Pulm Patho Flashcards
1
Q
dyspnea
A
difficult of painful breathing
2
Q
orthopena
A
easier breathing while up right, difficult lying down. (usually a sign of pulm edema or pulm effusion)
3
Q
parxoysmal nocturnal dyspnea
A
attacks of SOB at night
4
Q
kussmaul resp
A
rapid deep breaths (running to class); blowing out CO2, if doing this at rest- compensation for metabolic acidosis (often ketoacidosis)
5
Q
Cheyne-Stokes resp
A
sign that patient is going to die; brain stem damage (NTS not working properly) O2 plummets during apnea, O2 detector sends alarm message to NTS resulting in fast, deep rapid breaths, alarm turns off, apnea, rapid respirations, apnea, etc. (alternating apnea and tachypnea)
6
Q
hypoventilation
A
hypercapnia-high PaCO2–respiratory acidosis
7
Q
hyperventilation
A
hypocapnia–low PaCO2–resp alkalosis
8
Q
hypoxemia
A
low O2 tension
low O2 sat
9
Q
Hypoxia
A
low O2 content one cause is hypoxemia, another is anemia
10
Q
clubbing
A
enlargement of the distal ends of fingers due to chronic hypoxemia
11
Q
hemoptysis
A
coughing up blood
12
Q
pain with breathing
A
usually pleuritic causing rubbing of visceral and parietal pleura
13
Q
acute resp failure
A
inadequate gas exchange
ex: dive into pool and can’t swim
14
Q
pulm edema
most common, most acute
A
excess fluid in interstitium or alveoli
- most common: increased vascular pressure ex: 2nd to heart failure: Increased pulmonary venous pressure due to left-sided heart problem → edema
- most acute: increase permeablility ex: injury to capillary endothelia cells ex: ARDS: Injury to capillary endothelium → inflammation → increased vascular permeability → water gets into lumen of alveoli due to vascular permeability → Fluid (water) not good substitute for surfactant → some alveoli hyperventilate, some collapse
15
Q
Atelectasis
A
collapse of lung tissue (failure to ventilate alveoli)
Compression-compression of alveoli but something heavy
Absorption-obstructed airway and gas absorption alveoli shrivel up.
16
Q
Bronchiectasis
A
chronic abnormal dilation of bronchi
17
Q
Bronchiolitis
A
inflamm obstruction of bronchioles
18
Q
Pneumothorax 4
A
gas in the pleural space
- open pneumothorax: rib wants to go out, lungs want to go in; stick knife or syringe into patient so that gas can fill vacuum, chest will go up, lungs will go down and air will fill in the middle
- tension: as we are expanding lung, as we inhale more gas into area, exhalation can’t get it out: pneumothorax increases with each inhalation
- spontaneous: idiopathic
- secondary pneumothorax: caused by other lung problem
19
Q
Pleural effusion 5 types
A
fluid in pleural space
1 Transudative – low protein content (usually systemic problem, e.g. heart failure) pressure problem
2 Exudative – high protein content (usually local inflammation) permeability problem ex: CA or infection
3. Hemothorax – blood in pleural space
4. Chylothorax – lymph in pleural space
5. Empyema – pus in pleural space: results in orthopnea; if standing, fluid accumulates at bottom
20
Q
mechanical problems with chest wall
A
chest wall restriction- impairs breathing
flail chest- fractured ribs interfere with normal ventilation
21
Q
Restrictive lung disease
A
Loss of compliance: difficulty opening up lungs → difficulty getting air IN
Decreased FVC
1Acute intrinsic: (pulm edema) ARDS
2Chronic intrinsic: (diseased lung parenchyma) pulm fibrosis
3Chronic extrinsic: 9chest wall, intra-bad and neuromuscular disease) spinal cord damage
4Disorders of Pleura and Mediastinum
PNA
Many!
Fibroblasts lay down collagen, thicker membrane impairs gas exchange and makes lung less compliant although maintains good recoil
22
Q
Obstructive lung disease
A
Difficulty getting air OUT loss of recoil or obstruction of airways; decreased FRV1/FRC, decreased FEV1: amount of air getting out quickly is highly decreased Asthma COPD -dyspnea and wheezing
23
Q
Resp tract infection
A
PNA-6th most common cause of death in US
bacterial (most common ex: strep) and viral
TB
Acute bronchitis
Abscess formation in cavitation- often result of PNA
24
Q
Cystic fibrosis
A
genetic
25
pulm vascular disease
pulm embolism
pulm HTN
Cor pulmonale: right-sided heart failure due to lung problem
26
Lung CA
Non-small cell lung cancer: Squamous cell carcinoma, Adenocarcinoma, Large cell carcinoma,
Small cell carcinoma
27
Asthma
Triggered by allergen or irritant exposure → immune activation/mast cell degranulation
want to get irritant out of lung so you want conductive airways to get smaller to help, but in asthma, this is over-reactive,
*airways over-constrict → bronchoconstriction/spasm + immune mediated damage to airways → asthma
Tx: Epinephrine: vasodilator,
S/S: recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and in the early morning.
