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Jess Resp > First Aid: Pathology Pt 2 > Flashcards

First Aid: Pathology Pt 2 Flashcards

1
Q

What is mesothelioma? What is it associated with and what can it result in?

A

What is mesothelioma? What is it associated with and what can it result in?

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2
Q

What is mesothelioma? What is it associated with and what can it result in?

A

Smoking

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3
Q

What can be seen on histology of mesothelioma,

Name one other positive finding in almost all mesotheliomas

A

Psammoma bodies

Calretinin and cytokeratin 5/6 is positive in almost all mesotheliomas

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4
Q

Describe the pathophysiology of ARDS

A
  1. Alveolar insult results in the release of pro-inflammatory cytokines
  2. leading to neutrophil recruitment, activation and release of toxic mediators (i.e ROS, proteases, etc)
  3. This causes capillary endothelial damage and increased vessel permeability
  4. allowing for leakage of protein-rich fluid into the alveoli and forming intra-alveolar hyaline membranes and noncardiogenic pulmonary edema
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5
Q

What else contributes to alveolar collapse in ARDS?

A

Loss of surfactant

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6
Q

What are intra-alveolar hyaline membranes composed of and what do they cause?

A

Dead cells, surfactant and proteins - they deposit along the walls of the alveoli making gas exchange difficult

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7
Q

Name four causes for ARDS

A

STAPP: Sepsis, trauma, aspiration, pneumonia, pancreatitis

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8
Q

How is ARDS diagnosed?

A

Diagnosis of exclusion with the following criteria

A: abnormal CXR (i.e bilateral lung opacities)
R: Resp failure within 1 week of alveolar insult
D: decreased PaO2/FiO2 (the ratio is <300, this indicates hypoxemia due to increased intrapulmonary shunting and diffusion abnormalities)
S: symptoms of resp failure are NOT due to HF/fluid overload

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9
Q

Define a pulmonary shunt, what does it cause?

A

When parts of the alveoli are filled with fluid, so parts of the lung are unventilated but still perfused. Intrapulmonary shunting is the main cause of hypoxemia

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10
Q

What happens to the lungs as a result of ARDS?

A

Impaired gas exchange, decreased lung compliance and pulmonary hypertension

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11
Q

How is ARDS managed?

A

By treating the underlying cause and with mechanical ventilation

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12
Q

Define sleep apnea and describe its complications

What are the 3 types?

A

Repeated cessation of breathing for >10 seconds during sleep, this leads to disrupted sleep and daytime somnolence

Sleep apnea leads to

  1. Hypoxia: stimulates EPO and erythropoiesis
  2. Nocturnal hypoxia: can cause systemic and pulmonary hypertension, arrhythmias and sudden death

3 types: obstructive sleep apnea, central sleep apnea and obesity hypoventilation syndrome

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13
Q

Define obstructive sleep apnea, what are its commonly associated features (including how it can be caused in adults and children)? How does it affect daytime PaO2?

A

A respiratory effort against airway obstruction

Associated with: obesity, loud snoring and daytime sleepiness and can be caused by excessive parapharyngeal tissue in adults and adenotonsillar hypertrophy in children

Normal daytime PaO2

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14
Q

How is obstructive sleep apnea treated?

A

Weight loss, CPAP and dental devices

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15
Q

What is central sleep apnea and what can it be caused by? How can it be treated?

A

Impaired respiratory effort due to the 3 Cs…

  1. CNS injury/toxicity
  2. Congestive HF
  3. Cheyne-stokes respirations (changing between apnea (not breathing) and hyperpnea (increased depth and rate of breathing))

Treated with positive airway pressure

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16
Q

How does obesity hypoventilation syndrome affect daytime and nocturnal PaO2 and PaCO2 and why? What else is it known as?

A

Also known as Pickwickian syndrome

When BMI>30 -> leads to hypoventilation and increased PaCO2 during waking hours and increased PaCO2 and decreased PaO2 during sleep

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17
Q

What is the normal pulmonary artery pressure, and what pressure defines pulmonary hypertension?

A

Normal: 10-14 mmHg
PH: >25 mmHg at rest

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18
Q

What can pulmonary hypertension result in?

*both in terms of arterial damage and longer-term?

A

I AM P: Arteriosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries and plexiform lesions

Longer-term: severe respiratory distress -> cyanosis and RVH and death from decompensated cor pulmonale

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19
Q

What are the causes of pulmonary arterial hypertension?

