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352 Cards in this Set
- Front
- Back
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what is different about the R bronchus?
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more vertical therefore aspirations will empty into this bronchus
the left bronchus is a differnt angel |
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what size particles will enter the nasopharynx? lower resp tree? alveoili?
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nasopharynx: >5microns
lower resp tree: 3-5 alveoli: <2 |
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what is classic respitory epithelium?
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pseudostratified columnar
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what epi will you find in the vocal cords?
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stratified squamous
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histologically, how will the bronchus appear?
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ring of hyaline cartilage plus sero mucus glands
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compare bronchus with bronchioles?
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bronchus: ring of cartilage with sero mucus glands
bronchioles: NO cartilage |
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what happens to the epi in bronchioles?
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becomes less like pseudo
colm/cuboidal epi |
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what are the cellular components of blood air barrier?
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alveolar lining cells (95% type I, 5% Type II)
capillary endothelial cells occasional interstitial cell and alveolar macrophage |
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what is the area/connexn b/n alveolar spaces?
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Pores of Kohn
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normally the lungs bud off wht?
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foregut tehrefore can have agenesis or hypoplasia that is seen w/ compression during congenital state (potter seq)
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is pulmonary hypoplasia common?
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yes
seen in 10% neonatal autopsies |
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what is the most common type of tracheoesphageal fistula?
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esophagotracheal fistula: blind esophagus with the distal esophagus connexted to trachea
surgical correction b/c of rapid damage that could occur |
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what is a congenital foregut cyst? where do you normally see this?
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detached section of maldeveloped foregut located at mediastinum and hilar areas normally
NOT connected to airways consists of cystic spaces up to 5cm mimicing tumor |
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when do congenital foregut cysts present? what are they lined with?
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present in adulthood as mass
lined with resp epi: bronchogenic and filled with mucin |
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what is a bronchopulmonary sequestration?
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congenital lung disease
area of lung not connected to airways with blood supply from systemic arteries |
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what is a extralobar bronchopulmonary seqestration
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found in thorax or mediastinum
EXTERNAL to lung Dxed as mass lesions solid, NOT cystic Extralobar = External |
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what is a intralobar bronchopulm seqestration and where do you find them?
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intralobar
w/n lung associated with recurrent infxn most likely an aquired lesion |
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bronchopulmnary sequestrations are usually in Right or Left lungs?
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Left sided
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compare intralobar and extralobar bronchopulmonary sequestrations
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intralobar: solid, aquired, w/n pulmonary parenchyma, no bronchial connexn
extralobar: spongy, not w/n lung, no bronchial connxn, seen early |
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waht supplies bronchopulmonary sequestratoins ?
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systemic arteries
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what are the 3 ways in which atelectasis can occur in adult?
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acquired collpase-common
1. resorption: mucus, foreign body, tumor, aspiration of peanut 2. compression: tension pneumothorax 3. contraction usually b/c fibrosis |
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in a airway collapse due to resorption, in which way does the mediastinum shift?
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toward area of abnormality
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in an airway collapse due to compression, in which way does the mediastinum shift? in a contraction?
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away
no shift in contraction |
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in atelectasis, is the airway aerated?
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no, not anymore b/c of colapse
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what is the most common cause of linear atelectasis?
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diaphragm
afraid to take deep breath in *will see this on basal surface of lung |
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what is happening in tension pneumothorax?
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compression atelectasis
life threatening chest wall puncture when try to exhale, air won't escape cuasesing pressure to bulid up causing lung to collapse |
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what can acute lung injury progress to?
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ARDS (DAD) or AIP
most acute lung injury is short lived acute injury can be due to congestion, edema, surfactant disruption, atelectsis |
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what are the 2 types of pulmonary edema?
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hemodynamic :most common
microvascular (alveolar injury): leakage of protein rich fluids |
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what is happening in hemodynamic pulmonary edema?
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increased hydrostatic pressure b/c of Left heart failure
occurs mostly in lower basal lobes b/c of gravity hallmark histologically: heart failure cells; macrohage mopping up RBC therefore have Fe in them |
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what is happing in terms of pressure in pulmonary edema?
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increasing hydrostatic pressure
decresed oncotic presure increasd vascular permeabilty |
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microvascular injury that causes pulmonary edema can lead to what?
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ARDS/DAD
fluid and protein leakage |
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what are teh 4 big cuases of ARDS/DAD?
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diffuse pulm infxn
gastric aspiration sepsis trauma **not releated to surfactant defi as in newborns |
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what is the onset and severity of Adult Acute Resp Distress syndrome/ diffuse alveolar damage?
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rapid onset
life threatening in pts with severe disease all cuases have diffuse damage to alveolar cap walls which lead PMNs inside |
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what plays a key role in ARDS?
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PMNs
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what do we see in an ARDS alveoli?
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proteinaceous fluid
necrotic type I cells PMN sequestration and migration into alveoli hyaline membrane fomation IL-1 and IL-8 activated |
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clincally how does ARDS present? what does it progress to? mortality rate?
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rapid onset
in pts who are already ill after intial nl CXR progresses to diffuse bilateral infiltrates high mortality, 60% permanet damage |
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what is the most commonly used pulm diagnostic sampling technique?
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thorascopy, video assisted
invasive but benign way to get tissue |
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ARDS-Diffuse Alveolar Damage is called this because of?
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hyaline membranes: protein condensed on alveolar walls
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what lung disease is similar to ARDS?
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acute interstitial pneumo (AIP) but there is no associated causative disorder unlike ARDS
think of AIP as Idiopathic ARDS |
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waht is idiopathic ARDS?
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AIP
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age, mortality for AIP?
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50 yrs
M=F >50% mortality rate, usually w/n 2 months (very serious) **no underlying cause progres rapidly, white out, cyanosis |
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compare obstructive and restrictive lung disease?
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obsructive: limit rate of flow (low FEV) due to resistance:problem = air flow
restictive: low TLC and RV, normal flow rate; problem = lung capacity, stiff |
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ex of obstructive disease? restictive?
