Respiratory Disorders Flashcards
(141 cards)
1
Q
What kind of infection is influenza? Where does it occur? When?
A
Acute viral. URT. Seasonally
2
Q
What types of influenza are there? Which is the most common?
A
A, B, C.
A
3
Q
How long is the incubation period for influenza?
A
1-4 days
4
Q
Who are most likely to contract influenza?
A
elderly, young, HC workers, chronically ill
5
Q
Patho of influenza?
A
viral injury to cells in URT = cells lyse = inflammatory tissue damage
6
Q
What will happen if influenza extends to the LRT?
A
bronchial and alveolar damage
7
Q
Complicating sofà influenza?
A
Pneumonia and bronchitis
8
Q
What can we do to prevent influenza prophylactically?
A
immunization
9
Q
Amantidine treats what? Does what? what gen?
A
ANTIVIRAL
influenza, prevents unraveling of DNA, 1st gen
10
Q
Relenza treats what? Does what? What gen/
A
ANTIVIRAL
influenza, inhibits replication of viral particles and prevents cell lysing, 2nd gen
11
Q
Why do we give Abx to those with influenza?
A
Given prophylactically to prevent a secondary bacterial infection in the respiratory tract
12
Q
Another name for pneumonia
A
Pneumonitis
13
Q
What kind of infection is pneumonia?
A
Nosocomial
14
Q
Where does the inflammation occur in pneumonia?
A
alveoli and bronchioles (terminal end)
15
Q
What is an example of atypical pneumonia? Where does the activity occur?
A
Viral etiology. Within the cells of the lung wall
16
Q
Example of typical pneumonia causes. Where does the activity occur
A
bacterial, toxic fumes. within the alveoli
17
Q
Example of non infectious pneumonia
A
inhalation of toxins, aspiration
18
Q
Pneumonia classified by what area of the lung affected is…
A
Lobar (one lobe)
Bronchopneumonia (diffuse)
19
Q
What does pulmonary edema result in
A
Increased diffusion distance = impaired gas exhange
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
21
Q
What 6 manifestations pneumonia
A
fever, chills, dyspnea, sputum (mucus + exudate), headache, chest pain
22
Q
What is inflamed in COPD?
A
airways, parenchyma, vasculature
23
Q
What 2 disorders are included in COPD? What does COPD often coexist with?
A
chronic bronchitis and emphysema. asthma
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
25
4 Et COPD
smoking, recurrent respiratory infections, genetic defect of alpha 1 antitrypsin gene, aging
26
What is chronic bronchitis?
inflammation and obstruction of airways, usually due to smoking/chronic inf
27
Where do changes happen first in chronic bronchitis? What are they? Second? What are they?
large airways
hypertrophy of submucosal glads = hyper secretion
smaller airways
hyperplasia of goblet cells
28
What is the normal inspiration to expiration ratio?
1:2 or less
29
Why is there prolonged expiration in chronic bronchitis?
Air flow to and from the lung is impeded so it takes a longer time to exhale the air within the lungs
30
Patho of chronic bronchitis
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
31
What happens in chronic bronchitis when the ventilation perfusion ratio is imbalanced?
Hypoxemia
32
Dx chronic bronchitis
productive cough for other 3 months per year in 2 consecutive years
33
Manifestations of chronic bronchitis and why
```
hypoxemia and hypercapnia due to impaired resp fx
activity intolerance ( less o2 = less ATP production)
sputum, dyspnea, wheezing, crackles, prolonged expiration
```
34
What is emphysema
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
35
Et emphysema
smoking, genetic defect of alpha 1 antitrypsin
36
What is the connection between alpha 1 antitrypsin and emphysema
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.
37
How does one get an alpha 1 antitrypsin problem?
smoking or inherited
38
How does smoking effect A1AT?
inhibits A1AT
39
What role does smoking play in emphysema's pathology?
smoking inhibits A1AT and attracts inflammatory cells, causing tissue damage. With increased proteases, alveolar walls are destroys, alveoli merge and surface area is lost.
40
How would one describe the airspaces in emphysema?
permanently distended
41
How does dead space develop in emphysema?
alveoli walls are damaged, so air moves out of alveoli and gets trapped between alveoli
42
What is dead space? An example of normal area this is?
area within respiratory tract when no gas exchange
trachea
43
Dead space in emphysema ultimately results in
impaired work of breathing
44
Why is there impaired perfusion in emphysema?
Capillary walls have been destroyed
45
Bullai? Blebs?
air trapped pushing against pleural membrane and form bubbles. blebs are smaller as above
46
Which accessory muscles are used in emphysema?
Trapezius, sternocleidomastoid
47
Why does a barrel chest occur? What diameter changes?
Increased WOB and use of accessory muscles in breathing. Traverse diameter gets closer to anterior posterior diameter and decreases
48
What other breathing manifestations would one see with emphysema?