A

HPHDCSIC: Have pulmonary hypertension? Damn cocaine sure is crazy

  1. Often Idiopathic
  2. Heritable: inactivating mutation in the BMPR2 gene (which normally inhibits vascular smooth muscle proliferation)
  3. Portal hypertension
  4. HIV disease
  5. Drugs (i.e cocaine and amphetamines)
  6. CT disease
  7. Congenital heart disease
  8. Schistosomiasis
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20
Q

What happens as a result of the pulmonary vasculature endothelial dysfunction in pulmonary arterial hypertension?

A

Increased vasoconstrictors (i.e endothelin) and decreased vasodilators (i.e NO and prostacyclins)

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21
Q

What does L heart disease cause?

A

Systolic/diastolic dysfunction and valvular disease

22
Q

Name three major causes of lung diseases or hypoxia

A
  1. Destruction of the lung parenchyma (i.e COPD)
  2. Lung inflammation/fibrosis (i.e interstitial lung diseases)
  3. Hypoxemic vasoconstriction (i.e obstructive sleep apnea, high altitudes, etc)
23
Q

What is chronic thromboembolic disease?

A

Recurrent microthrombi decrease the cross-sectional area of the pulmonary vascular bed

24
Q

What are some ‘multifactorial’ causes for pulmonary hypertension?

A

Hematologic, systemic, metabolic disorders and compression of the pulmonary vasculature by a tumour

25
Q

Describe the breath sounds in the following abnormalities

a) pleural effusion
b) atelectasis
c) simple pneumothorax
d) tension pneumothorax
e) consolidation (lobar pneumonia, pulmonary edema)

A

Breath sounds are DECREASED in pleural effusion, atelectasis, simple pneumothorax and tension pneumothorax

Bronchial breath sounds can be heard in consolidation, including late inspiratory crackles, egophony, whispered pectoriloquy

26
Q

Describe the percussion in the following abnormalities

a) pleural effusion
b) atelectasis
c) simple pneumothorax
d) tension pneumothorax
e) consolidation (lobar pneumonia, pulmonary edema)

A

a) Dull
b) dull
c) hyper resonant
d) hyper resonant
e) dull

27
Q

Describe the fremitus in the following abnormalities

a) pleural effusion
b) atelectasis
c) simple pneumothorax
d) tension pneumothorax
e) consolidation (lobar pneumonia, pulmonary edema)

A

DECREASED: for pleural effusion, atelectasis, simple pneumothorax and tension pneumothorax

e) increased

28
Q

Describe the degree (if any) of tracheal deviation in the following abnormalities

a) pleural effusion
b) atelectasis
c) simple pneumothorax
d) tension pneumothorax
e) consolidation (lobar pneumonia, pulmonary edema)

A

a) None if small and away from the side with the lesion if large
b) Towards the side of the lesion
d) none
d) away from the side of the lesion
e) none

29
Q

Name four causes for alveolar collapse and at least one example of each

A

COCA
1. Compressive: external compression on the lung will decrease the lung’s volume (i.e pleural effusion, space-occupying lesion)

  1. obstructive: airway obstruction prevents new air from reaching the distal airways and old air is resorbed (i.e foreign body, mucous plug, tumour)
  2. Contraction: scarring of the lung’s parenchyma distorts the alveoli (i.e sarcoidosis)
  3. Adhesive; due to lack of surfactant (i.e NRDS in premature babies)
30
Q

What is pleural effusion and what does it cause? How can it be treated?

A

Accumulation of fluid between the pleural layers, this restricts the lung’s ability to expand during inspiration.

Can be treated with thoracentesis to remove/reduce the fluid

31
Q

What are the three types of pleural effusion?

A

Lymphatic, exudate, transudate

32
Q

What causes a lymphatic pleural effusion and how do they appear? What else it is known as?

A

Also known as chylothorax

Caused by a thoracic duct injury from trauma or malignancy, the fluid is milky white and has increased TAGs

33
Q

What is exudate composed of and how does it appear? How must it be treated?

A

Increased protein content and is cloudy (cellular), must be drained right away due to the risk of infection

34
Q

What can cause abnormal amounts of exudate?

MIT

A
  1. Malignancy
  2. Inflammation/infection (i.e pneumonia, collagen vascular disease)
  3. Trauma (occurs in states of increased vascular permeability)
35
Q

What is transudate composed of and how does it appear? What causes it?