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obstructive: emphysema, bronchitis, asthma
restrictive: chest wall disorder, obesity, ARDS, interstital fibrosis (infxns) |
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what are the 4 main categories for COPD?
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Bronchiectasis
Asthma chronic Bronchitis Emphysema |
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what are the 2 forms of emphysema and which is more common?
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centriacinar/centrilobar >95%
Panacinar/panlobar 2-5% |
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where is centrilobar/centriacina r emphysema located and waht is it due to?
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smoking
predom upper lobes/ apices |
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panacinar/panlobar emphysema is found where? what is it due to?
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predom lower lobes/anterior
alpha 1 antitrypsin def, defintely smoking |
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what is emphysema due to?
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proteolytic digestions of alveolar walls
alpha Anti trypisin major anti-protease, but in emphysema this is inactivated causing an increase in neutrophil secreted elastase |
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when do persons with a genetic alpha 1 antitrypsin deficiency (PiZZ) develop emphysema?
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young
made worse with smoking |
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waht is the primary villian of emphysema?
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neutrophil secreted elastase: turned off proteases allow PMN elastase to cause damage
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waht are the clinical symptoms of emphysema?
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as airspaces enlarge expiration is difficult
barrel chest dyspnea, LOW FEV1, high TLC, High RV forward leaning in attempt to squeeze air out pink puffer |
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who is called pink puffer and why?
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emphysema pts
still have gas exchange, but have to breathe a lot b/c expieration is difficult |
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what is obstructive overinflation?
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overexpansion be/c of trapped air
ball valve obstruction by object or collaterals feeding around obstruction, life threatening |
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what can bullous emphysema cause?
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spontaneous pneumothorax
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what is considered chronic bronchitis? what is it related to?
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3 months of productive cough/year for 2 consecutive years
smoking! hypersecretion of mucus hypertrophy of bronichial submucusal glands(increaed Reid index) |
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what lung disease is this referring to: hypersecretion of mucus, hypertrophy of bronchial submucosal glands (increased Reid), cor pulmonale, gas exhange impaired?
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chronic bronchitis
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who is referred to as a blue bloater?
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chronic bronchitis pts due to impaired gas exchange with cyanosis : abnormalities in bronchi, no air in distal alveoli
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what is the reid index? in what diesease is it increased?
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the ratio of the thickness of mucuos glands to wall form epi to cartilage
chronic bronchitis |
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is dyspnea more severe chronic bronchitis or emphsyema? which do you see corpulonale?
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emphysema-sever dyspnea
bronchitis: cor pulmonale |
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when is asthma most often? what is the problem?
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most often night, early morning
reactive airpace disease with episodie (brief attacks) bronchoconstriction |
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describe the incidence of asthma? is it due to smoking at all?
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increasing in western society (are we too clean?)
not due to smoking |
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waht is atopic asthma and when does it begin?
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genetic tendency to develop IgE antibodies to inhaled allergens
begins in childhood |
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what is happening in atopic asthma?
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mucosal mast cells react releasing inflammatory mediator
stimulation of subepithelial vagal R's (PNS) provokes bronchoconstriction bronchial smooth muscle constricts |
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what is nonatopic asthma associated with?
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pulmonary infxns mainly viral
no allergic indicators |
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what is drug induced asthma?
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classic cause is aspirin
it inhibits COX and thus shunt arachidonic acid to lipoxygenases |
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overinflated lungs
over prodxn of thick mucus eosinophils in inflammatory bronchial wall infiltrates hypertrophy of submucusal glands and smooth muscle and goblet cell hyperplasia? |
asthma
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what is happening in asthma at the cellular level?
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eosinophils
thick/overprodxn of mucus goblet cell metaplasia smooth muscle thickening mast cells |
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in which lung disease do you see smooth mm hypertrophy and fibrosis along with mucous plug?
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asthma
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what is the hallmark of asthma?
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eosinophils, mast cells
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waht are the 3 things you look for in the sputum of asthama pt?
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charcot leyden crystals
curschmann spiral (mucus plug) eosinophils |
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what is bronchiectasis?
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permanent dilation of bronchi and bronchioles caused by tissue destrxn 2nd to infxn
associated with CF, obstruction, and many infxns |
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what lung condition is associated with CF, obstructions, and many infxns?
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bronchiectasis
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diffuse interstial lung diseases involve what part of lung? what is the end stage of these diseases?
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involve interstitium and alveolar walls (see expansion)
end stage: honeycomb lung |
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what are some resrictive disorders of unknown cause?
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nonspecific intersitial pneumo
COP/BOOP Sarcoidosis Pulm eosinophilia |
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what are some restricitve disorders of known cause?
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pneumoconioses
therapy related fibrosis |
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waht is the classic restrictive disease of unknown cause?
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IPF: Idiopathic Pulmonary Fibrosis
injury to alveolar wall (alveolitis) type I pneumocyte death type II hyperplasia collagen deposition |
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what is the hallmark of Idiopathic Pulm Fibrosis? clinically how will it present?
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collagen deposition
insidious dyspnea, dry cough mean survival 3 years |
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waht is the survival for IPF?
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3 years
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in idiopathic pulm fibrosis, what do you have repeated cycles of ? what is the end stage?
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repeated cycles of alveolitis with hypertrophy and hyperplasia of type II
end stage: honeycomb lung |
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where will you see the changes first in idiopathic pulmonary fibrosis?
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subpleural see fibrosis
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what is the appearance of a honeycomb lung?
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seen in end stage IPF
fibrotic-thick can't collapse down |
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what is nonspecific interstial pneumo and how does it compare to IPF?
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wastebasket term
not as sick as IPF better prognosis |
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what does COP stand for and why?
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Cryptogenic Organizing Pneumo b/c freq unknown etiology
organizing= al the connective tissue of same age and no interstial fibrosis so does not progress to honeycomb lung |
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does COP progress to honeycomb lung? what do you use to Tx?