28
What is the strongest identifiable predisposing factor for developing asthma
Atopy- the genetic predisposition for the development of an IgE- mediated response to common aeroallergens.
29
COPD: simple answer
Chronic Obstructive Pulmonary Disease
Combination of chronic bronchitis and emphysema
Both cause obstructive pulmonary disease
30
Chronic Bronchitis
inflamed and mucus-filled bronchi
large airway: trachea, bronchi: have mucus hypersecretion, inflammation
sm airways: peribronchiolar fibrosis
airway obstruction
*chronic infection
chronic productive cough, last for at lease 3 months of the year for at least 2 years
mucus is thicker
31
Emphysema
walls between alveoli are damaged and alveoli blow up to big balloons instead of clusters of little balloons which causes loss of surface area for gas exchange,
lung loses recoil elasticity because elasticity came from septa between alveoli
lose recoil so can't get air out, need to increase intrathoracic pressure to exhale
**Loss of Elastic Recoil
-centriacinar
-Panacinar
32
COPD risk factors
```
Cigarette smoking
Passive smoking?
Ambient air pollution?
Hyper-responsive airways ?
Occupational factors?
Alpha1-antitrypsin deficiency: Only known genetic abnormality that leads to COPD < 1% of cases
```
33
Characteristic Changes in Restrictive Lung Disease
(Normal VC is >70ml/kg.)
All lung volumes have decreased (total lung capacity, RV, VC, RVC)
Lost compliance: Harder to get in air, but easy to get air out once you get it in
FEV1 decreased because lung is smaller
Normal:
Expiratory flow rates
ratio of FEV1/FVC is normal
34
Inherited a-1 antitrypsin deficiency
basically break down elastin too fast lose recoil
Antitrypsin -trypsin-elastate-elastin
elastase and elastin need to be the same amt., make and break down--want elastin to be fresh so constantly replace.
Trypisn breaks down elastase, if don't have enough then elastase breaks down elastin too fast.
Antitrypsin breaks down trypsin so don't have enough with this inherited deficiency then don't break down trypsin.....rats i hate rats they drive me crazy...
35
Absorption Atelectasis
caused by lack of collateral ventilation through pores of Kohn
-plugged alveoli can be ventilated still with deep breathing...opens pores of Kohn
36
Restrictive disease
inspiration is limited-reduced compliance of lung or chest wall= stiff lungs
reduction in lung compliance= increased WOB, Dyspnea
Rapid, shallow breathing pattern= increased dead space ventilation
*normal gas exchange
until advanced disease-increased PaCO2, decreased PaO2 with pulm HTN and Cor pulmonale
37
Pulm edema
Fluid leakage from the intravascular space into the lung interstitium and alveoli caused by:
1 Increased capillary/hydrostatic pressure: (example: cardiogenic, valcular dysfunction, coronary artery disease, LV dysfunction-- lead to increased L atrial press--increase pulm capillary hydrostatic press
2 Increased capillary permeability: endothelium--increased capillary permeability and disruption of surfactant production--mvmt of fluid and plasma proteins from capillary to interstitial space and alveoli
*both CXR will show bilateral symmetrical opacities
38
Acute resp distress syndrome ARDS
Diffuse pulmonary endothelial injury
H2O, solutes, and macromolecules diffuse from intravascular space/capillaries into lung parenchyma and alveoli
Atelectasis: because of obstruction or decreased surfactant Harder to get air into lungs due to lack of surfactant
Loss of surfactant causing gas exchange to decrease; Greater impairment of O2 transport than CO2 transport; even if you give them O2 you don’t raise their O2 sat (unresponsive hypoxemia)
Sepsis often co-exists producing further lung injury via inflammatory mediators
Often ARDS signals the beginning of multiple organ system failure
39
ARDS flow chart
acure insult--release of cytokines--influx of inflamm cells to lung--release of ROS and cytomkines/ activation of complement system: all leads to:
- damage to type II pneumocytes--atelectosis, and decrease lung compliance
- disruption of alveolar-cap membrane--noncardiogenic pulm edema
- microthrombi in pulm circulation--pulm HTN
- release of fibroblast--pulm fibrosis
40
Aspiration Pneumonitis
Acidic gastric secretions destroy surfactant-producing cells & damage the pulmonary capillary endothelium
increased permeability pulmonary edema with atelectasis
s/s:Hypoxia,
Tachypnea
Bronchospasm
Pulmonary vascular constriction can develop into pulmonary HTN CXR changes 6-12 hrs later – usually right lower lobe
41
Tx of Aspiration Pneumonitis
#1 treatment is delivery of increased FiO2
PEEP
B-2 agonists for bronchospasm
+/- lavage of 5ml NS
Fiberoptic bronchoscopy – if suspected solid material aspirated
Abx, steroids?
