Week 5 Flashcards
Ventilation - define
air coming in through the atmosphere going into the alveoli
Diffusion - define
Air going from alveoli into capillaries
Gas levels in alveoli -PaO2–effect? - PaCO2
-High because it’s coming in; makes it goes into capillary - 0; allows for CaO2 to diffuse in
Gas level in blood - PaO2; importance? - CO2; importance?
- when O2 first enters the blood it is at 100 but after it goes through the body and then makes it back to the lungs the pressure has dropped to 40; having low pressure allows for oxygen from lungs to diffuse in because it goes from high to low - allows for CO2 to diffuse from capillary into alveoli
Define exertional dyspnea
Difficulty breathing with exertion
Common lung infection in HIV patients?
Tuberculosis
mechanisms behind pulmonary HTN
it could be backup from Lt side of heart (she’s got an ejection murmur so there’s obviously some dysfunction there) increase in left ventricular pressure could backup and cause increased left atrial pressure which would cause increased pressure on the pulmonary veins.
What happens to the vessels when you have endothelial damage?
You lose compliance, fibrosis- intimal thickening, vascular tone increases so you don’t get dilation.
do opioids cause lung damage?
Flash pulmonary edema
what can HIV do to vasculature?
- HIV Is associated with valvular defects in the heart and it is also associated with vascular changes. - thickens up, radius of vessels decreases –> resistance increases
How to differentiate between heart failure and pulmonary edema (pulmonary htn) due to opioid use? - order; why?
- order Echocardiogram and BNP - if BNP is low then not coming from heart but if BNP is high there is higher chance it is heart failure
what could increases in pulmonary pressure do to the right side
right side of heart could be undergoing changes in pressure, changes in contractile function leading to failure which is why you see the pitting edema.
Differences of pulmonary vasculature vs systemic vasculature?
. Arterioles in systemic vascular really hold their shape, but here is pulmonary vasculature the arterioles are a lot more expandable and collapsible.
Types of vasculature in lungs
- alveolar: inside/in between the alveoli - extralveolar: outside the alveoli.
Alveolar vasculature changes during inspiration. why? what happens to resistance?
Vessels are gonna get compressed and elongated because alveolar volume increases - Resistance increases and therefore bloodflow decreases
Extra alevolar vasculature changes during inspiration. - why?
- Resistance decreases - Interpleural pressure become more negative. Because of that, transmural pressure across the extraalveolar vessels increases and pulls the vessels open decreasing the resistance and increasing blood flow
What happens to alveolar and extra-alveolar vasculature during expiration?
- alveolar vessels are going to shorten and increase their radius so resistance starts to decrease whereas in the extra alveolar vessels, resistance increases.
How does pumonary HTN alter pulmonary vasculature resistance - what happens to vascular reactivity?
- She has intimal thickening and narrowing of some of the vessels so her resistance is increased - decreased vascular reactivity
What happens to blood flow in lungs during exercise? - what happens to MPAP? - term for this? - what can help with this?
- You increase blood flow d/t increased production of metabolites. The whole point of the pulmonary/circulatory system is to get O2 in and CO2 out. - Your mean arterial pulmonary pressure (MPAP) decreases because as your blood flow/perfusion pressure starts to increase with exercise, you oppose hydrostatic pressure, and so it helps to open up new arteries (increased distension). And so you recruit more blood vessels. - Recruitment: recruiting more arterioles to have more blood flow - Distension: distending the arterioles to reduce the pressure. It allows for more blood flow so that you can pick up more O2 and meet the metabolic demand.
What happens when a patient with pulmonary htn tries to exercise? - what happens to MPAP
- She would not be able to meet metabolic demand because she can’t distend due to the vascular changes in her vessel - MPAP stays elevated because they don’t have recruitment and distension
Effect of gravity on pulmonary blood flow - standing up - laying down
- gravity pulls blood to the bottom of the lungs when standing up - gravity is more proportional, so your blood flow is more proportionate.