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will not progress to honeycomb lung b/c tissue is of SAME stage and no interstial fibrosis so does not progress to "honeycomb lung"
will respond to oral steroids |
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thin alveolar walls
all connective tissue is same age waht does this describe? |
COP
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what is a common collagen vascuar disorder?
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RA (30-40% have abnormal pulmonary fxn tests)
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in which conditions will we see follicular bronchiolitis and what else will we see?
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RA related lung disease
w/ chronic inflammatory cells also see rheumatoid nodule and honeycomb lung when end stage |
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what is the most dangerous particle size in environmentally related lung diseases?
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1-5 microns
also the amount/volume matters |
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what are the 4 Pneumoconiosies?
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coal workers pneumoconioses
asbestos silicosis berylliosis |
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is coal workers pneumoconiosies severe?
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no usually benign disease
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currently, what is the most prevalent chronic occupational disease in the world?
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silicosis
occurs in sandblasters and miners |
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what is the progression of silicosis like and what is happening?
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slowly progressive
silica ingested by macrophages and kills see inflammatory response with release of TNF that stimulates fibroblasts |
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when considereing silicosis, what should you do?
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1st look under polarized light: see birefringment silica particles
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what will silicsis look like histolgicallly?
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scattered silicotic nodules
dense center |
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what are amphiboles?
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brittle asbestos that is harmful
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where does asbestos normally occur in the lung? what diseases are related to asbestos?
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fibrotic lung disease that begins in lower lobes and subpleurally
common: pleural plaques mesothioloma lung cancer (more common than mesothioloma) |
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a smoker exposed to asbestos is more likely to get what disease?
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lung cancer than mesothilioma
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what do asbestos bodies look like?
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brown b/c of coating of Fe and protein
with iron (prussian) stain see "q tip" amphibole fibers |
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typical calcified pleural plaques are diagnostic of ?
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asbestos exposure
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which disease of unknown origin is characterized by the formation of numerous non-caseating granulomas?
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sarcoidosis
however, the granulomas are diagnosis of exclusion: when we find granulomas we stain for organisms b/c not always sarcoidoss |
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what are the levels of CD4, IL2 in sarcoidosis?
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increased CD4
increased IL-2 and cytokines may suggest a poorly degradeable antigen |
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what percent of sarcoidis pts recover?
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65-70% *majority recover
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what histological findings are associated with sarcoidosis but not diagnostic?
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asteroid body
schaumann body |
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where do hypersensitivity pneumonitis develop?
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unlike asthma it occurs at alveolar level (asthma is a central bronchiole disease)
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what will you see in distal lung of hypersensitivity pneumonitis?
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noncaseating granulomas
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waht is desquamatative intersitial pneumonia (DIP)? and who does it occur in? what will cure it?
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large collections of macrophages in alveoli that were initially thought to be desquaumated epi cells
greater than 50y.o males steroids and cessation of smoking curative |
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desquamatative intersitial pneumo
pulmonary Langerhans cell histiocytosis Respiratory bronchiolitis associated lung disease are all related to waht? |
cig smoking
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birbeck granules?
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Pulmonary langherans cell histiocytosis
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whhat will you see histologically in resp bronchiolitis associated interstitial lung disease (RBILD)
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pigmented macrophages in BrONCHIOLES (not in alveolar space like in DIP-desquamative interstitial)
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histologically, what does Pulmonary Alveolar Proteinosis look like and what are the 3 classes?
|
accumulation of ACELLULAR surfactant in the intra-alveolar and bronchiolar space
Aquired (90%) 20-50y/o Congenital (rare) FATAL |
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in what age range will you see pulmonary alveolar proteinisis? is it serioius?
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20-50y.o
Congential is fatal |
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what is there an accumulation of in pulmonary alveolar proteinisis? how do you treat?
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acellular surfactant
pulmonary lavage: wash out lungs w/ saline like soln |
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what is a significant cause of sudden death (>50K/yrUS)?
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pulmonary embolism
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where do thrombi of pulmonary embolisms form?
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most often in deep leg veins in pts with underlying conditions and/or immobilized
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is pulmonary embolism over or underdx?
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underdx
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why do only a small percentage of pulmonary embolisms result in infarction?
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only 10% b/c of the dual supply to the lung
clot in leg breaks free travels to the systemic vv and then to Right heart, it is then lodged in pulm artery |
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pulmonary embolism dx is made by?
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lung scan V/Q
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what will a Q scan show if there is a pulmonary embolism?
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area won't be purfused see wedge shaped abnormality but when you do a V scan it will appear filled in b/c it is only a problem with Q
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fat emboli are normally due to?
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trauma ex: car accidents
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when is pulmonary pressure abnormal?
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normally low pressure system
abnormal when equals 1/4 of the systemic P |
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94% of primary or secondary pulmonary hypertension is idiopathic?
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94% of primary is idiopathic
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is primary or secondary pulm hypertension more commone?
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secondary
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who do we see primary pulm hypertension in?
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females 20-40
mostly idiopathic with rare familial form that is AD with only 20% penetrance |
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what is primary pulmonary hypertension due to?
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mutation in the bone morphogenic protein receptor type 2 (BMPR2) that normally inhibits proliferation and favors apotosis in vascular smooth muscle cells
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what protein is mutated in primary pulm hypertension?
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BMPR2 that normally inhibits proliferation of smooth mucsule
when mutated get pulm vascular thickenening and occulusion |
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is there a mutation involved in secnodary pulm hypertension?
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no
2ndary depends on normal rxn of pulmonary arteries to increaed pressure increaed pressure from any cause induces medial hypertrophy if increaesd pressure continues then hypertrophy narrows arteries to where the narrowing furter increase P |
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glomerulonephritis and hemorrhagic interstitial pneumo is seen in what syndrome?
|
goodpasture syndrome
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what is the cuase of Goodpasture? who do we see it in?
|
autoimmune, anti BM Ab
Males teens-20's |
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what is the most common cuase of death in goodpasture?
