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119 Cards in this Set

  • Front
  • Back
who hi risk TB in PPD test
recent contact, HIV, IVDA, CXR old TB w/o tx (positive PPD > 5mm)
med risk TB in PPD test
from area hi incidence (Asia, Africa, Latin America)
hospital personnel, nursing home
positive PPD>10mm
UL v LL pneumoconiosus
UL=coal, silicosis, (hypersensit PNA, sarcoid, TB)
risk factors silicosis
stone, foundry, mining, sandblast
risk factors asbestosis
shipyard, brake repair, insulation, refinery, demolition, plumbers
beryllosis presentation
like asbestosis
hypersensitivity lung dz
can be acute (6hrs) or chronic (noncaseating granuloma) due to organic particles
whorls of collagen and LN egg shell calcific...what lung dz
two types asbestosis
1) amphiboles(straight)-amosite, crocidolite (worst)
2)chrysotitile(serpentine)-most commercial, less toxic
presentation sarcoidosis? pt?
Asx hilar LAN, ILD upper 2/3, F, arthralgia, rash,
AA female 30-40
Curschman spirals
seen in asthma
causes bronchiectasis (3)
bronchial obstruction, CF, kartageners/ciliar
T/F Both obstructive and restrictive lunf dz have decrease in FEV and FVC
on physical exam chronic bronchitis v emphyseam
bronchitis-wheezing, crackles, cyanosis
emphysema-decr breath sounds, decr I/E ratio, dyspnea, tachycardia
2 histol of emphysema
panacinar=alpha anitrypsin, see also liver cirrhosis
triggers asthma
viral URI, Ag, stress
T/F I/E decr in asthma
T (also with emphysema)
T/F can see pulsus paradoxus in asthma
2 main types restrictive lung dz
1) muscular and bony (polio, MG, scoliosis)
2) ILD
restrictive lung dz: ILD (8)
acute, chronic, immune
acute: ARDS, neonatal RDS, chronic: pneumoconiosis, sarcoid, IPF
immune: goodpasteur, wegeners, eos granuloma
incr/decr fremitus indicates
incr in lobar PNA, decr in pl eff
bronchial breath sounds at exterior
lobar PNA
dx Neonatal RDS before born
lecithin/sphingomyelin <1.5
what makes surfactant? when? chemical composition of surfact? mech NRDS?
pneuII make surfactant (DPPC) most abundantly >35wks
DPPC=dipalmitoyl phosphatidylcholine
mech: alveolar collapse
histol pathognomonic finding in asbestosis
ferruginous bodies=asbestos fibers coated in hemosiderin
defect in Kartageners, clinical present
recurrent sinusitis, bronchiectasis, infertility +/- situs inversus
responses to hi altitude
(hormone, cell changes, acid/base)
increases in ventilation (both acute and chronic), incr EPO (incr H/H), incr mitochondria, incr 2,3 DPG, respir alkalosis compensated with incr excretion of HCO3
possible cxn hi altitude
chronic hypoxic vasoconstriction leading to RVH
activates bradykinin
products of lung (3 unique to lung)
1) surfactant
2) ACE (turn angI to angII, inactivates bradykinin)
3) Kallikrein (acitv bradykinin)
others: PG, Histamine
vital capacity
TV+IRV+ERV (everything but RV)
the whole shubang! (IRV+ERV+RV+RV)
functional reserve capacity
volume in lung after normal expiration=RV+ERV
(not real inspir counterpart, see IC= biggest breath ever, IRV=volume can breathe in on top of normal inspiration)
volume of largest breath ever
volume can take in on top of normal inspiration
causes L shift Hb curve and its effects
decr PCO2, H+, temp, 2,3 DPG
incr pH
fetal HB
effects: increase O2 affinity, decr P50
causes R shift Hb curve and its effects
incr CO2, T, H+, 2,3DPG,
decr pH
hi altitude
effects: decr O2 affinity so can deliver more O2 to tissues, incr P50
def diffusion limited pul circulation
gas does not equilibrate by the time blood reaches end of capillary
(normal lung)
ex-N2O, O2
def perfusion limited pul circulation
when do you see?
