membranes of URT red swollen and bathed in secretions

70
Q

What 2 drugs and their effects for common cold

A

antihistamines dry up secretions and anticongestants construct blood vessels and decrease swelling

71
Q

What is rhinosinusitis

A

inflammation of nasal passages and paranasal sinuses

72
Q

What sinuses are involved in rhinusinusitis

A

frontal, ethmoid, maxillary

73
Q

Patho rhinusinusitis

A

URTI obstructs ostia and impairs mucociliary clearance (nasal polyps can also obstruct)

changes in barometric pressure such as swimming or diving can effect

74
Q

What kind of infection can rhinusinusitis be?

A

acute, subacute, or chronic

bacterial, viral, or mixed

75
Q

Complications of rhinusinusitis and where do they occur

A

INTRACRANIAL
related to infection of frontal/ethmoid sinuses

ORBITAL
edema of eyelids, orbital cellulitis, subperiosteal access, facial swelling, periorbital edema

76
Q

Tx COPD pharmacologic stages

A

short acting beta agonist + anticholinergic
add inhaled steroid
long acting beta agonist + inhaled steroid
theophylline (bronchodilator)

77
Q

What happens in acute phase asthmatic episode? (5)

A

allergen + IgE = degranulation mast cell, mediators released= inflammation
intracellular junctions open, allergens enter submucosa and bind to mast cells there
increased perm + muc sec = edema
PNS = bronchospasm
AW constriction

78
Q

Late phase asthmatic episode?

A

new trigger (eg. cold air) attracts NFs, Bfs, Eos = epithelial damage, edema, changes in mucociliary fx, decreased clearance of resp tract secretions and increased AW responsiveness

79
Q

What receptors involved in bronchoconstriction/dilation in late phase asthmatic episode?

A 
bronchoconstriction = alpha adrenergic receptors (epinephrine)
bronchodilation = beta adrenergic receptors
80
Q

What is the inhalation challenge test and what does it aim to diagnose?

A

Tests responsiveness to potential allergens

Asthma

81
Q

Drug steps asthma

A

inhaled short action bronchodilators PRN
+ inhaled steroid
inhaled steroid + long acting bronchodilator
short course steroid PO + leukotriene receptor antagonist/theophylline

82
Q

Is atelectasis reversible?

A

Yes if no damage

83
Q

Obstructive/Resorptive Atelectasis

A

AW obstruction = air trapped, reabsorbed = local collapse

84
Q

Compression Atelectasis

A

external pressure on lungs by e.g. tumor

85
Q

Contraction Atelectasis

A

scar tissue contraction = lung collapse

86
Q

Why tachypnea in atelectasis

A

Lung capacity decreased, so to increase air/min increase rate since depth cannot be increased

87
Q

Pleural effusion is also known as

A

Hydrothorax

88
Q

Where is the fluid accumulation in a pleural effusion

A

Pleural cavity

89
Q

Exudative fluid in pleural effusion is

A

inflammatory fluid with high protein content

90
Q

Transexudate fluid in pleural effusion is

A

non inflammatory fluid with low protein content

91
Q

Empyema fluid in pleural effusion is

A

purulent

92
Q

Hemothorax in pleural effusion is

A

blood

93
Q

Chylothorax in pleural effusion is

A

lymph

94
Q

Et pleural effusion (4)

A

CHF, infection, CA, pulmonary infarction (obstruction leads to congestion and fluid shift preceding ischemia and infarction)

95
Q

Pathologically, what happens during a pleural effusion that allows the fluid to accumulate?

A

fluid entry into tissues > lymphatic drainage

96
Q

Why does pleuritic pain occur in pleural effusion?

A

membranes stretched = pain

97
Q

Why dyspnea in pleural effusion?

A

pressure in lungs against pressure of fluid against lungs

98
Q

Tx pleural effusion

A

thoracentesis & fluid analysis, chest tube for continual drainage

99
Q

Why are volume expanders not needed for pleural effusion?

A

Not necessary, pleural cavity not large

100
Q

Where is the fluid accumulation in pulmonary edema?

A

Alveoli

101
Q

What are the 2 main problems in pulmonary edema?

A

increased diffusion distance and loss of compliance

102
Q

Embolism
Embolus
Thrombus

A

process
moving clot
clot within tissues

103
Q

Where do PE arise from usually? which veins?

A

DVT. Popliteal, iliac, femoral

104
Q

How could a fat emboli occur to cause a PE?

A

fractured bone (fat from bone marrow enters circulation)

105
Q

What causes bronchial and pulmonary artery constriction during a PE? What does this lead to?