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renal failure
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how will goodpasture syndrome look with immunofluorescence?
|
linear appearance of anti BM Ab
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who does idiopathic pulm hemosiderosis occur in? what is it?
|
children
episodes of diffuse hemorrhage diffuse hemosiderin deposition |
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how will the lungs appear in idiopathic pulm hemosiderosis?
|
brown, firm, heavy due to diffuse hemosiderein deposition
|
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what is wegener granulomatosis?
|
necrotizing granulomatous arteritis of lungs
necrotizing glomerulonephritis |
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who is wegeners seen in?
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males
5th decade |
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what Tx is used for wegners?
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immnosupprussion
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most pulm infectious diseases are where and due to what?
|
upper tract
viral |
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what is the major cuase of mortality and morbidity in pulm infectious diseases?
|
lower tract pneumo
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what are the 2 basie types of bacterial peumo? which is the predominant type?
|
bronchopneumo
lobar pneumo bronchopnumo is the predominant type |
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lobar pnuemo is caused almost always by what?
|
pneumococcus but now rare b/c of effectivness of antibiotics
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when considering bacterial pneumo, what is the 1st thing you are concerned with?
|
first figure out what organism it is via sputum specimen or gram stain
then where it was aquired: community or *need to do a CXR |
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how can you tell the difference grossly b/n bronchopneummo and lobar?
|
broncho: involving more than 1 lung
lobar: entirely confined to 1 lobe |
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b/c strep pneumo is common in sputum of healthy, what must you see in association with the G+ dipplococci?
|
numerous acute inflammatory cells
|
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what are the stages of pneumococcal lobar pneumo?
|
edema to red hepatization to grey hepatization then to resolution
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atypical pneumo due to? typical?
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atypical: viral
typical: bacterial |
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to create a pulmonary abscess, need what?
|
a destructive organism like Staph aureus, many G- or anearobic org
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what sequalae aspirations?
|
pulmonary abscesses: alveolar wall eaten away
|
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what causes chronic pneumo?
|
Tb
Fungi |
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characteristic of primary Tb ifxn?
|
Ghon complex (parenchymal lesion + involved lymph node)
rarely Dx, not sick enough to present |
|
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what is characteristic of secondary Tb?
|
reactivation of walled off lesions, usualy apical
Miliary Tb |
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when does Miliary Tb occur?
|
when tubercle erodes into a vessel
|
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when the Ghon complex heals and calcifies it is known as?
|
Ranke complex
|
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Histoplasma capsulatum is found where? Coccidiodes? Blastomyces?
|
Histoplasma: Ohio River Valley
Coccidiodes: SW US Blastomyces: Central, SE US |
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how does Histoplasma appear on lungs?
|
present as discrete coin lesions
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what is true about the ppl living in southwest US?
|
80% have Ab to coccidiodes but have never had s/s unless immunocomp
|
|
|
what are the unusual diffuse pneumos seen in HIV?
|
pneumocystis jiroveci
CMV |
|
|
what are the unusual focal pneumos seen in HIV?
|
aspergillius
candida |
|
|
what are the hallmarkes of viral pneumonitis?
|
giant cells
|
|
|
localized abscess
fungal balls broad brr hyphae? |
aspergillus lung disease in immunocomp
|
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most lung tumors are?
|
malignant therefore anytime mass found in lung needs to be Dx
*benign neoplasms are uncommon |
|
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what are the most common cause of cancer death, M/F, USA ?
|
primary lung tumors
|
|
|
most who develop lung cancer ___
|
die from it (not true in breast cancer)
|
|
|
what is the 2ndmost common cancer in both genders in USA?
|
lung cancer
*but it is the #1 cause of mortality in both genders almost equal number of cases and deaths therefore it you get it you will die of it |
|
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what accounts for 90% of all lung cancer deaths?
|
cig smoking
|
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what percent of smokers get cancer?
|
only 20%
|
|
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what happens to your death risk when you stop smoking?
|
when you stop smoking your risk descrease over time
|
|
|
what are some environmental risk factors for lung cancer?
|
radiation
asbestos radon |
|
|
what are the 3 non small cell lung cancers?
|
SSC 25-40%
Adenocarcinoma (25-40%) Large Cell Carcinoma (10-15%) |
|
|
what is the neuroendorcine tumor that causes lung cancer?
|
small cell carcinoma
|
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which of the non small cell and small cell carcinomas are associated most highly with cig smoking?
|
SSC (98%)
Small cell carcinoma (99%) Large cell carcioma (93%) *all have central lesions adenocarcinoma is only 82% and is peripheral |
|
|
what is usually the presenting sign in lung cancer?
|
metastatic effects ex: R occipital lobe giving visual defects
|
|
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b/c mets is common in lung cancer, where should you look?
|
adrenals : not uncomon to see metastatic loci
|
|
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is metastastis common in lung cancer?
|
yes very common
check adrenals! |
|
|
if you see a central mass, what types of lung cancer can you consider?
|
small cell
SCC large cell |
|
|
how you can you tell the diff b/n SCC and small cell cytologically?
|
scc: keratinized cells
small: very little cytoplasm, nuclei jammed together"nuclear molding" |
|
|
central endobronchial growth
98% smokers keratinization may cavitate |
SCC
|
|
|
what are some precursor lesions see with SCC?
|
metaplasia
dysplasia carcinoma in situ |
|
|
central mass in lung with hypercalcemia?
|
always think SCC
|
|
|
keratinized strap cells
squamous pearl |
SCC
|
|
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who is adenocarcinoma of lung commmon in?
|
womean and nonsmokers
|
|
|
charactristics of adenocarcinoma of lung?
|
women and nonsmokers
more peripheral mucin prodxn common related to scaring "scar carinoma" |
|
|
zellballen with vacoules
mucin present w/n cells |
adenocarcinoma (not squamous perals
|
|
|
characteristics of Bronchioalveolar carcinoma?
