Lung CA + CF + Resp Failure

Question 1

What qualities of CA does Lung cancer have?

Answer 1

• Primary and secondary site
• Is largely avoidable
• Major cause of death (mortality = about 30%)
• Aggressive progression, invasive, metastasizes early…everything you don’t want about a tumour is present here!

Question 2

What are the 3 preferred secondary sites from lung CA?

Answer 2

bone, liver, brain

Question 3

2 Main categories of lung cancer?

Four major primary types and how they fit into the above?

Answer 3

• “Non-Small Cell Lung Cancers” - NSCLC (types 1-3)
• “Small cell Lung Cancers” SCLC (type 4)

1) Adenocarcinoma (~30%)
2) Squamous cell carcinoma (~30%)
3) Large cell carcinoma (~12%)
4) Small cell carcinoma (~22%)
5) “Mixed group” is 5th category which contains mixtures of the above

Question 4

What is an adenocarcinoma?

Answer 4

a malignant tumor formed from glandular structures in epithelial tissue

Question 5

Et of lung cancer?

Answer 5

• Smoking (>80%)

* Toxins (eg: asbestos)

Question 6

Describe squamous cell carcinoma in terms of:

1) Origin
2) Where it spreads to
3) Who is most common in

Answer 6

1) Arises in central bronchi (hilum) –> Said to be central in origin (not down in alveoli)
2) Spread to hilar nodes; Because is hilar region, as it progresses, it could impact the heart
3) More common in men

Question 7

95% of lung cancer is _______ (term used to describe origin)

Answer 7

“bronchogenic” – originate it the bronchi

Question 8

What is the lung hilum?

Answer 8

the point at which the bronchi, pulmonary arteries and veins, lymphatic vessels, and nerves enter the lung.

Question 9

Adenocarcinoma

1) Origin
2) More common in?

Answer 9

• Peripheral origin (in association with alveoli and bronchioles)
• More common in women & non-smokers

Question 10

Large Cell Carcinomas

1) Origin?
2) why called this?
3) When does it met
4) GOod prognosis?

Answer 10

• Peripheral origin
• Large cell = large, undifferentiated cancer cells
• Metastasizes early
• Poor prognosis in comparison to those we have discussed so far

Question 11

What is the most common cause of small cell carcinomas?

Answer 11

Smoking - 99% in smokers!

Question 12

What is characteristic of small cell carcinomas?

WHy are these CAs particularly bad?

Answer 12

• “Oat grain cancer” – tiny oval cells
• Aggressive, invasive, early mets
• Is worst form!!!
• Mets at Dx
• Non resectable because are tiny grains, not necessarily massed together

Question 13

Where do small cell carcinomas typically met to?

Answer 13

brain

Question 14

What tx do SCLC’s respond to?

Answer 14

Radiosensitive - radiation

Question 15

What kind of CA are paraneoplastic syndromes seen in? What occurs here?

Answer 15

Notes say: “same as ectopic tumour but not endocrine so can’t call it this”….hmm?

Due to its high grade neuroendocrine nature, small-cell carcinomas can produce ectopic hormones, ACTH + ADH….resulting in things like Cushing’s and SIADH.

Paraneoplastic syndromes are symptoms that occur at sites distant from a tumor or its metastasis. Although the pathogenesis remains unclear, these symptoms may be secondary to substances secreted by the tumor or may be a result of antibodies directed against tumors that cross-react with other tissue.

Question 16

Manifestations of lung CA?

Answer 16

• Based on type and site, extent and mets, whether have paraneoplastic syndromes or not,
• If central → impairs ventilation → coughing, wheezing, dyspnea
• Hemoptysis (tumour damages blood vessels)
• Pain (why?)
• Cardiac mnfts??? If impacts pericardium and the heart

Question 17

Dx of lung CA?

Answer 17

• Hx, px (excluding chronic bronchitis, etc..)
• Chest x-ray, US, CT, MRI
• Bronchoscopy – can collect biopsy with this
• Needle biopsy (have to find tumour first, then take from there)
• Cytology (sputum or bronchial wash)

Question 18

Tx of lung CA?

Answer 18

• NSCLC: sx, radiation & chemo
• SCLC: chemo & radiation
• Very hard to have early detection because is no screen process…so likely have poor prognosis once it has been diagnosed

Question 19

What is cystic fibrosis?