Zones of pulmonary blood flow and gravity - ventilation - resitance to blood flow - zone 1
- Ventilation becomes more proficient as you move down the zones. As you get further and further down the lung, the alveoli are more of their normal shape, so they can change their volume to allow for more efficient ventilation. - As you get further and further down the lungs, resistance to blood flow decreases, and so you get increased blood flow. □ Zone 2: ® Arterial pressure is higher than alveolar pressure ® You have matched ventilation and perfusion –> proper gas exchange ® Zone 2 is what happens during exercise. As you start to exercise, your zone 2 starts to expand. □ Zone 3 ® Arterial pressure is the highest and venous pressure is higher than alveolar pressure ® Greatest amount of blood flow in this zone ® Perfusion>ventilation so no proper V/Q matching, so gas exchange not that efficient ® Too much perfusion and little ventilation, and nothing gets in ® There’s so much blood flow in this zone, but the alveoli are smaller and although there is some ventilation, the blood just goes right through
Zone 1 - where is it? - alveolar pressure - Perfusion - Factors increasing size of alveoli - young vs old - terminology for this zone - things that can increase in zone 1
- At the top of the lung -Alveolar pressure is the highest - There is ventilation here, but no perfusion -> there is so much ventilation that the alveoli get really big and there is no perfusion. - Alveoli are also getting big/expanding because gravity is just pulling them down - So even though your alveoli here are bigger because of gravity pulling them down, your efficiency to move air in and out isn’t that great. - Zone 1 usually doesn’t happen in a healthy young person during exercise, but as you age, you might start to get some increases in zone 1. - This is called dead space. - PEEP (positive end-expiratory pressure), Hemorrhage, General anesthesia
Zone 2 - arterial vs alveolar pressure - perfusion; effect? - what happens during exercise
- Arterial pressure is higher than alveolar pressure - You have matched ventilation and perfusion –> proper gas exchange - Zone 2 is what happens during exercise. As you start to exercise, your zone 2 starts to expand.
Zone 3 - arterial vs alveolar pressure - perfusion - what happens?
- Arterial pressure is the highest and venous pressure is higher than alveolar pressure - Greatest amount of blood flow in this zone; Perfusion > ventilation so no proper V/Q matching, so gas exchange not that efficient - There’s so much blood flow in this zone, but the alveoli are smaller and although there is some ventilation, the blood just goes right through
Type 1 Pulmonary HTN - O2 - calcium channel blocker - what do you give if CCB causes ortho hypotension - surgery? - prognosis
- not going to help this patient, could cause oxygen toxicity - reduce calcium cycling –> vasodilation - PDE5 inhibitors: inhibit the degradation of cGMP by PDE5, increasing blood flow to the penis during sexual stimulation. These meds work well for this and they don’t cause orthostatic hypotension. Ex: Viagra - If it progresses to the point where it’s going to kill her, which is a good possibility, it might be her only chance of survival. – lung transplants - Prognosis: Est median survival: 2.8 years
Acute pulmonary vasodilator testing - nitric oxide - specificity - other option
- Inhaling nitric oxide is testing the ability of her vessels to react. If her vessels don’t respond, you don’t have vascular reactivity, and so they won’t respond to CCB d/t significant endothelial damage. - Nitric oxide has the unique advantage of being rendered chemically inactive in the presence of hemoglobin, which isolates its effects to the pulmonary vasculature and virtually eliminates the risk of significant systemic side effects that are common with other agents - Another test is giving IV vasodilator and performing an echo
What happens with Inhalation injury? - hyaline membrane
Inhaling smoke–>pneumocyte injury (Type I and Type II alveolar cells)–>resident macrophages start recruiting neutrophils–>neutrophils degranulate and release inflammatory mediators–>accumulation of fluid and formation of a hyaline membrane–>necrosis–>damage–>Type II cells secrete surfactant and those are damaged –> less surfactant being released–>surface tension and elastic recoil increases–> everything collapses–>FRC decreases - Hyaline membrane makes lungs more rigid which also decreases compliance
VQ Matches
§ V=Ventilation § Q=Perfusion § When we talk about V/Q needs to match, this is what determines gas exchange
What happens to VQ with destruction of alveoli?