|
70% smokers
very peripheral mutifocal/lobar and diffuse therefore difficult to Dx grow along alveolar septa, rare invasion |
|
|
which lung cancer grows along the aveolar septa?
|
bronchioalveolar: less associatied with smokers, unique presentation, less aggressive
|
|
|
small percentage of large cell carcinoma are actually..
|
neuroendocrine
|
|
|
99% smokers
neuroendocrine orgin very aggressive respond to chemo paraneoplastic syndomes |
small cell carcinoma
|
|
|
what Tx is used for small cell?
|
they respond well to chemo b/c all cells are dividing
|
|
|
what must you do if considering small cell in terms of biopsy?
|
take a deep biopsy b/c normally small cell will grow under squamous metaplatic epi b/c it arises from neural crest cells
|
|
|
nuclear molding
|
small cell carcinoma
|
|
|
prognosis for non small cell and small cell
|
non small: 5 yr survival
small: 2 yr survival (high stage-months survival) |
|
|
where does lung cancer mets to?
|
regional nodes
adrenals liver brain bone |
|
|
what do the lungs receive mets from
|
hematogenously and lymphatic from breast
GI sarcomas H/N melanoma *anything that spreads hemoatogenously |
|
|
if in pleura think?
|
metastasis most common esp lung and breast
|
|
|
what is calretinin stain used for?
|
malignant mesothelioma
|
|
|
what is the most useful gold standard for looking for microvilli?
|
EM (studies of pleural lesions)
|
|
|
dx gold standard for malignant mesothelioma?
|
microvilli via EM
|
|
|
what is fluid homeostasis?
|
maintainence of vessel wall integrity
maintianence of intravascular pressure and osmolarity maintianing blood as a liquid until injury when it becomes a clot |
|
|
edema definition?
|
increased fluid in the interstial space
|
|
|
what are teh 3 basic fluid compartments?
|
intravascular
interstitial intracellular |
|
|
RBC contribute to what volume?
|
intravascular volume therefore hardest to replace
give transfusions in acute hemorrhage to maintain volume |
|
|
hemorrhage definition?
|
presence of blood outside the intravascular space
|
|
|
bleeding def?
|
active process producing hemorrhage
|
|
|
clotting def?
|
physiologic process involved in forming an insoluble plug (clot) form platelets and fibrin
|
|
|
what makes a clot?
|
plateltes and fibrin
|
|
|
what is a thrombus?
|
clot that has pathologic consequences
|
|
|
what is anasarka?
|
severe generalized edema
|
|
|
what amt of fluid stays in interstitium and becomes lymph?
|
small amt: 2-4%
lymph carries fluid to LN |
|
|
nodes are impt in what
|
staging system
|
|
|
normally, as interstital fluid vol increases, what happens?
|
tissue lymphatics remove excess volume eventually returning it to the circuation via the thoracic duct
|
|
|
what happen when the ability of the lymphatics to drain the interstial tissue is exceeded?
|
persistant tissue acumulation of fluid occurs and edema results
|
|
|
what are the 2 basic causes of edema?
|
increased hydrostatic pressure
diminished plasma osmotic pressure |
|
|
what can cause increased hydrostatic pressure?
|
R heart failure: heart can't keep up with venous return
constrictive pericarditis lower extremity inactivity (on a plane) liver cirrhosis |
|
|
how can decreased plasma oncotic P effect the heart?
|
decreased plasma oncotic P-decreased blood volume- decreased CO evenutally leading to edema
|
|
|
what is pitting edema?
|
type of edema in which the skin surface, when pressed by a finger leaves an indentation which persists long after removal of the pressure
*accumulation of interstial fluid in tissues |
|
|
which is more common, upper or lower extremity edema?
|
lower
upper seen in more serious cases |
|
|
what is another name for reduced plasma osmostic pressure?
|
hypoproteinemia
|
|
|
what are some situations that cause hypoproteinemia?
|
nephrotic syndrome
liver cirrhosis malnutrition (don't make enough albumin) protein losing gastroenterophathy (not breaking down protein) |
|
|
ascites develops in ppl with what problem?
|
reduced plasma oncotic pressure (hypoproteinemia)
|
|
|
where is the common place to spot edema in kids?
|
face: periorbital edema usually in nephrotic syndrome
|
|
|
lymphatic obstruction is a cause of edema. how can lymphatics be obstructed?
|
inflammatory
neoplastic: tumor post surgical: removed for breast cancer; take LN out the lymph has no where to go postradiation: radiate axilla |
|
|
what is pulmonary edema?
|
water in lungs particularly alveolar spaces frequently due to leave heart failure
*medical emergency, high mortality |
|
|
if there is a exudate associated with inflammatory edema what does this indicate?
|
protein rich with specific gravity >1.020
|
|
|
if there is inflammatory edema with transudate what does this mean?
|
protein poor with specific gravity <1.012
|
|
|
the prefix Hydro- indicats waht?
|
fluid accumulation in body cavity: hydrothorax
|
|
|
what is the diff b/n hyperemia and congestions
|
hyperemia: active process resulting from arteriolar dilatation (red skin when embarrased)
congestion: accumulation of deoxy Hb (blue-red color) by CO poisoning |
|
|
hyperemia leads to?
|
erythema: flushing due to increased inflow engorgement with oxy blood
|
|
|
congestions results in?
|
cyanosis: dimished outflow leads to a capillary bed swollen with deoxy venous blood (due to local obstruction or congestive heart failure)
|
|
|
in both hyperemia and congesion there is what?
|
1. increased vol and pressure of blood in a given tissue
2. associated capillary dilation and potential fluid extravasation |
|
|
a liver with chronic passive congestion can look like waht?
|
nutmeg liver
|
|
|
what is this: extravasation of blood outside the confines of the intravascular space ?
|
hemorrhage
freq due to vssl rupture caused by trauma or b/c of loss of vascular integrity b/c of erosion of endothelium |
|
|
what is the key to stopping bleeding?
|
direct pressure-induce stasis
|
|
|
what is bleeding diatheses?
