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Respiratory > Diseases (Pleura, Cancer, Vascular, ARDs, RF) > Flashcards

Diseases (Pleura, Cancer, Vascular, ARDs, RF) Flashcards

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1
Q

The visceral + parietal pleura shares many things in common:

  • rich network of lymphatics
  • blood supply from the systemic circulation

What is the difference then?

A

Parietal pleura receives innervation from intercostal + phrenic n and their lymphatic networks contain stoma

Visceral pleura does NOT have any innervation and does NOT contain stoma.

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2
Q

Pleura consists of 4 layers:

Which layer contains the lymph and vasculature?

Which layer is most susceptible to developing cancers as a result of asbestos exposure?

A

1) mesothelium - frequent site of mesotheliomas as a result of asbestos exposure

2) loose connective tissue
3) elastic tissue

4) areolar tissue - lymph and vasculature

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3
Q

What is the purpose of stoma present in the lymphatic networks?

A

drains fluid, large molecules, particles, and cells from the pleural space

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4
Q

Physiologically, how does pleural effusions develop?

What are examples of altered states that cause this?

A

When the rate of fluid formation/filtration&raquo_space; rate of fluid reabsorption (via lymphatics)

examples:
- increased systemic Pcap (ie RHF, increase fluid filtration from parietal layer)
- increased pulmonary Pcap (ie LHF, increase fluid filtration from visceral layer)
- increased capillary permeability
- decrease lymphatic outflow (tumor)
- decrease pleura pressure (atelectasis)
- decrease transdiaphragmatic transport (cirrosis)

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5
Q

How does RHF cause pleural effusions?

A

increased systemic Pcap (ie RHF, increase fluid filtration from parietal layer of pleura)

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6
Q

How does LHF cause pleural effusions?

A

increased pulmonary Pcap (ie LHF, increase fluid filtration from visceral layer)

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7
Q

Movement of fluid across the pleural space is governed by Starling’s Law, which is influenced by these 4 factors:

A

1) surface area
2) hydrostatic pressure
3) oncotic pressure
4) size of pore

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8
Q

Fluid in the pleural space is mostly derived from which layer of the pleura?

A

Parietal pleura - due to a net hydrostatic pressure from the systemic capillaries that moves fluid into the pleural space

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9
Q

Pleural effusions can be of two types:

A

transudate (low protein)
- due to change in systemic factors (hydrostatic pressure, oncotic pressure); likely due to CHF, cirrhosis, nephrotic syndrome, hypoalbuminea

exudate (high protein)
- due to change in the capillary permeability of the pleura; likely due to malignancy, infection, inflammation of the pleura

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10
Q

What is the Light Criteria? What is it used for?

A

if pleura/serum protein >0.5 and if pleura/serum LDH >0.6, then the fluid is EXUDATE.

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11
Q

What are some of the symptoms observed in a patient with pleural effusions?

A

dysnpea, pain, cough (due to atelectasis, vagal stimulation, and some underlying disease)

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12
Q

What is indicative of a friction rub?

A

inflammation, exudative pleural effusion

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13
Q

What are some of the physical findings observed in a patient with pleural effusions?

A 
less chest wall expansion
decreased tactile fremitus (palpable vibration)
dullness
decreased breath sounds
friction rub
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14
Q

What type of defect is pleural effusions?

A

restrictive defect

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15
Q

What are some tests that can be performed to diagnose the etiology of pleural effusion?

A

cell count, cytology, culture
glucose, amylase, pH

CCC, GAP

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16
Q

What is a chylothorax?

How do you know if this has happened?

What are some common causes of this?

A

damage to the thoracic duct that results in a leakage of chyle (lymphatic fluid of intestinal origin) into the pleural space.

fluid has high TG or cholesterol content and/or a milky apperance

causes: malignancy (metastatic dz, lymphoma), trauma

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17
Q

What is the difference between a spontaneous and traumatic pneumothorax?