- You have blood flow but decreased ventilation so gas flow does not really occur - right to left shunt so it is bypassing the ventilated alveoli. The mixed venous blood and alveoli are going to equilibrate so there is no increase in oxygen content
What happens to VQ with airway obstruction
- Causes complete blockage and creates absolute shunt
What happens to VQ with Alveoli dead space? - prime example - emphysema
- V/Q=infinity and we have no perfusion. The alveoli are not being perfused - Emboli is blocking blood, so not perfusing those alveoli. - Emphysema is destruction of alveoli septal tissue, and septal tissue has capillaries in there, and with destruction of that septal tissue so we lose those capillaries to get more dead space
What happens to VQ with COPD?
- will have areas of dead space and shunting depending where it is.
What happens to VQ with inhalation injury?
- the alveoli collapsed because our FRC decreased. So we are going towards zero - We lose surfactant, and increase surface area we collapse alveoli, so we would probably have absolute shunts
1st thing you do with patient who has been inside any enclosed burning area, hoarse voice with singing of facial or nasal hair
- they get an endotracheal tube IMMEDIATELY
What is RSI
- rapid sequence intubation. - We put them on ventilation, at 100% oxygen setting in ER.
Explain PEEP - transmural pressure - oxygen
- increase because you’re raising the positive pressure in the alveoli - high concentration of oxygen makes the alveoli even more unstable -> ○ They are more delicate, more responsive to changes so they will try to take more areas and ventilation or perfuse more areas, but end up closing off those airways. So they become more fragile
why at what point does oxygen be poisonous or damage the alveoli, but how can oxygen damage the alveoli
- When you have large areas in which V/Q is absolute shunt or shunt like state, then they become very unstable. So the concentration that high makes them more unstable.
Which alveoli are being opened in mechanical ventilation?
- With positive ventilation the alveoli further from the chest wall have greater distension
should you use neuro block on patient who has ARDS and is on ventilator
With severe ARDs, if we do neuromuscular block, they don’t do as well as when they aren’t blocked. Consensus is try and not do neuromuscular block. We don’t know why
Tx for inhalation injury from fire - Antibiotics - Bronchodilators - Steroids - Vasopressors - ECMO
- NO, Infectious process not going on (yet) - Bronchodilators: maybe, maybe not - Steroids: massive anti-inflammatories but increases infection risk. - Vasopressors: only if you try everything else first. - ECMO: Yes because oxygenating his blood outside of his body and putting it back in his body. Gives his lungs a chance to recover while his body gets oxygen from some other source, but keep him on ventilation. We want to keep alveoli open and they repair themselves. Could help this guy!
Fick’s Law of diffusion - equation - dependent upon?
- V= A x D x (P1-P2) / T - Partial Pressure (P1-P2 is the difference in partial pressure of gas on either side of the barrier of diffusion.); Thickness (T is the thickness of the barrier to diffusion or the distance the gas has to travel); Surface Area (A is the area available for gas exchange); Diffusion coefficient of each of the gases (D is the diffusion constant which is dependent upon the solubility of gas and temperature)
Examples of pathologies that affect Fick’s law - Surface Area - Thickness - Partial Pressure
-Surface Area (A): Emphysema is an example of a loss of surface area because the alveolar walls get destroyed so you lose some of the alveolar-capillary barrier. Exercise is an example of increasing surface area because you recruit more alveoli and allow for distention. This allows for an increase in gas exchange to meet the metabolic demands of an exercising individual. - Thickness (T): Fibrosis and pulmonary edema are examples of increasing thickness of the barrier resulting in decreased gas exchange - Partial Pressure (P1-P2)–> Bronchitis is an example of decreased partial pressure gradient because the mucus causes an obstruction. The alveoli of the obstructed area now have a blocked airway, causing a decreased partial pressure gradient as compared to the surrounding, unblocked alveoli that are getting adequate ventilation.