|
tendency for severe bleeding even in response to insignificant injury b/c of deficients in the normal clotting mxns
|
|
|
what is a hematoma?
|
accuulation of blood w/ a tissue frequently as a localized mass
|
|
|
is an external hemorrhage subject to tamponade?
|
yes, external= wound to skin
|
|
|
is an internal hemorrhage surbject to tamponade?
|
some: not subject to tamponade: GI tract, rupture liver or spleen
subject to tamponade: retroperitoneal space, intracranial |
|
|
what are petechiae?
|
1-2mm punctate hemorrhages into skin, mucous membranes or serosal surfaces; freq associated with thrombocytopenia
|
|
|
what are purpura?
|
3mm or greater areas of hemorrhage in same location as petechiae
|
|
|
ecchymoses ?
|
large (1-2cm) subcutaneous hematoma seen after trauma which "changes color" as the hematoma clears
-red to blue green to gold brown -bruises |
|
|
who are ecchymoses common in?
|
pts on anticoagulants that lack sub cut tissue (elderly)
|
|
|
what is the percent of blood loss that is acute in healthy adults and tolerated before hypovolemic symptoms such as hypotension appear?
|
less than 20%
|
|
|
1 unit of blood loss is equal to how many ml what percent of loss in 140lb person?
|
1 unit blood = 500mL
10% acute loss |
|
|
when does clinical shock from blood loss become apparent?
|
at 30% loss or greater (3 units)
|
|
|
what is considered chronic blood loss?
|
300-400mL/day
eventually can't make enough RBC which leads to anemia |
|
|
what are some additional factors that affect clinical findings related to hemorrhage?
|
body site: small amts of hemorrhage (200-400ml) can have severe consequences in intracranial sites or w/n pericardial sac or upper/lower GI
Cause of hemorrhage |
|
|
what are the 3 major components involved in hemostasis?
|
blood vssl: endothelial cell
platelets coagulation cascade (fibrin prodxn) |
|
|
what are the 5 steps of hemostasis?
|
1. endothelial injury-vssl injury
2. clot intiations and formation: primary hemostasis 3. clot propogation and stabilization: secondary hemostasis 4. clot inhibition and cessation: antithrombic activity 5. clot dissolution: fibrinolysis |
|
|
what is the prothrombotic role?
|
the intact endothelial cells of the vssl immediately adjacent to the injury promote the formaiton of clot
|
|
|
what components are prothrombus?
|
thromboxane A2: vasoconstrictor
vWF: allow platelets bind collagen thromboplastin/tissue factor coaguation factors |
|
|
what components are antithrombic?
|
prostaglandin-vasodilator
protein C and S: S is the precursor for C thrombomodulin: activates protein C TPA: plasminogen becomes plasmin heparin-like molcules bind circulating antithrombin 3 |
|
|
what makes vWF?
|
endothelial cells which is released both into circulation and to the subendothelial surface
|
|
|
what is tissue factor and what is its role?
|
tissue factor made by endothelial cells that is released when endothelilal cells are damaged.
tissue factor activates extrinsic portion of the clotting cascade and intrinsic factor 9 |
|
|
what procoagulant activates extrinsic factor?
|
tissue factor
|
|
|
endothelial cells secrete what that is antifibrinolytic
|
secrete inhibitors of activated plasmingoen (PAI's) which prevent dissolution (fibrinolysis of clots)
|
|
|
waht do heparin-like molecules combine with
|
combine with circulating antithrombin III to form a molecular complex that activates circulating IIa (thrombin), IXa and Xa
|
|
|
action of thrombomodulin
|
surface thromboodulin with thrombin to form a molecular complex that converts circulating Protein C into activated protein which is a potent inhibitor of Va and VIIIa
|
|
|
job of vWF?
|
signal platelets to attach w/o it nothing for platelets to recognize
made by subendothelial cells |
|
|
what allows aggregation of platelets?
|
platelts link via fibrinogen bridges bound to platelet GpIIb-IIIa R's
|
|
|
activated platelets release what?
|
ADP (potent stimulus for platelet aggregation) and thromboxane A2 both for vasocontriction and platelet aggregation
|
|
|
job of fibrin
|
glue for platelets to stay and stabilize clot
|
|
|
how do you stabilize the clot?
|
fibrin cross-linking stabilizes the fibrin-platelet clot
|
|
|
what happens in coagulation?
|
formation of insoluble structural protein, fibrin, from circulating proteins in the blood to form a coagulum which along with plateltes forms a clot and if the clot is large with clinical sequallea other than just hemostasis then the clot is termed a thrombus
|
|
|
what factors are part of the common pathway? extrinsic? intrinsic
|
10, 5, 2, 1: common
7: extrinsic 12: intrinsic |
|
|
what are the fibrin split products
|
D-dimers
|
|
|
which clotting pathway is activated first?
|
extrinsic
then intrinsic pathway and used to amplify fibrin prodxn at least 100fold |
|
|
prothrombin is factor what? thrombin is factor what?
|
prothrombin: Factor2
thrombin: Factor 2a |
|
|
action of Xa?
|
converts factor 2 (prothrombin) to factor 2a (thrombin)
|
|
|
what is assembled on the phospholipid surface of platelets?
|
factor IXa, Factor X and F8a
|
|
|
first step of hemostasis?
|
vasoconstriction: injury to endothelium
-transient vasoconstrxn by endothelin which leads to stasis -tissue factor released which stimulates F7 -collagen exposure stimulates F12 |
|
|
2nd step of primary hemostasis?
|
platelets adhere to exposed ECM via vWF and are activated
release ADP and thromboxane A2 lead to further platelet aggregation to form the primary hemostatic plug (platelets bound via soluble fibrinogen) |
|
|
what is the 3rd step of hemostasi?
|
secondary hemostasis-coagulation
need platelets to come together b/c occurs on surface of platelets activation of coagulation cascade results in insoluble fibrin polymerization, "cementing" platelets into a definitive 2ndary hemostatic plug |
|
|
waht is the 4th step of hemostasis?