Pursed lip breathing, nasal flaring, dyspnea
49
Centriacinar emphysema
Destruction in terminal and respiratory bronchioles
50
Panacinar emphysema
destruction of alveoli, terminal bronchioles, and respiratory bronchioles
51
How do we limit profession of emphysema
smoking cessation, avoid airway irritants
52
What are the staged based drug regimes for emphysema?
short acting beta agonists and anticholinergics (bronchodilators)
add inhaled steroids
inhaled steroid and long acting beta agents
theophylline (bronchodilator)
53
What bacteria causes TB
Mycobacterium tuberculosis
54
How can one get TB
drinking milk (Bowvine form) airborne, inhaled (human TB)
55
What happens when a person inhales TB for the first time?
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
56
What is the Ghon focus? What is in it?
The primary lesion in TB. Contains tubercle bacilli, immune cells and modified macrophages
57
When does the Ghon focus under go necrosis?
When the numbers of orangisms increases, and therefor the hypersensitivity reaction increases too
58
What forms the Ghon complex?
The primary lesion and granulomas
59
How can someone develop secondary TB?
inhalation of TB again, or reactivation of previously healed primary lesion... HS reaction begins
60
Manifestations of primary TB
night sweats, fever, weight loss, fatigue
61
Manifestations of secondary TB
low grade fever, night sweats, anorexia, dyspnea, orthopnea
62
What 2 screening tests are done for TB
skin test and CXR
63
What 2 diagnostic tests are done for TB and why they are done
culture from DNA for active TB
| Genotyping to identify strains
64
What tx for TB
drugs (INH, streptomycin, rifampin)
chemotherapy
BCG vaccine prophylaxis
65
What kind of infection is the common cold?
Viral infection of the URT
66
What 5 viruses can cause the common cold?
rhinovirus, parainfluenza virus, respiratory syncytial virus, coronavirus, adenovirus
67
How long is the incubation period for the common cold?
~5 days
68
How long does the common cold lasT?
7-10 days
69
Manifestations of common cold
dry/stuffy nasopharynx
excessive production of nasal and eye secretions
mucus membranes of URT red swollen and bathed in secretions
70
What 2 drugs and their effects for common cold
antihistamines dry up secretions and anticongestants construct blood vessels and decrease swelling
71
What is rhinosinusitis
inflammation of nasal passages and paranasal sinuses
72
What sinuses are involved in rhinusinusitis
frontal, ethmoid, maxillary
73
Patho rhinusinusitis
URTI obstructs ostia and impairs mucociliary clearance (nasal polyps can also obstruct)
changes in barometric pressure such as swimming or diving can effect
74
What kind of infection can rhinusinusitis be?
acute, subacute, or chronic
| bacterial, viral, or mixed
75
Complications of rhinusinusitis and where do they occur
INTRACRANIAL
related to infection of frontal/ethmoid sinuses
ORBITAL
edema of eyelids, orbital cellulitis, subperiosteal access, facial swelling, periorbital edema
76
Tx COPD pharmacologic stages
short acting beta agonist + anticholinergic
add inhaled steroid
long acting beta agonist + inhaled steroid
theophylline (bronchodilator)
77
What happens in acute phase asthmatic episode? (5)
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
Late phase asthmatic episode?
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
What receptors involved in bronchoconstriction/dilation in late phase asthmatic episode?
```
bronchoconstriction = alpha adrenergic receptors (epinephrine)
bronchodilation = beta adrenergic receptors
```
80
What is the inhalation challenge test and what does it aim to diagnose?
Tests responsiveness to potential allergens
| Asthma
81
Drug steps asthma
inhaled short action bronchodilators PRN
+ inhaled steroid
inhaled steroid + long acting bronchodilator
short course steroid PO + leukotriene receptor antagonist/theophylline
82
Is atelectasis reversible?
Yes if no damage
83
Obstructive/Resorptive Atelectasis
AW obstruction = air trapped, reabsorbed = local collapse
84
Compression Atelectasis
external pressure on lungs by e.g. tumor
85
Contraction Atelectasis
scar tissue contraction = lung collapse
86
Why tachypnea in atelectasis
Lung capacity decreased, so to increase air/min increase rate since depth cannot be increased
87
Pleural effusion is also known as
Hydrothorax
88
Where is the fluid accumulation in a pleural effusion
Pleural cavity
89
Exudative fluid in pleural effusion is
inflammatory fluid with high protein content
90
Transexudate fluid in pleural effusion is
non inflammatory fluid with low protein content
91
Empyema fluid in pleural effusion is
purulent
92
Hemothorax in pleural effusion is
blood
93
Chylothorax in pleural effusion is
lymph
94
Et pleural effusion (4)
CHF, infection, CA, pulmonary infarction (obstruction leads to congestion and fluid shift preceding ischemia and infarction)
95
Pathologically, what happens during a pleural effusion that allows the fluid to accumulate?
fluid entry into tissues > lymphatic drainage
96
Why does pleuritic pain occur in pleural effusion?
membranes stretched = pain
97
Why dyspnea in pleural effusion?
pressure in lungs against pressure of fluid against lungs
98
Tx pleural effusion
thoracentesis & fluid analysis, chest tube for continual drainage
99
Why are volume expanders not needed for pleural effusion?