Carrying Capacity of O2 - When oxygen diffuses into the capillaries, one of two things can occur - how many molecules can bind each hemoglobin - how do you reduce carrying capacity? increase?
- Cars= hemoglobin molecules - One is they can physically dissolve which will contribute to the partial pressure of O2 (PaO2), Two is they will bind hemoglobin (cars) - 4 oxygen molecules can bind each hemoglobin -We can lose carrying capacity by reducing the number of hemoglobin/cars; Less cars–> less oxygen can hitch a ride–> lower carrying capacity - increase carrying capacity by increasing the number of hemoglobin molecules/cars
Oxygen saturation
The number of O2 molecules actually bound to hemoglobin (how many of the 4 seats in the car are taken up by oxygen)
How is CO2 carried?
- Physically Dissolved - Bound to hemoglobin - Bound to bicarb -> Need carbonic anhydrase for this rxn
Types of Therapeutic Breathing - 4-7-8 Breathing - Kapalabhati and Bellows breathing - Body area/ muscle-focused Breathing - Breathing with Increased Airway Resistance
- 4 sec inhalation, 7 seconds holding, 8 second exhalation
Types of Therapeutic Breathing - 4-7-8 Breathing - Thoracic pattern breathing - Diaphragmatic/abdominal breathing - Breathing with Increased Airway Resistance - Movement with Breathing Work
- 4 sec inhalation, 7 seconds holding, 8 second exhalation - We use this pattern physiologically during exercise, or pathologically during something like an asthma exacerbation - We switch to this type of breathing during a really relaxed state. Otherwise, it takes conscious effort to do this. - This keeps alveoli open. Can be used to help COPD patients by creating a more positive pressure at the mouth. Pursing the lips creates a pressure gradient (high at mouth and low at alveoli) that creates an internal positive pressure that pushes the collapsed alveoli back open during expiration. - Timed breathing with movement such as inhaling and exhaling to a certain number of steps while running.
Bellows Breathing (Bhastrika) - how its done - physical movement
- Breath in and out of nose as fast as you can. There are other variations of this technique that involve use of the arms as well) - Can use hands/arms when doing it: Hands open and up on inhalation, Hands Closed and elbows in on exhalation, Do for 50 cycles for best results
Balancing: Alternate Nostril Breathing (Nadi Sholhana) - how to do it? - steps - effects
- Use thumb and ring finger to alternate closing one nostril at a time - Inhalation and exhalation should be through the nose: Close right nostril with thumb, Breath in through left nostril, Close left nostril will ring finger, Breath out through right nostril, Hold finger placement, Breath in through right nostril, Close right nostril with thumb, Breath out through left nostril, Hold finger placement, Breath in through left nostril, Continue pattern… alternating fingers/nostrils…. Repeat at least 30 times - Improves cognitive function
Why is there not a decrease in arterial O2 during exercise?
You have a bigger volume (tidal volume), so your breathing frequency increases and you increase alveolar O2 to increase arterial O2; you get slight increase in alveolar O2 bc you’re bringing in more O2, which keeps your arterial O2 constant bc you need to supply it to tissues
If you measure partial P concentration of O2 in venous side of blood, it’s decreased more than normal bc you’re putting more O2 into tissues where it’s needed What causes changes in ventilation? What else is going on in blood during exercise?
Increase acidity
What causes initial changes in tidal volume?
neural input-mechanoreceptors, you have anticipatory effect (getting ready to work out), increases BP set point, so you can increase sympathetics so you don’t pass out. Now you have a ventilatory effect as well, increase TV as you increase your O2 demand.
What happens to ventialtion as you increase lactic acid
minute to minute ventilation increases
How does O2 get into tissues?