What are complications of either one of these?

A

spontaneous (2 types)
1˚ = healthy patients that have apical blebs
2˚ = Dz patients (COPD, CF)

traumatic (2 types)
surgical = thoractomy
non-surgical = rib fracture, blunt trauma, iatrogenic

Can lead to tension pneumothroax

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18
Q

What is tension pneumothorax?

What are the physiological consequences of this?

A

where the pressure in the pleural space is increased due to a one-way valve that prevents egress of air during expiration.

consequences:
- impaired venous return due to increased intrathoracic/pleural pressure
- severe hypoxia, since the collapsed lung functions as a massive SHUNT

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19
Q

What are some of the symptoms of a pneumothorax?

What are some of the physical exams findings?

Therapy?

A

symptoms: breathlessness, cough, chest pain, tachycardia, cyanosis, hypotension

physical exam:
hyper-resonance
decreased breath sounds
decreased tactile fremitus (palpable vibration)
asymmetry in chest wall size
tracheal shift away from side of pneumothroax

Therapy:

  • air aspiration from pleural space
  • oxygen to reverse hypoxemia
  • pleurodiesis
  • surgery
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20
Q

What are the two major types of lung cancer? subtypes?

A 
I - small cell lung carcinoma (SCLC)
II - non-small cell lung carcinoma (NSCLC)
   a) adenocarcinoma
   b) squamous cell carcinoma
   c) large cell carcinoma
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21
Q

What is small cell lung carcinoma?

In what population does it occur most often in?

How is SCLC classified? What is the purpose of treatment at these stages?

A

aggressive cancer that tends to grow and spread quickly and often metastasizes

occurs almost exclusively in smokers

classified as:
LIMITED - cancer is within one lung and/or mediastinal lymph nodes
trmt: chemo + radiation to cure the patient of cancer

EXTENSIVE - cancer has spread to the other side of the chest or to distant locations in the body
trmt: chemo to relieve the patient of symptoms, prolong life, and limit spread of cancer

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22
Q

What are the genetic mutations observed in SCLC and NSCLC?

A

both have decreased p53 and Rb, but increased myc.

Adnenocarcinoma has increased ras as well.

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23
Q

What are general clinical presentations of lung cancer?

What are paraneoplastic manifestations of SCLC? NSCLC?

A

general: cough, dyspnea, obstructive pneumonitis, SVC syndrome, hemoptysis, chest pain, fatigue, weight loss

paraneoplastic SCLC:

  • ectopic ADH secretion
  • SIADH
  • Eaton lambert syndrome (muscle weakness due to autoimmune rxn aganist VG Ca channels)
  • neuropathy

paraneoplastic NSCLC

  • cachexia (dramatic weight loss and muscle atrophy)
  • hypercalcemia (squamous cell carcinoma)
  • skeletal, CT syndromes (adenocarcinoma)
  • gynecomastia (large cell carcinoma)
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24
Q

How is prognosis of lung cancer determined?

A

1) performance status (ability to do daily activities)
2) stage of cancer
3) LDH levels