A

Decreased protein content and is clear (hypocellular), caused due to…

  1. Increased hydrostatic pressure (i.e HF, Na+ retention)
  2. Decreased oncotic pressure (i.e nephrotic syndrome, cirrhosis)
36
Q

What are six features of pneumothorax on the affected side?

A

DDCCTH

Dyspnea, diminished breath sounds, uneven chest expansion, chest pain, decreased tactile fremitus and hyper resonance

37
Q

Name the four types of pneumothorax

A
  1. Primary spontaneous pneumothorax
  2. Secondary spontaneous pneumothorax
  3. Traumatic pneumothorax
  4. Tension pneumothorax
38
Q

What causes primary spontaneous pneumothorax and who is commonly affected?

A

Caused by the rupture of apical subpleural bleb or cysts, commonly occurs in tall, thin, young males and smokers

39
Q

What causes secondary spontaneous pneumothorax?

A
  1. Diseased lung: bullae (blister containing serous fluid) in emphysema, infection
  2. Mechanical ventilation with the use of high pressures can cause barotrauma
40
Q

What can cause a traumatic pneumothorax?

A
  1. Blunt, i.e rib fracture
  2. Penetrating, i.e gunshot
  3. Iatrogenic, i.e central line placement, lung biopsy, barotrauma (due to mechanical ventilation)
    Other trauma
41
Q

What can cause tension pneumothorax? Describe its pathophysiology

A

Can be caused by anything that causes the other types of pneumothorax

Pathophysiology:
1. Air enters the pleural space and cannot exit, the increase in trapped air leads to a tension pneumothorax

  1. This can increase the intrathoracic pressure -> causing mediastinal displacement -> kinking of the IVC and therefore decreased venous return and decreased cardiac output
  2. The trachea deviates away from the affected lung
42
Q

How is a tension pneumothorax immediately managed?

A

Needle decompression and chest tube placement

43
Q

Name four types of pneumonia

A
  1. Lobar pneumonia
  2. Bronchopneumonia
  3. Interstitial (atypical) pneumonia
  4. Cryptogenic organizing pneumonia
44
Q

Name three organisms that can cause lobar and bronchopneumonia

A

Lobar pneumonia: S. pneumonia, legionella (L-L) and klebsiella

Bronchopneumonia: S. pneumonia, Klebsiella, S. aureus (and H.influenza)

45
Q

Compare the characteristics of lobar and bronchopneumonia including which zones of the lung are affected

A

Lobar: intra-alveolar exudate leads to consolidation that may involve the entire lobe or the whole lung

Bronchopneumonia: acute inflammatory infiltrates from bronchioles into adjacent alveoli results in a patchy distribution involving 1 or more lobe(s)

46
Q

Name four organisms that tend to be involved in interstitial (atypical) pneumonia

A

Mycoplasma, chlamydia pneumonia, legionella, viruses (influenza, adenovirus, RSV and CMV)

47
Q

Describe the pathology of interstitial (atypical) pneumonia, how does it appear on a CXR?

A

Diffuse patchy inflammation localized to interstitial areas at alveolar walls

CXR: shows bilateral multifocal opacities

48
Q

What causes cryptogenic organizing pneumonia?

A

Etiology is unknown, secondary organizing pneumonia (has a specific cause) can be caused by

  1. Chronic inflammatory diseases (i.e rheumatoid arthritis)
  2. Medication side effects (i.e amiodarone)
49
Q

Describe the pathology of cryptogenic organizing pneumonia, what else was it formerly known as?

What does it (and what does it not) respond to?

A

Noninfectious pneumonia characterized by inflammation of the bronchioles and surrounding structure, formerly known as bronchiolitis obliterans organizing pneumonia (BOOP)

Often responds to steroids but not antibiotics!

50
Q

Describe the natural history of lobular pneumonia (in terms of days and their corresponding findings, including the features of the exudate)

A

Days 1-2: Congestion, red-purple, partial consolidation of the parenchyma. Exudate with mostly bacteria

Days 3-4: Red hepatization, red-brown consolidation. Exudate has fibrin, bacteria, RBCs and WBCs

Days 5-7: Grey hepatization, uniformly grey consolidation, exudate has WBCs, lysed RBCs and fibrin

Days 8+: Resolution, enzymatic digestion of exudate by macrophages

Jess Resp (20 decks)

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