- Increase acidity (decreasing pH) - Increase temperature (working out, get hot, increase temperature) - 2, 3 BPG (DPG)-binds directly to Hb and releases O2 - CO2 increases - All these factors causes R shift and easier unloading of O2 into tissues
What causes left sided shift
Fetal hemoglobin, less CO2, decrease temperature, opposite of stuff above.
How can you differentiate between restrictive and obstructive lung disease?
- Obstructive shows increase in TLC and RV and FEV1/FVC decreased - Restrictive lung dx will have increased or normal FEV1/FVC
How can you differentiate between restrictive and obstructive lung disease?
- Obstructive FEV1/FVC decreased - Restrictive lung dx will have increased or normal FEV1/FVC
How would you be able to tell a patient has emphysema off of spirometry testing?
- Emphysema-destruction of septal tissue. You lose traction on airways, when you do forced inspiration you get more dynamic compression at higher volumes, which is why you get reduction in FVC. With FEV1 you have airway flow altered. So together you get decrease in FEV1/FVC ratio. - Loss of alveolar septa causes collapsing of airways, traps air in there, increase in RV and then increase in TLC
What would happen to DLCO in COPD patient?
DLCO is down in COPD patient, bc reduction in surface area
what other ways would you see decrease in DLCO?
- Decreased Hb–> but in COPD (chronic smoking) amount of Hb goes up (polycythemia) - fibrosis (thickness of barrier changes diffusing capacity)
What’s your normal paO2 and paCO2?
80-100 normal PaO2, whereas 35-45 normal for PaCO2.
Why would patient with emphysema have further decrease in DLCO? - what can cause this?
- CO2 retention - Heavy air pollution in her area->she’s in a state of exacerbation of her COPD.
What would increasing arterial CO2 do?
Increase ventilation. Her carotid sinus and aortic arch (carotid sinus has greater effect) chemoreceptors stimulated.
peripheral vs central chemo receptors?
- Central chemoreceptors mediate chronic long term breathing.
How do central chemoreceptors work?
So CO2 in CSF–>under normal circumstance, brain produces more CO2 bc byproduct of metabolism, and CO2 diffuses into arterial blood from CSF. If you have normal arterial CO2, then it should diffuse into arterial blood. But if you start to increase arterial CO2 like in patient, you lost the diffusion gradient, so you get more CO2 in the CSF and that accumulates in brain stem and triggers central chemoreceptors.
What does hypoxia do to peripheral chemoreceptors?
Potentiates it
Why does work of breathing increase in patient with COPD?
bc lost elastic recoil making it harder to expire
What is driving force of ventilation in patient with COPD? - Why do you have to be careful with supplemental oxygen with these patients? - What happens if you were to abruptly stop O2 therapy and start and stop again?
hypoxia. Bc while they have increase in CO2 they reduce their arterial PO2 so their ventilatory drive is the hypoxia. This helps potentiate peripheral chemoreceptors to keep having increase in breathing - You lose the hypoxic drive that drives her respiration -> Can lead to respiratory depression - CO2 can continue to build up and you get more CO2 retention
What would you see in spirometry for restrictive lung dx?
- Increase in FEV1/FVC ratio and Decrease in both FVC & FEV
What are some of the health benefits of coherent HR variability?