Not necessary, pleural cavity not large
100
Where is the fluid accumulation in pulmonary edema?
Alveoli
101
What are the 2 main problems in pulmonary edema?
increased diffusion distance and loss of compliance
102
Embolism
Embolus
Thrombus
process
moving clot
clot within tissues
103
Where do PE arise from usually? which veins?
DVT. Popliteal, iliac, femoral
104
How could a fat emboli occur to cause a PE?
fractured bone (fat from bone marrow enters circulation)
105
What causes bronchial and pulmonary artery constriction during a PE? What does this lead to?
when platelets aggregate and degranulate they release mediators which cause bronchial and pulmonary artery constriction
Hemodynamic instability
106
Why does CO decrease during a PE?
LA not receiving blood from pulmonary circuit
107
Why would RSHF occur eventually in PE?
RV pumping harder to move blood into the pulmonary circuit
108
CP during PE is related to what?
ischemia
109
Why does atelectasis occur during PE?
loss of surfactant (no o2 to surfactant cells)
110
What is a specific serum marker in diagnosing a PE?
LDH3 (lactate dehydrogenase) = specific to lung tissue
111
How is a contrast lung scan done to diagnose a PE?
131 I-HSA (human serum albumin) marked with iodine 131 is given IV
112
What is the ultimate diagnostic for a PE?
pulmonary angiogram
113
Why is shock a possibility in PE?
decreased return to LA = decreased CO = risk for shock
114
What is pulmonary HTN? in mmHg?
sustained increase in pressure in pulmonary circuit
| >25 mmHg.
115
3 etiologic categories for pulmonary HTN?
| Examples of each?
increased pulmonary volume (cardiac septal defects)
hypoxemia (hypoxia in lung = vasoconstriction)
increased pulmonary venous pressure (LSHF)
116
What would one see on an XRAY if one had pulmonary HTN?
RV hypertrophy & distended pulmonary arteries
117
Why would syncope occur in pulmonary HTN?
Brain deprived of O2
118
Etiology for ARDS (5)
aspiration, inhalation of noxious fumes, septicaemia, fat embolism, DIC
119
What causes the pathologic increase in permeability in ARDS
Endothelial and alveolar damage from free radicals, phospholipids and proteases being released from NFs
120
Early/Late acid/base problems in ARDS
early: respiratory alkalosis
late: metabolic acidosis
121
Where do primary malignancies in the lung spread to?
Brain, bone, liver
122
4 major primary malignancies in Lung CA and their categories
NSCLC: adenocarcinoma, squamous cell carcinoma, large cell carcinoma
SCLC: small cell carcinoma
123
Et Lung CA
smoking, toxins (asbestos), genetic predisposition
124
Adenocarcinoma Lung CA
peripheral origin, common in females and non smokers
125
Squamous cell Lung CA (4)
central (hilum) origin, spreads to local hilar nodes, more common in men, can cause cardiac tamponade if on L side
126
Large cell carcinoma Lung CA
peripheral origin, large undifferentiated cells, early metastasis
127
Small cell carcinoma Lung CA
SMOKERS, early metastasis to brain, radiosensitive cells, non resectable, paraneoplastic syndromes (SIADH, Cushings)
128
Common presentation for all types of lung CA?
hemoptysis
129
How can a specimen for cytology be done for lung CA?
sputum collection
| bronchial wash to collect and analyze neoplastic cells
130
What systems are affected in cystic fibrosis?
GIT, Resp, reproductive
131
Main problem in cystic fibrosis?
defective Cl channel in cell membrane
132
Et cystic fibrosis
monogenic (CFTR gene on Chr 7: cystic fibrosis transmembrane regulator)
autosomal recessive
133
What does CFTR form?
Cl channels in epithelial cell membranes
134
Why are Na/H20 reabsorbed after being secreted as part of exocrine secretions?
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
2 problems associated with cystic fibrosis within the respiratory tract?
recurrent bacterial infections & decreased respiratory function
136
What does the sweat test for cystic fibrosis measure?
Na, Cl
137
Why is trypsinogen tested in new borns with CF?
pancreatic secretions obstructed
138
Why is DNAase used in CF? What does it ultimately do?
breaks down DNA strands within the mucus (released when cells were damaged and lysed)
Decreases stickiness of mucus
139
What Tx is available for CF?
control infections with gamma globulins
DNAase
diet modification
pancreatic enzyme supplements
140
What 2 ABG changes would one see in respiratory failure? Levels? What do they indicate?
hypoxemia (Pa02 45)
| = respiratory acidosis
141
Et respiratory failure (7)
COPD, pneumonia, atelectasis, Guillain-Barre, pulmonary edema, ARDS