Answer 19

• Defective Cl- channel in cell membrane

* Will end up with hypersecretion of exocrine fluids (mucous in resp tract, GI, or reproductive tract)

Question 20

Et of cystic fibrosis?

Answer 20

• CFTR gene on Chr 7 – Cystic Fibrosis Transmembrane Regulator
• Is monogenic problem (not complex trait!)
• Is autosomal recessive

Question 21

Patho of CF?

Answer 21

SEE FIG 29-13 p. 692
• CFTR codes for Cl- channels on epith cells
• Mutation makes cell impermeable to Cl- –> Cl- doesn’t move out of secretory cells into lumen
- H2O and Na+ excessive absorbed…less liquid in lumen
o Abn secretion – thickening of mucuous in the airway

• Mucus = h20 + Cl- + Na+
• Contents move from blood cells into secretory cells before being able to secrete things like mucus
• With CF: chloride will not move into the airway, will instead accumulate in the cell after coming in through the blood → cell now more concentrated than mucus in the lumen → water and sodium will flow back from the mucus back into the cell…now more viscous, thick and sticky.

Question 22

What is the ultimate effect of thickened mucuous in the airway in CF?

Answer 22

o Thick mucus → dec ciliary fx → plugs airways → dec resp function
o Bacterial infection d/t dysfunctional mucociliary blanket

Question 23

How do people usually die from CF?

Answer 23

o >90% die with severe pulm disease

Question 24

Dx of CF?

Answer 24

• Sweat test
• CF in a sibling (genetic link)
• Newborn screen (trypsinogen)
• GI and resp manifestations

Question 25

How does sweat test work with CF?

Answer 25

measure NaCl concentration in perspiration; those with CF will have 2-5 fold higher conc than normal
(in sweat glands, it’s the reabsorption of the Cl-, not the secretion that’s impacted…so extra salty)

Question 26

Trypsinogen test in newborn?

Answer 26

• measured in blood, will see elevated trypsinogen in blood of baby because secretion of this is obstructed and so will accum in blood

Question 27

Tx of CF

Answer 27

• No cure
• DNAase (dec mucus stickiness)
• Control infection
• Diet mod and pancreatic E supplementation
• Anti-inflm (because is substantial inflm here)

Question 28

Why do you use DNAase for thickened mucous?

Answer 28

• is NOT causing destruction of DNA within intact cells, but rather that which has appeared in the mucus from damaged cells; mucus now less thick and can be expectorated more easily

Question 29

Lung failure

what will you see on the ABG’s?

Answer 29

• Lungs fail to fx
• No gaseous exchange
• Hypoxemia + Hypercapnia

Question 30

Causes of resp failure?

Answer 30

see chart 29-3 (some selected here…he said to choose familiar ones)

• COPD
• severe pneumonia
• Atelectasis
• Weakness or paralysis of resp muscles (d/t brain injury, drug overdose, Guillain-Barre,
• Pulm edema
• ARDS
• Upper airway obstruciton d/t infection, tumours, etc.

Question 31

Manifestations of resp failure.

Answer 31

• Hypoxemia (PaO2 45mmHg)
• Respiratory acidosis
• Manifestations of underlying cause

Question 32

Why does resp acidosis occur in resp failure?

Answer 32

d/t CO2 + H2O → H2CO3 → H+ + HCO3- — excess of CO2 means will form more H2Co3

Question 33

What kind of blood would be tested for hypoxemia + hypercapnia?

Answer 33

Arterial

Question 34

Tx of resp failure?

Answer 34

• Can progress through to acute resp failure
• Restore gas exchange eg: O2 admin
• Mechanical ventilation
• Bronchodillators??
• Abx?? if indicated because of (risk for) infection
• Underlying cause

Question 35

Why must you give O2 judiciously?

Answer 35

because if give too much O2, suppress patient’s urge to breath on own

Question 36

Are you able to reduce the hyaline membrane that forms in ARDS?

Answer 36

No…

Question 37

Is the extend of damage in lung failure as extensive as liver failure?

Answer 37

• Funciton of lungs is purely d/t respiration…the issues that result from this failure is not nearly as extensive as liver failure (which is caught up in several systems/organs)