42
Cardiogenic pulm edema
Left ventricular failure with increased pulmonary vascular hydrostatic pressures
Signs of SNS activation usually more dramatic than with increased capillary permeability edema (transudate, no protein bc problem with pressure.)
s/s:
Extreme dyspnea Tachypnea Hypertension Tachycardia Diaphoresis
43
Neurogenic Pulm edema
Occurs minutes to hours following an acute brain injury (medulla (part of resp center, especially)
Secondary to massive SNS discharge in response to CNS insult
Generalized vasoconstriction with shift large blood volume into pulmonary vessels = vessel injury and transudation of fluid into lung parenchyma/alveoli
Tx: supportive, control ICPs, increased FiO2, Positive press vent, PEEP
diuretics not indicated
resolution of edema occurs within a few days
44
drug induced pulm
Herion- high permeability type
Cocaine- pulm vasoconstriction and or MI can result in pulm edema
Tx: supportive
45
High altitude pulm edema
intense hypoxic pulm vasoconstriction after 48-96hrs at 2500-5000m altitude (rapid ascent)
increased pulm vascular pressure result in high permeability pulm edema
treated with O2, prompt descent from altitude, and inhaled NO
46
Re-expansion pulm edema
transudate ?
enhance capillary membrane permeability
occasionally follows evacuation of pneumothorax or pleural effusion.
more common in >1L taken out of pleural space and >24hr duration of collapse, and if re-expansion occurs rapidly
supportive tx NO diuretics
47
Negative-pressure pulm edema, when does it occur and due to what
occurs min to 2-3hrs after acute upper airway obstruction in a spont breathing pt. Due to:
*post-extubation laryngospasm
*Obstructive sleep apnea
epiglottitis
tumors
obesity
hiccups
*the attempt in inspiration against occlusion creates excessive intrathoracic Neg pressure causes: increased venous return and increased afterload. Leads to :
increased pulm blood volume and increased venous pressure.
48
Negative-pressure pulm edema
| patho
development related to generation of highly negative intraplueural pressures agains a closed glottis/upper airway
1. Decreased interstitial hydrostatic pressure
2. increased venous return
3. increased afterload on L ventricle
4. Increased SNS outflow- HTN, central pooling
5. Hypoxemia with further SNS activation
Tachypnea, cough, failure to maintain SaO2 >95%
Usually self-limited 12-24hrs duration
Treat with supplemental O2, maintenance of airway and if necessary mechanical ventilation
49
Chronic Intrinsic Restrictive Lung Disease: Overview
Pulm HTN and Cor pulmonate are likely to happen as a result of progressive fibrosis= loss of pulm vasculature
Pneumothoracies are common with advanced disease
dyspnea prominent- rapid and shallow breathing, breathing doesn't move much
decreased compliance
compression of pulm capillary so R heart has to work harder
50
Sarcoidosis where, patho
systematic granulomatous disorder, often found in thoracic lymph nodes and lungs
Cor pulmonale and pulm HTN likely
decreased alveolar diffusion capacity
Laryngeal sarcoid 1-5% of patients- can interfere with passage of ETT
Myocardial sarcoid rare (heart blood, dysrhythmias, restrictive cardiomyopathy)
liver spleen, optic, and facial nerve often involved,
51
Sarcoidosis diagnosis
pt often present for mediastinoscopy for diagnosis
watch fo hypocalciema
pt many need a stress dose of steroids peri-op often on chronic corticosteroids for tx
(slide has dose stuff)
52
Hypersensitivity pneumonitis
Chronic intrinsic restrictive lung disease
something with protein- something that was alive and get immune system to react
diffuse interstitial granulomatous reactions in the lungs after inhalation of dust containing fungi, spores, or animal/vegetable material.
Bird fancier’s lung, farmer’s lung, etc.
53
Pneumoconiosis
Chronic intrinsic restrictive lung disease
non-protein, NO B and T cell response
Silicosis, coal worker pneumoconiosis (e.g. black lung),
asbestosis
54
other chronic intrinsic restrictive lung disease
- Eosinophilic Granuloma-pulmonary fibrosis is common.