|
thrombus and antithrombytic events
release of tPA, thrombomodulin by neighboring endothelium which limits the hemostatic process to the site of injury |
|
|
protein C and S inactivate what?
|
V a and VIIIa
|
|
|
antithrombin inhibits and deactivates waht?
|
activated forms of 9, 10, 11, 12
|
|
|
how do you initiate fibrinolysis?
|
activate plasminogen to form plasmin: plasmin is the active enzyme that degrades fibrin in soluble fragments (D-dimers)
|
|
|
what is the problem in vWF disease?
|
deficit in platelet plug: lack of adhesion
noral platelets but not enough-quantititive problem |
|
|
what is a qualitative platelt problem?
|
enought platelts but they don't work
lack of aggregation so cannot form effective plug uremia aspirin Glanzmann thromasthenia Bernard-Soulier syndrome |
|
|
if you have vWF disease what also might you lak?
|
circulating F8
|
|
|
what is the most common congenital bleeding disorder in humans?
|
vWF disease
1/100 1% in US population AD |
|
|
type I and 3 vWF disease make up waht percent of vWD? due to waht?
|
70%
decresed quanitiy of circulating vWF decreaed F8 ability mild bleeding |
|
|
type 2 vWD? waht percent? what is the problem?
|
25% vWD
QUALITATIVE defect in vWF (type 1 and 3 are quanitity problem) nl F8 circulating pletny of vWF but doen'st work well |
|
|
primary hemostasis is a problem with? secondary hemostasis is a problem with?
|
primary: problem w/ platelets
secondary: problem w/ formation of fibrin |
|
|
what is the most common anticaogulation cause of bleeding?
|
coumadin
|
|
|
what are some common acquired factor deficiencies?
|
washout from massive hemorrhage: lose clotting factors when you bleed
hepatic failure-can't make all factors to produce fibrin *both problems of secondrary hemostasis: fibrin prodxn problem |
|
|
if you have diffuse bleeding, you dont' have enought of what?
|
fibrin
|
|
|
what are the 2 uncommon cascade factor defiencies?
|
Hemophilia A: factor 8
Hemophilia B: factor 9 (1/10 as common as A) rare: hemo C: factor 11 |
|
|
Hemophila A result in what?
|
decreased syn or impaired fxn of factor 8
|
|
|
do pts with Hemo A blled from cuts?
|
dont bleed from cuts bc nl platelet fxn b/c they make enought fibrin to control small cuts
problem bleeding is b/c of surgery, trauma |
|
|
what are some clinical manifestation of classic hemophilia?
|
joint and muscle bleeding
traumatic, operative and post op bleeding easy bruising minimal bleeding from small cuts* |
|
|
what is the pathologic process opposite to hemostasis?
|
thrombosis: inappropriate activation of nromal hemostatic process b/c of endothelial injurty plus initial platelt participation is a prereq
|
|
|
what is a clot that has consequences other than just acting asa hemostatic plug? what does it lead to
|
thrombus
leads to alteration of normal blood |
|
|
waht is a thrombus?
|
a clot with patholgical sequelae: edema, tissue ischemia, infarction, embolism
|
|
|
what re the components of the Virchow triad in thrombosis?
|
endothelial injurty: most impt factor
abnormal blood flow hypercoaguability abnormal blood flow and hypercoag can be caused by endothlal injruty |
|
|
waht are some expampes of injury of endothelium?
|
endocardial injury due to MI
ulcerated plaques trauma vasculitis |
|
|
alteration of normal blood flow can result from/
|
turbulence: on arterial side
stasis: developing venous thrombi |
|
|
what are some clinical conditions associated with stasis?
|
aneurysms: dissection of wall
noncontractile portions of endomyocardium following infarct left atrium dilatation atrial fib hyperviscosisty syndrome prolonged bed rest *economy class syndrome: sittin on plane for 12hrs |
|
|
what is a hypercoaguable state? mxn?
|
increased propensity to clot
inability of individuals to stop or inhibit the activated clotting cascade..Failure to stop clot formation |
|
|
what tissue is responsible for stopping the clot?
|
normal adjactent tissue therefore activated thrmobomodulin to stop thrombin on NOrMAL endothelium
|
|
|
waht are some natural anticoagulants:
|
protein C and S: inactivate F5a and 8a
plasminogen and plasmin |
|
|
waht is thrombophilia?
|
hypercoaguability
|
|
|
waht are the primary (genetic) causes of hypercoaguability?
|
mutations in F5: Factor Leiden
|
|
|
what is a blood clot (plateltes + fibrin) larger than a hemostatic plug?
|
thrombus with patholgical sequelae: obstruct or alter blood flow distal to its location
fragmentation of the thrombus that rsults ina protion of the thrombus traveling to distant sites (emoblus) and causes obstruction |
|
|
what do you acall a thrombus that forms in cardiac chambers and aorta?
|
mural thrombus
|
|
|
wha do you call a thromus that forms in cardiac valve leaflets and cusps?
|
vegetations
|
|
|
waht do you call a thromus that forms in blood with localization to arterioles and capillaries?
|
microthrombi
|
|
|
what is a mural thromus?
|
thrombu that forms in cardiac chambers or along the aorta (aneurysm) where the thrombus has a Mass appearance
|
|
|
what do mural thrombi exhibit on cross section?
|
lines of Zahn
|
|
|
what are lines of Zahn?
|
alterating layers of fibrin clot fund in mural thrombi
alternating pink bands (platelets + fibrin) and red bands of RBC |
|
|
what are the 3 thrombus associated with heart valve abnormalities?
|
infective endocarditis: bacterial or fungal with associated formation of thrombus where the infections agent triggers the clotting mxn
Nonbacterial endocarditis Libman sachs endocarditis |
|
|
what are nonbacterial thrombotic endocartitis?