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25
What are the 4 stages of NSCLC?
1 - tumor confined within lung parenchyma and has NOT spread to regional lymph nodes, <3 cm, surrounded by lung or visceral pleura, not invading into a main bronchus 2 - tumor confined within lung parenchyma and has spread to regional lymph (intrapulmonary/hilar) nodes 3 - tumor spread to mediastinal lymph nodes or to contralateral lung 4 - tumor spread outside of the lung
26
Explain the significance of the following lab values for lung cancer: - anemia - LDH - CRP - a1-acid glycoprotein
Anemia LDH - tissue breakdown releases LDH, increased in cancer and inflammatory diseases CRP - acute phase reactant protein that is elevated in inflammation a1-acid glycoprotein - acute phase reactant protein that is elevated in inflammation
27
What is the ideal tumor therapy? (4)
targets tumor specific molecules that drive tumor growth reversible dispensable in normal cells measurable
28
What are examples of non-small cell carcinoma? What are examples of neuroendocrine tumors (tumors that secrete hormones directly into the blood)
non-small cell carcinomas (LAS) - adenocarcinoma - squamous cell carcinoma (SCC) - large cell carcinoma neuroendocrine tumors (CS) - small cell carcinoma - carcinoid tumor
29
What type of carcinoma is an adenocarcinoma?
non-small cell carcinoma
30
What type of carcinoma is an squamous cell carcinoma?
non-small cell carcinoma
31
What type of carcinoma is an carcinoid tumor?
neuroendocrine tumor
32
What type of carcinoma is an small cell carcinoma?
neuroendocrine tumor
33
What are the main histological features of invasive squamous cell carcinoma?
(non-small cell carcinoma) keratin formation (whorls, pearls) intracellular bridges mitotic cells present arise CENTRALLY
34
What are the main histological features of invasive adenocarcinoma?
(non-small cell carcinoma) glands present mucin production (luminal or cytoplasmic) mitotic cells present arises PERIPHERALLY
35
What are the main histological features of carcinoid tumors? What populations is this most common in?
(neuroendocrine tumors) low power: RIBBONS of cells with nuclei of uniform size and salt/pepper pattern common in smokers + non;smokers
36
What are the main histological features of small cell carcinomas? What populations is this most common in?
(neuroendocrine tumors) low power: SHEETS nuclei that "mold" to adjacent nuclei and salt/pepper pattern common in smokers
37
What do these histological markers stain for: ``` TTF (thyroid transcription factor) Keratin Vimentin Desmin Neurofilament, Synaptophysin, chromgranulin GFAP ```
TTF (thyroid transcription factor) = Lung or thyroid tissue Keratin - epithelial cells Vimentin - connective tissue/mesoderm Desmin - muscle cells (think desmosomes connect muscle cells Neurofilament, Synaptophysin, chromgranulin: neuronal cells GFAP: glial cells
38
What are the most common cancers of the H&N? Most lethal?
most common: laryngeal + oral mucosal most lethal: hypopharynx, esophageal, sinus
39
Of all of the salivary glands, which one are the most likely to harbor a malignancy?
smallest ones
40
Where do cancers generally spread to first?
lymph nodes of the neck, then to the liver, lungs, and bones
41
What type of cancer makes up the majority of all H&N cancers?
squamous cell cancers (SCC)
42
What is the mechanism by which HPV cause cancers? Where does it occur most frequently? What are clinical manifestations?
HPV 16/18 disrupts cell cycle/tumor suppressor genes (p53/Rb) via E6/E7 proteins, leading to cell proliferation and immortalization location: tonsil + base of tongue (Waldeyer's Ring) clinical manifestations: leukoplakia - "smoker's keratosis" erythroplasia - flat, red, patchy lesions on mucosal surfaces
43
Why are T3/T4 tumors more likely to recur at or near the primary site? (2)
radioresistance | undetected spread of cancer cells
44
# Define: pulmonary hypertension pulmonary arterial hypertension cor pulmonale RH failure
pulmonary hypertension - PH - increase in pulmonary artery pressure pulmonary arterial hypertension - PH caused by an abnormality in the pulmonary vasculature cor pulmonale - R heart disease caused by a lung problem (ILD, COPD, sleep apnea) RH failure - compromised RV pump function that results in increased RV preload; evidenced by peripheral edema, elevated JVP, hepatomeagly