- Pulmonary Alveolar Proteinosis-unknown cause, deposition of lipid-rich proteinaceous material in the alveoli.
- Lymphangiomyomatosis- proliferation of smooth muscle in the abdominal and thoracic lymphatics, veins, and bronchioles.
- Idiopathic pulmonary interstitial fibrosis
55
inhalation disorders
exposure to toxic gases
| pneumconiosis: silicosis, coal worker pneumoconiosis (coal workers, black lung), asbestosis
56
hypersensitivity pneumonitis
bird fancier lungs-bird feather and droppings
| farmers lungs- moldy hey
57
patho of chronic restrictive lung disease
in haled agent, dust, blood-borne toxins, unknown antigens
activated macrophage leads to
*recruitment of neutrophils
*oxidants proteases--injury to type 1 pneumocytes
*fibrogenic and chemotactic cytokines--fibroblast
fibrogenic and chemotactic cytokines also from hypertrophy and hyperplasia of type 2 pneumocytes also cause fibroblast
58
chronic extrinsic restrictive lung disease
thoracic cage abnormalities
interference with lung expansion
compressed lung result in increased WOB:
1. decreased lung volumes with corresponding increase in airway resistance
2. abnormal chest wall mechanics
with thoracic deformity: right ventricular dysfunction common with chronic compression of pulmonary vasculature, can also compress heart
impaired cough= chronic infection, development of obstructive component
59
obesity
diaphragm and chest wall movement restricted by excessive weight/abdominal panicles
dyspnea especially with exercise- increased resistance to breathing and increased work to move excess weight
FRC decreased with V/Q mismatch
Supine position exacerbates
60
costovertebral skeletal structure deformities
Scoliosis: lateral curvature with rotation of the vertebral column
Kyphosis: anterior flexion of vertebral column
60 degrees-dyspnea with exercise
100 degrees- alveolar hypoventilaiton, decreased PaO2, erthrocytosis, pulm HTN, cor pulmonale
110 degree, VC<45%, resp failure
**de careful with CNS depressants- increased risk of hypoventilation and pneumonia
61
deformities of the sternum
pectus excavatum- inward concavity of sternum
pectus carinatum -outward protuberance of sternum
*somet pts asymptomatic, others require surgical correction to reduce pulm restriction and resultant cardiovascular dysfunction
62
flail chest
2nd to rib fx/sternotomy dehiscence- paradoxical inward mvmt of the unstable portion of the thoracic cafe during inspiration
lung increased volume durning exhalation and decreases volume during inhalation
decreased PaO2 and increased Pa CO2 2nd to alveolar hypoventilation
positive pressure ventilation required until thoracic cage stabilization occurs
63
Neuromuscular disorders patho
spinal cord, peripheral nerve, neuromuscular junction or skeletal muscle pathology that prevents the generation of normal resp pressures
impairment of effective cough generation, retained secretions, pneumonia, and resp failure may result
very sensitive to CNS depressants
Vital Capacity useful to measure extent of impact of disease on ventilation,
*still have phrenic nerve (3,4,5) of diaphragm works
same with CN11 for sternochiedomastoid
64
Neuromuscular disorders
| names
```
Diaphragmatic paralysis
Spinal cord transection C4
Guillian-Barre syndrome
Myasthenia gravis
Myasthenic syndrome
Muscular dystrophy
```
65
disorders of the pleura and mediastinum
mechanical changes interfere with effective lung expansion
66
pleural abnormalities
| penuomthorax
Open pneumothorax- hole from rib side
Tension pneumothorax-- air from damaged lung side, as breathe gets bigger
Spontaneous pneumothorax
Secondary pneumothorax- some other lung problem
67
idiopathic pneumothorax
Gas in the pleural space secondary to a defect in the parietal or visceral pleura
68
Tension pneumo
medical emergency when air enters the pleural space during inspiration and is not allowed to exit on expiration – common after rib fracture or barotrauma – symptoms more sudden and severe
69
pneumo s/s
```
acute dyspnea
ipsilateral chest pain
decreased PaO2 increased PaCO2
hypotension and tachycardia
decreased chest wall movement
decreased/absent breath sounds
hyperresonant percussion
decreased CO bc increased pulm vascular resistance
```
70
pneumothorax
catheter aspiration or chest tube
life saving tx of tension pneuma- small bro plastic starter into 2nd anterior intercostal space
Increased fiO2 improves the rate of air resorption by pleura 4X
-tissue wants O2 pressure gradient, then tissue keeps using so gradient continues in favor.