○ Less risk of death–decreased morality rate ○ We see improvements in cardiovascular morality for HR variability
What happens to partial pressure of O2 at high altitude? - hemoglobin at acute, 72 hrs, and a couple weeks later? - hemoglobin sat curve - Erythropoietin
- Decreases bc barometric pressure has decreased - Minute ventilation increases across all 3 of them bc you have a lower partial pressure gradient of oxygen - Initially shifts LEFT bc you’ve lost O2 & there’s more CO2 there so you get the Left shift -> After 72 hrs & a couple weeks it shifts RIGHT bc you have an ↑ in 23-BPG - Erythropoietin → ↑RBC production after 72 hrs & in a couple weeks → more ability to have unloading to the lower partial pressure
Diffusion of oxygen - normally? - high altitude
- O2 is perfusion limited meaning that the partial pressure of O2 quickly equilibrates into the blood of that capillary - diffusion limited bc you don’t have that partial pressure gradient in there
Small Cell carcinoma - risk factors - molecular pathogen - morphology - typical location - prognosis and treatment
- smoking - TP53, RB, MYC - small round tumor with scant cytioplasm, high mitotic activity, lots of necrosis - central or peripheral - really bad, chemo/radiation
Adenocarcinoma - risk factors - molecular pathogen - morphology - typical location - prognosis and treatment
-smoking - gain of function mutations in growth factor receptors, TK family - many patterns with common theme glandular or mucinous - peripheral - bad, surgery targeted therapies
Squamous Cell carcinoma - risk factors - molecular pathogen - morphology - typical location - prognosis and treatment
- smoking - TP53, CDK2NA, RB - Sheets of squamoid cells and sometimes with keratinization - central - surgery/radiation if extensive
Squamous cell carcinoma
It looks like skin.
You’ve got intercellular bridges, squamous pearl, keratinized cell
- what is this?
- differentiation
This is a less well differentiated squamous cell carcinoma
This is a moderately differentiated
The squamous pearls go away, you start getting these little holes that would fool you into thinking “oh could this be an adenocarcinoma” but he would still call this a squamous, you’ve got this jigzaw puzzle look, but its not always as clear cut
What is this?
Adenocarcinoma bc its making glands
This is what an adenocarcinoma should look like
What are these?
- pattern at upper right
- Adenocarcinoma of the lung has many faces
- lepidic pattern you’ve got these strx that look like alveolar septa and you’ve got these tumor cells that are just lining up and the stick out like little thumbs
- very well differentiated pattern and when that is all you see w/o tissue invasion, that used to be called bronchoalveolar carcinoma, it is now considered an in situ lesion if that is all you have
What is this??
- specific features
- small cell carcinoma
- soft tumor cells and they press up against each other and they take on the shape of the cell next to them
Carcinoid Syndrome
- what does it cause?
Characterized by intermittent attacks of diarrhea, flushing, and cyanosis.
What’s the difference between a carcinoid and an atypical carcinoid?
Typical is a lot less pleomorphic, have less mitotic activity, don’t metastasize as much, don’t invade lymphatics, and they’re non-necrotizing
What do carcinoids look like under the microscope
Under the microscope, typical and typical carcinoids look kind of like an adenocarcinoma except they’re really bland and boring looking, so they’re carcinoma-like carcinoids
Neuroendocrine tumors
- occur?
- what does it look like?
- immuno stain
- can occur anywhere in the body
- ugly large tumor
- neuroendocrine markers will light up, so that’s what puts it in the neuroendocrine box
Carcinoid prognosis
- typically curable, behave in a benign fashion , can still metastasize
What are these?
- Top left; description?
- Top right; description
- Bottom left; how do you know?
- Bottom right; description
- Top left: carcinoid- Very bland cells; they’re classically described as being in nests, can be in tubules, in rosettes, or rings
- Top right: atypical carcinoid- This is a little bit uglier and you’re starting to get more mitotic activity, and the pink stuff is necrosis; We literally start counting mitotic cells per high-powered field and we can get to atypical carcinoid
- Bottom left: large cell neuroendocrine carcinoma, It’s getting really ugly, but the cells are still kind of big and we throw our neuroendocrine markers on; You can’t get to large cell neuroendocrine carcinoma by just looking through a microscope, you have to do a bunch of studies to prove that it’s not only a large cell carcinoma, but that it’s in the neuroendocrine family of tumors, and we have tests to do that
- Bottom right: small cell carcinoma; Very scant cytoplasm and nuclei mold into each other.
What type of epithelium lines the respiratory tract?
Ciliated Pseudostratified columnar
Most typical precursor lesion of…?