45
Pulmonary circulation is dependent on these 3 factors:
1) CO 2) Pulmonary vascular resistance (PVR) 3) L atrial pressure (LAP)
46
What two factors modulate pulmonary vascular resistance?
lung volume and blood flow @ low lung volume/TV: HIGH PVR @ high lung volume/TLC: HIGH PVR (PVR is lowest at an intermediate lung volume) @ low blood flow: HIGH PVR @ high blood flow: LOW PVR (as blood flow increases, PVR decreases)
47
Blood flow in pulmonary vasculature is governed by which 3 pressures? Where is the greatest blood flow in the lungs?
pulmonary arterial pressure pulmonary venous pressure alveolar pressure base of lungs receive greater blood flow than the apices (simply due to gravity)
48
What does hypoxia do to the lungs? Why?
Vasoconstriction - reduces blood flow to poorly perfused areas to minimize VQ mismatch
49
Describe whether these factors decrease or increase PVR: ``` Thromboxane Prostacyclin NO Endothelin-1 5HT a-adrenergic agonist (NE) b-adrenergic agonist (albuterol) ```
``` Thromboxane: increase PVR Prostacyclin: decrease PVR NO: decrease PVR Endothelin-1: increase PVR 5HT: increase PVR a-adrenergic agonist (NE): increase PVR b-adrenergic agonist (albuterol): decrease PVR ```
50
What are the mechanisms of pulmonary HTN? (3 main ones) and what are some of the causes of each one?
increase pulmonary blood flow (CO) - VSD/ASD increase PVR - hypoxia increase L atrial pressure - mitral valve dz/diastolic dysfunction
51
How is pulmonary HTN quantified?
R heart catheterization/pulmonary wedge pressure provides measures of - pulmonary arterial pressure - L atrial pressure - cardiac output can calculate PVR from these 3 factors: P(PA) = (CO*PVR)+P(LA)
52
Pulmonary HTN is classified into 3 groups. What are they?
Group 1 - abnormality w. pulmonary vessels (idiopathic, 1˚, familial, drugs, etc) Group 2 - abnormality w. L side heart Group 3 - abnormality due to lung disease (aka cor pulmonale) Group 4 - abnormality due to thromboembolic disease
53
What is idiopathic PAH? Which pulmonary HTN group is it classified into? What is it caused by? How does it present clinically? What is the pathology? How would you diagnose it? how would you treat it?
classification: group 1 (abnormality with pulmonary vessels), aka 1˚ pulmonary HTN cause: disease of endothelial function, genetic predisposition presentation: insidious onset of dyspnea and evidence of RHF (increased JVP, edema, hepatomeagly) plexiform lesions - loss of lung parenchyma + thickening of small arteries Dx: ECHO, R heart catheterization Trmt: O2, anti-coagulation, vasodilators, lung transplant
54
What are plexiform lesions? In what patients would you normally find them?
vascular lesions characterized by concentric intimal obliteration of pulmonary vessels. normally found in patients with primary pulmonary HTN
55
Group 3 pulmonary hypertension due to lung disease is also known as..... What are examples of lung diseases that do this? What is the pathophysiology behind the increased PVR in these diseases?
cor pulmonale COPD, ILD, chronic hypoxia, sleep apnea COPD: increased lung volume -> PVR decreased PAO2 -> NO production -> PVR ILD: decrease cross-sectional area of capillary bed Chronic hypoxia: increased hypoxic-induced pulmonary vasoconstriction -> PVR increased polycythemia -> increase Hb -> increase blood viscosity -> PVR Vascular remodeling: - medial hypertrophy in arterioles -> PVR
56
ARDs is characterized by (3)
1) severe hypoxia 2) diffuse, bilateral pulmonary infiltrates 3) reduced lung compliance it is a form of pulmonary edema accompanied by inflammation + fibrosis that occurs in response to injury
57
What's the difference between cardiogenic and non-cardiogenic pulmonary edema?
Cardiogenic: hydrostatic edema, due to increased pulmonary venous hypertension that results from LV failure (increase Pmv - hydrostatic pressure in capillary lumen - of Starling's equation) Non-cardiogenic: edema that is due to increased permeability of the vessels (since the lungs receive the entire CO, it has the greatest exposure to any inflammatory mediators present in the blood)