71
disorders of the pleura and mediastinum
pleural fibrosis: pleurodesis-pleural stuck together
pleural effusion
for recurrent effusion, stick them together by using talcum powder "gravel" causes inflame and scare tissue then stick together
mediastinal tumors
acute mediastinhtis
pneumomediastinum
bronchogenic cysts
72
pleural abnormalities: Pleural effusion
transudative effusion: just fluid- high pressure, standard edema ex: ankle from standing
Exudative effusion: protein ex: sprained ankle
pleurisy: inflamm of pleural, painful breathing, infection
hemathorax
73
pleural abnormalities: Empyema
pus in pleural space from infection
| infected pleural effusion
74
FVC
mesures getting air in
75
FEV1
getting air out in 1 sec, normal is 90%
76
diseased with NORMAL FVC
obstructive
77
diseases with NORMAL FEV1
restrictive, can be reduced
78
disease with NORMAL FEV1/FVC%
restrictive
79
Pulm Embolism
occlusion of a portion of the pulm vascular bed by a thrombus, embolus, tissue fragment, lipids, or an air bubble
commonly arise from the deep being in the thigh
-lungs act as filter, letting clots break down, micro emboli
80
Virchow triad
venous statsis, hypercoagulabability, and injuries to the endothelia cells that line the vessels
81
pulm embolism causes
```
hypoxic vasoconstriction
decreased surfactant
release of neruohumoral and inflamm substances
pulm edema
atelectasis
```
82
pulm embolism s/s
```
tachypnea
dyspnea
chest pain
increased dead space
V/Q imbalances
decreased PaO2
pulm infarction
pulm HTN
decreased CO
systemic hypotension
shock
```
83
pulm HTN, definition and classifications
mean pulm artery pressure 5-10mmgh above normal or above 20mmhg
pulm art HTN
pulm venous HTN
pulm HTN due to a resp disease of hypoxemia (ex COPD, vasoconstriction from poor vent
pulm HTN due to thrombi or embolic disease
pulm HTN due to disease of pulm vasculature
84
pulm HTN patho
endothelial dysfunction:
*overproduction of vasoconstrictors--thromboxane, endothelin
*under production of dilators--prostacyclin, nitric oxide
usually idiopathic: environmental, genetic
85
Cor pulmonale
R heart failure 2ndary to pulm HTN
86
chronic pulm HTN cause by....
```
COPD, interstitial fibrosis, OHS leads to:
Chronic hypoxemia/chronic acidosis leads to:
pulm art vasoconstriction leads to:
increased pulm art pressure leads to:
*intimal fibrosis and hypertrophy of medial smooth muscle layer of pulm art leads to :
CHRONIC PULM HTN which can then lead to:
Cor Pulmonale (hypertrophy and dilation of Right ventricle)- R heart failure.
* progression of pulm HTN can be reverse at this point with effective tx of primary or underlying disease.
```
87
lung CA risk factors
most common cause is smoking:
heavy smokers have a 20 times greater chance of developing lung CA then nonsmokers
smoking is related to CA of larynx, oral cavity, esophagus, and urinary bladder
environmental or occupational risk factors are also associated with lung CA
88
lung CA types
small cell carcinoma (oat cell)
| non-small cell: squamous cell carcinoma, adenocarcinoma, large cell carcinoma
89
Squamous cell carcinoma
slow
near hills
obstructive with cough (irritating bronchus) and hemoptysis
90
small cell (oat cell) carcinoma
vary rapid
most correlated with smoking
very high mortality
ectopic hormone production
91
adenocarcinoma
moderate growth rate
LEAST correlated with smoking
usually on periphery
92
Large cell carcinoma
rapid
93
Cystic fibrosis general, normal sweat duct, Cl channel, where else are these channels
Autosomal recessive need 2 bad genes
normal sweat duct: Na reabsorbed and Cl follows.
Cystic fibrosis: defective Cl channel. If just Na was reabsorbed then sweat would be negatively changed, this doesn't happen. SO with the defective Cl channel Na just stops going in, get salty sweat
CF has hypertonic sweat
Same defective Cl channel is in other organs: lungs, pancreas, gallbladder
94
CF big problem
BIG problem in lungs: normal pump mucus and release chloride into it, bring small amount of sodium back in;
If defective: chloride doesn’t go out into mucus, and bring back (out of mucus) more sodium and more water, therefore mucus is dehydrated and therefore too thick for cilia to move and it stays in the lungs
lots of lung infections because mucus doesn’t move out of lungs and bacteria can grow in the mucus (mucus doesn’t kill the bacteria, it just traps them)
pts can live into 30s, with daily percussion tx