- squamous cell carcinoma
- adenocarcinoma (2)
- pulmonary carcinoid tumors
- squamous metaplasia w/ or w/o squamous dysplasia
- atypical adenomatous hyperplasia and adenocarcinoma in-situ (bronchoalveolar carcinoma)
- diffuse idiopathoc pulmonary neuroendocrine cell hyperplasia
How do you get squamous cell carcinoma from psuedostratified ciliated columnar cells?
- which cells are affected?
- metaplasia: change from one cell shape to another
- basal cells change; in the epithelium there’s supposed to be ciliated columnar cells, but for whatever reason due to irritation, the reserved cells at the basal layer start turning off the ciliated genes and turning on the squamous genes
why might metaplasia of any kind, if it’s not neoplastic and nothing abnormal has happened here, why might it be a precursor lesion?
You’re turning genes on and off, and you’re messing with the DNA. You’ve unfolded the DNA and you’re messing with it. That is fertile soil for something bad to happen. Because neoplasia occurs from wrong genes turn on, or genes mutate
What should squamous dysplasia look like?
- are there mutations?
- Disordered squamous epithelium
- yes, lots
bronchoalveolar carcinoma
- now known as adeno carcinoma in situ (AIS)
- usually seen on the periphery of more conventional adeno carcinomas under the microscope
- patient will probably still get a lobe-ectomy and when the lobe come out we are going to look at a whole bunch of areas of this tumor and we are going to find the area of invasion. If we don’t find an area of invasion and we are convinced we have thoroughly sampled then we may make a diagnosis of BAC.
What is happening in each stage??
A:
Ciliated epithelium
Entire respiratory track should be lined with this, except for a few areas like the larynx
B:
Squamous metaplasia
Looks like skin–> well actually mucus membrane because it doesn’t have the dead layer on the top
Normal squamous epi (mature)
Between A and B there is transitional layer immature squamous metaplasia (this is something for a pathologist to worry about, not us)
C:
Nuclei on the bottom are getting bigger and a little darker-> immature nuclei a little further up
D:
Similar to C but a little more
E:
A whole lot of ugly
F:
Completely disorganized all the way through
Some people say full thickness dysplasia but this is misnomer because this is full thickness immaturity
Dysplasia is present in all the cells even before immaturity is seen in all the layers because the mutation is already present in C the cells just have a greater ability to still mature than the cells in E
What is this?
Adenocarcinoma- invasive
What is this?
- neoplastic cells that are lining these alveolar septa that is atypical adenomatous hyperplasia
- When these become confluent, a continuous line of these neoplastic cells that are lining the alveolus but not invading anything that is adenocarcinoma insitu also know as bronchial alveolar carcinoma
These cells are called Hobb nail cells
What is this?
Idiopathic neuro endocrine hyperplasia
Paraneoplastic syndromes
- 60 yr old male w/ lung mass with decreased Na and decreased urination
- 56 yr old woman w/ lung mass with post menopausal bleeding
- 62 yr old man w/ lung mass and hypercalcemia
- Syndrome of inappropriate ADH –> Most associated with small cell carcinoma
- Syndrome causing increased estrogen –> not usual but can cause post menopausal bleeding
- Increased parathyoid hormone -> common with squamous cell carcinoma
Is carcinoid syndrome a paraneoplastic syndrome?
YES
buzz words for Asbestos
Ship-building and commercial construction
DDX for asbestos
Mesothelioma or Bronchogenic Carcinoma
Statistically speaking, is mesothelioma or bronchogenic carcinoma more common?
- lung cancer
Mesothelioma
- histological subtypes
- most typical mutation
- immuno stain
- what do pathologists look for?
- Epitheliod and sarcomatoid
- CDKN2A/INK4a
- cal retnin that will light up mesothelioma but not cancer cells
- invasion of fat and lighting up with this stain in order to dx
1st test on pleural fluid out of a female and there are tumor cells in it
- Test for breast CA