58
What roles do the alveolar endothelium and the pulmonary capillary endothelium play in terms of fluid movement? What happens if these barriers are compromised? What does this result in?
alveolar endothelium - prevents fluid accumulation in the alveoli pulmonary capillary endothelium - prevents fluid accumulation in the interstitial space compromised barriers: - alveolar flooding - decreased surfactant production - fibrosis all results in: - HYPOXEMIA due to impaired gas exchange - COMPLIANCE is decreased - PULMONARY HTN
59
What are the 3 pathologic changes in ARDs patients? Hint: there are 3 stages
1) Exudative (crackles, hypoxemia, tachypnea) - alveolar + interstitial EDEMA (crackles) - type I death, type II hyperplasia - inflammatory cells are present - diffuse alveolar damage 2) Fibroproliferative (refractory hypoxemia, non-compliant lungs, PEEP responsive) - granulation deposits - fibroblasts present - presence of HYALINE MEMBRANE 3) Fibrotic (persistent hypoxia, PEEP UN-responsive) - fibroblasts predominate - collagen deposition in walls/septa - vascular obliteration - pulmonary HTN
60
How do you treat ARDs?
these treatments improve VQ mismatch/oxygenation, AND it reduces mortality: - low-tidal volume ventilation (minimizes the injury caused by the ventilator) these treatments improve VQ mismatch/oxygenation, but does not reduce mortality: - inhaled NO - exogenous surfactant - prone positioning
61
Summarize ARDs in 7 bullet points: ``` think about histological features (2) pathophysiology (4) therapies (2) outcomes (1) causes ```
1) pulmonary edema + hyaline membrane in septa 2) diffuse alveolar damage (DAD)/alveolar inflammation -> increased permeability 3) thickened diffusion barrier -> hyoxemia + cyanosis 4) decreased compliance due to fibrosis+edema, and decreased surfactant production 5) limited effective therapies (PEEP, low tidal volume ventilation) 6) significant M&M 7) caused by: acute lung injury (trauma, sepsis, infections, gastric aspiration)
62
What is respiratory failure? What are the types of RF?
failure of respiratory system to 1) deliver enough oxygen into arterial blood 2) removal of CO2 from mixed venous blood ``` types: hypoxemia hypercapnia acute chronic ```
63
Which one is better tolerated by the body: hypoxemia or hypercapnia?
hypercapnia
64
Predict the Aa difference in these mechanisms that cause hypoxemia: ``` shunt VQ mismatch hypoventilation diffusion impairment decrease FiO2 ```
``` shunt: increase Aa VQ mismatch: increase Aa hypoventilation: normal Aa diffusion impairment: increase Aa decrease FiO2: normal Aa ```
65
What are the causes of hypercapnia?
CNS depression respiratory muscle weakeness imbalance btwn ventilatory O2 supply and demand, and CO2 production
66
How would you treat these hypoxemia that is due to: shunt VQ mismatch hypoventilation diffusion impairment
shunt: supplemental O2 if shunt is small hypoventilation: supplemental O2 diffusion impairment: supplemental O2 VQ mismatch: high FiO2
67
What is PEEP used for? What are the adverse effects of PEEP?
maintains expiratory pressure at a level that is sufficient to keep the alveolus from collapsing and to allow for a greater volume change to occur (thus, alveolar units are better ventilated) Adverse effects: increase intrathoracic pressure -> decreased venous return
68
What is iNO for?
potent pulmonary vasodilator - decreases pulmonary HTN and increases blood flow improves VQ mismatch and arterial PO2, but no improvement in mortality rates since few ARDs patients die from hypoxemia
69
When would you see a plateau pressure? how would you lower plateau pressure?
when the tidal volume is high and/or the compliance is low (ie ARDs) easy: increase lung compliance or reduce tidal volume delivered.
70
When would you see a normal PCO2 during increased minute ventilation?
when the physiological dead space is significantly increased.

Respiratory (5 decks)

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