|
sterile thrombi that occur in non-infected valves in pts with hypercoaguble disorders
|
|
|
waht is Libman Sachs endocarditis?
|
thrombi that occur subjacent to valves in pts with SLE
|
|
|
how would you describe vegetations?
|
admixture of clot and bacterial debri
friable: crumbly, breaks apart when picked at |
|
|
size of arterial clot? how do they grow?
|
small, tiny
occur at sites of endothelial injruy or turbulence clot grows or propogates in a retrograde direction agasint blood flow |
|
|
which thrombi grow retrograde? anterograde?
|
retro: arterial
anterograde: venous |
|
|
waht are the most common sites for arterial thrombus?
|
coronary:bc small and prone to atherosclertoic plaques
cerebral: occulsion = stroke femoral |
|
|
MI is due to what type of thrombus?
|
arterial: coreonary thrombosis
|
|
|
what is impt about tx arterial thrombus?
|
early intervention with agents taht provide fibrinolysis: urokinase and streptokinase (plasminogen activators) to reestablish blood flow
|
|
|
plasminogen activators? job?
|
streptokinase, urokinase
dissolve clot |
|
|
size of venous thromus? located where? direction ?
|
large
in zones of stasis or turbulence form in direction of flow: anterograde 90% occur in deep veins of lower extremity and iliac system |
|
|
where do 90% of venous thrombi form?
|
in deep veins of lower extremity and iliac system
|
|
|
major complications of venous thrombus?
|
edema
pulmonary embolism |
|
|
clot dissolution is called?
|
fibrinolysis
|
|
|
what are microtrhombi and where do they form
|
small 5-25 micron fibrin-platelet aggregates
form in circulating blood then may partially obstruct or occlude arterioles and capilllaries seen in DIC, TTP |
|
|
what is microangiopathic hemolytic anemia?
|
fragment and rupture RBC like jaggged endges
|
|
|
DIC is both a ....
|
thrombotic dissorder (excessive clotting)
and Hemorhagic disorder (propensity for increased or more severe bleeding) |
|
|
what is consumption coagulopathy?
|
as seen in DIC
consume all precurssores for clot formation |
|
|
when do yousee widespread fibrin thrombi in microcirculation that are present in all vesses, arterial and venous?
|
DIC
|
|
|
is DIX amenble to thrombolytic Rx?
|
NO
|
|
|
how do you Dx DIC?
|
lab testing: large number of platelets being consumed therefore decreased platelet #, decreased fibrinogen levels
|
|
|
widespread microvascuar thrombosis can cause?
|
consumption of clotting factors and platelets
activation of plasmin Fibrinolysis Iscchemic tissue damage all leading to bleeding |
|
|
what are the most common causes of DIC?
|
sepsis
massive tissue injury |
|
|
major clinical symptom of DIC?
|
bleeding: pts starts to bleed from everywhere
widespread deposition ofsmall particles of insoluble fibrin in microcirculation |
|
|
what is microangiopathic hemolytic anemia?
|
seen in DIC
widespread deposition of small particles of insoluble fibrin in microcirculation that causes ishemia and hemolytic anemia--b/c fragment RBC |
|
|
what do you have a decrease of in DIC?
|
fibrinogen
platelets coagulation factors RBCs (anemia) |
|
|
waht do you have an increase of in DIC?
|
elevated fibrin split products: D dimers
|
|
|
how do you Tx DIC?
|
remove source of coagulation activation
support with rBcs platelets, fresh frozen plasma |
|
|
what do you call a detached thrombus as it moves through the vascular system?
|
thromboembolism
|
|
|
95% of pulm thromboembolisms originate from ?
|
deep veins of lower extremities
|
|
|
what is a saddle embolus?
|
single large mass obstructing one or both pulm arteries..usually fatal
saddle the bifurcation |
|
|
what percent of pulm emboli are clinically silent?
|
most: 60-80%
|
|
|
for a pulm embolus to be fatal, how much obstruction must occur?
|
immediate obstruction of 60% or greater of pulm cirulation to be fatal (cor pulmonale)
|
|
|
where do systemic thromboemolisms arise frome?
|
embolic traveling w/n arterial circulation
80% arise from mural thrombi formed in cardiac chamber: left heart pumps it into sysemic circulation |
|
|
waht are the major sites of systemic thromboembolisms?
|
aries from heart to
lower extermities (70%) brain (10%) |
|
|
when does fat embolism occur?
|
after fx of long bones that have fatty marrow
in 90% ofppl with sevre skeletl trauma |
|
|
fat emboli are characteried by what type of insuffienciency?
|
pulmonary insuff, neurologic symptoms, anemia, dIC which begins 1-3 days following injruty
|
|
|
when do symptoms of fat emobli occur?
|
1-3 days follwoing injurty
|
|
|
what can cause an air embolus?
|
air bubble greater than 100ml
gas bubble behaves as theombus chest wall injuries, ob procedures, open IV lines |
|
|
what is the leading cause of maternal death at time of delivery?
|
amniotic fluid embolism: 1:50000 delieveries
|
|
|
waht cause amniotic emoblus?
|
entry of amniotic fluid into the maternal ciruclation via tear in placental membranes or rupture of uterine vv allowing entry into venous circulation
occurs in seconds |
|
|
onset of aminotic embolism characterized by sudden onset of what?
|
severe dyspnea
cyanosis profound shock and sudden death those that survive the acute resp syndrome develop DIC |
|
|
what is an infarction?
|
area of ischemic necrosis caused by occulstion of the arterial supply (white or anemic) and of the venous drainage (hemorrhagic) in a particular tissue
|
|
|
what are Red Infarcts?
|
venous occulsion (ovarian or testicular torsion)
occcur in ares of dual blood supply: lung and small bowel reperfusion |
|
|
what are White Infarcts?
|
arterial inclusion of solid organs with end artery circulation: brain, heart, soft tissue of leg
|
|
|
what type of infarct would occur in lugn? spleen? kidney?
|
lung: red (appear wedge shaped)
kidney: white spleen: white |
