Lung CA + CF + Resp Failure Flashcards
What qualities of CA does Lung cancer have?
- 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!
What are the 3 preferred secondary sites from lung CA?
bone, liver, brain
2 Main categories of lung cancer?
Four major primary types and how they fit into the above?
- “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
What is an adenocarcinoma?
a malignant tumor formed from glandular structures in epithelial tissue
Et of lung cancer?
- Smoking (>80%)
* Toxins (eg: asbestos)
Describe squamous cell carcinoma in terms of:
1) Origin
2) Where it spreads to
3) Who is most common in
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
95% of lung cancer is _______ (term used to describe origin)
“bronchogenic” – originate it the bronchi
What is the lung hilum?
the point at which the bronchi, pulmonary arteries and veins, lymphatic vessels, and nerves enter the lung.
Adenocarcinoma
1) Origin
2) More common in?
- Peripheral origin (in association with alveoli and bronchioles)
- More common in women & non-smokers
Large Cell Carcinomas
1) Origin?
2) why called this?
3) When does it met
4) GOod prognosis?
- Peripheral origin
- Large cell = large, undifferentiated cancer cells
- Metastasizes early
- Poor prognosis in comparison to those we have discussed so far
What is the most common cause of small cell carcinomas?
Smoking - 99% in smokers!
What is characteristic of small cell carcinomas?
WHy are these CAs particularly bad?
- “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
Where do small cell carcinomas typically met to?
brain
What tx do SCLC’s respond to?
Radiosensitive - radiation
What kind of CA are paraneoplastic syndromes seen in? What occurs here?
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.
Manifestations of lung CA?
- 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
Dx of lung CA?
- 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)
Tx of lung CA?
- 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
What is cystic fibrosis?
- Defective Cl- channel in cell membrane
* Will end up with hypersecretion of exocrine fluids (mucous in resp tract, GI, or reproductive tract)
Et of cystic fibrosis?
- CFTR gene on Chr 7 – Cystic Fibrosis Transmembrane Regulator
- Is monogenic problem (not complex trait!)
- Is autosomal recessive
Patho of CF?
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.
What is the ultimate effect of thickened mucuous in the airway in CF?
o Thick mucus → dec ciliary fx → plugs airways → dec resp function
o Bacterial infection d/t dysfunctional mucociliary blanket
How do people usually die from CF?
o >90% die with severe pulm disease
Dx of CF?
- Sweat test
- CF in a sibling (genetic link)
- Newborn screen (trypsinogen)
- GI and resp manifestations
How does sweat test work with CF?
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)
Trypsinogen test in newborn?
- measured in blood, will see elevated trypsinogen in blood of baby because secretion of this is obstructed and so will accum in blood
Tx of CF
- No cure
- DNAase (dec mucus stickiness)
- Control infection
- Diet mod and pancreatic E supplementation
- Anti-inflm (because is substantial inflm here)
Why do you use DNAase for thickened mucous?
- 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
Lung failure
what will you see on the ABG’s?
- Lungs fail to fx
- No gaseous exchange
- Hypoxemia + Hypercapnia
Causes of resp failure?
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.
Manifestations of resp failure.
- Hypoxemia (PaO2 45mmHg)
- Respiratory acidosis
- Manifestations of underlying cause
Why does resp acidosis occur in resp failure?
d/t CO2 + H2O → H2CO3 → H+ + HCO3- — excess of CO2 means will form more H2Co3
What kind of blood would be tested for hypoxemia + hypercapnia?
Arterial
Tx of resp failure?
- 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
Why must you give O2 judiciously?
because if give too much O2, suppress patient’s urge to breath on own
Are you able to reduce the hyaline membrane that forms in ARDS?
No…
Is the extend of damage in lung failure as extensive as liver failure?
• 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)