A

when platelets aggregate and degranulate they release mediators which cause bronchial and pulmonary artery constriction

Hemodynamic instability

106
Q

Why does CO decrease during a PE?

A

LA not receiving blood from pulmonary circuit

107
Q

Why would RSHF occur eventually in PE?

A

RV pumping harder to move blood into the pulmonary circuit

108
Q

CP during PE is related to what?

A

ischemia

109
Q

Why does atelectasis occur during PE?

A

loss of surfactant (no o2 to surfactant cells)

110
Q

What is a specific serum marker in diagnosing a PE?

A

LDH3 (lactate dehydrogenase) = specific to lung tissue

111
Q

How is a contrast lung scan done to diagnose a PE?

A

131 I-HSA (human serum albumin) marked with iodine 131 is given IV

112
Q

What is the ultimate diagnostic for a PE?

A

pulmonary angiogram

113
Q

Why is shock a possibility in PE?

A

decreased return to LA = decreased CO = risk for shock

114
Q

What is pulmonary HTN? in mmHg?

A

sustained increase in pressure in pulmonary circuit

>25 mmHg.

115
Q

3 etiologic categories for pulmonary HTN?

Examples of each?

A

increased pulmonary volume (cardiac septal defects)
hypoxemia (hypoxia in lung = vasoconstriction)
increased pulmonary venous pressure (LSHF)

116
Q

What would one see on an XRAY if one had pulmonary HTN?

A

RV hypertrophy & distended pulmonary arteries

117
Q

Why would syncope occur in pulmonary HTN?

A

Brain deprived of O2

118
Q

Etiology for ARDS (5)

A

aspiration, inhalation of noxious fumes, septicaemia, fat embolism, DIC

119
Q

What causes the pathologic increase in permeability in ARDS

A

Endothelial and alveolar damage from free radicals, phospholipids and proteases being released from NFs

120
Q

Early/Late acid/base problems in ARDS

A

early: respiratory alkalosis
late: metabolic acidosis

121
Q

Where do primary malignancies in the lung spread to?

A

Brain, bone, liver

122
Q

4 major primary malignancies in Lung CA and their categories

A

NSCLC: adenocarcinoma, squamous cell carcinoma, large cell carcinoma
SCLC: small cell carcinoma

123
Q

Et Lung CA

A

smoking, toxins (asbestos), genetic predisposition

124
Q

Adenocarcinoma Lung CA

A

peripheral origin, common in females and non smokers

125
Q

Squamous cell Lung CA (4)

A

central (hilum) origin, spreads to local hilar nodes, more common in men, can cause cardiac tamponade if on L side

126
Q

Large cell carcinoma Lung CA

A

peripheral origin, large undifferentiated cells, early metastasis

127
Q

Small cell carcinoma Lung CA

A

SMOKERS, early metastasis to brain, radiosensitive cells, non resectable, paraneoplastic syndromes (SIADH, Cushings)

128
Q

Common presentation for all types of lung CA?

A

hemoptysis

129
Q

How can a specimen for cytology be done for lung CA?

A

sputum collection

bronchial wash to collect and analyze neoplastic cells

130
Q

What systems are affected in cystic fibrosis?

A

GIT, Resp, reproductive

131
Q

Main problem in cystic fibrosis?

A

defective Cl channel in cell membrane

132
Q

Et cystic fibrosis

A

monogenic (CFTR gene on Chr 7: cystic fibrosis transmembrane regulator)
autosomal recessive

133
Q

What does CFTR form?

A

Cl channels in epithelial cell membranes

134
Q

Why are Na/H20 reabsorbed after being secreted as part of exocrine secretions?

A

Cl cannot be secreted with them, so there is a high concentration of Cl within the cell, which draws H20 and therefor Na back into the cell

135
Q

2 problems associated with cystic fibrosis within the respiratory tract?

A

recurrent bacterial infections & decreased respiratory function

136
Q

What does the sweat test for cystic fibrosis measure?

A

Na, Cl

137
Q

Why is trypsinogen tested in new borns with CF?

A

pancreatic secretions obstructed

138
Q

Why is DNAase used in CF? What does it ultimately do?

A

breaks down DNA strands within the mucus (released when cells were damaged and lysed)

Decreases stickiness of mucus

139
Q

What Tx is available for CF?

A

control infections with gamma globulins
DNAase
diet modification
pancreatic enzyme supplements

140
Q

What 2 ABG changes would one see in respiratory failure? Levels? What do they indicate?

A

hypoxemia (Pa02 45)

= respiratory acidosis

141
Q

Et respiratory failure (7)

A

COPD, pneumonia, atelectasis, Guillain-Barre, pulmonary edema, ARDS

Patho 2nd Semester (6 decks)

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