gas equilibrates early along the length of capillary, so diffusion can be increased only by incr BF
(O2 exercise, emphysema, fibrosis)
formula collapsing pressure in lung
formular dead space
describe 3 zones of lung and relative pressures
1 apex=A>a>v
2 middle=a>A>v
3 base=a>v>A
v/q at apex?
at base?
how exercise affect
exercise moves v/q at apex closer to 1
T/F v/q greater at base
F (apex)
T/F both ventilation and perfusion are less at apex
T (but q decreases much more than v, so v/q highest at apex)
haldane effect
oxygenation of Hb promotes dissoc of CO2 from Hb
name of CO2 travelling bound to Hb
carbaminoHb (5%)
bohr effect
in peripheral tissue, incr H+ causes curve to shift right, unloading O2 where it's needed
what type of immune response are the 2 rhiniti
acute rhinitis=none, adenovirus
allergic rhinitis=type I (IgE) with eosinophils in PBS and sxns
extrinsic v intrinsic asthma
extrinsic=type I hypersens with IgE begins childhood
intrinsic=adult onset, no hx allergy, incl cold induced, exercise induced, assoc w chronic bronchitis
key histological marker of ARDS
intra-alveolar hyaline mem
(also seen in NRDS)
cxns of NRDS
-bronchopulmonary dysplasia from hi O2 and mech vent
-PDA (continued hypoxia)
-intraventricular brain hemor
-necrotizing entercolitis (premies)
characteristic finding of eosinophilic granuloma
histiocytic prolifer (related to Langerhans of skin) with inclusions Birbeck granules, which look like tennis rackets
lab findings sarcoid
incr Ca, hypergammaglobulinemia, incr ACE****
Note: anergy on skin Ag test (PPD -)
IPF progression/histol
begins alveolitis, fibroses and ends in fibrotic lung with cystic air spaces (honey comb lung). die in 5 yrs.
basically chronic inflamm/fibrosis alveolar wall
lung ca frequ cavitate
lung ca develop at site prev injury/scar
bronchial adeno
lung ca that can mimic PNA
bronchioalveolar adeno
lung ca less assoc smoking
both adenos (broncho adeno and bronchoalveolar adeno)
CAP typical
Strep Pneu
CAP atypical: MC, be wary of...?
MC is Mycoplasma, (but be wary of Legionella and Chlamydia)
descrip legionella as CAP, course and dx
dx-flour Ab or urine Ag
most virulent of the atypical
incidence depends on geo
what is an uncommon cause CAP hard to dx
Mycoplasma PNA-epidemio, histol
may occur in epidemics
inflamm rxn is confined to inerstitium with no exudate in alveolar spaces, also has intraalveolar hyaline mem
dx Mycoplasma PNA
cold agglutination test (difft from dx mono via agglutinatio of sheep RBC bc of heterophil Ab)
when see viral PNA
childhood, usu influenza, Adeno, rhino, and RSV
giant cell PNA
the measles virus creates, numerous giant cells w tracheobronchitis
cause lung abscesses
bronchial obstruct (ie cancer), aspiration
can be cxn PNA
bugs in lung abscess
Staph, Pseudo, Kleb, Proteus often w anaerobic
extra pulmon TB dz
vertebral-Potts dz,
CNS-parenchymal tuberculoma, mening
paravertebral or psoas abscess
+ GI, renal cxns
usu gram - PSEUDO, also E coli, Kleb, Enterobacter.
if gram + usu Staph,
dx BAL>10^4CFU
MC is Strep Pneu, but PCP is most common AIDS indicator infxn
MC PNA in neonate
GBS, E coli
MC PNA <18
RSV, Myco, Chla, S Pneu
MC PNA 18-40
Myco, Chlam, S Pneu
MC PNA 40-65
S Pneu, H Flu, Anaer, virus, Myco
MC PNA elderly
S Pne, virus, anaerobe, H Flu, GNR
postviral PNA
Staph, H Flu, A Pneu
S Pneu
H flu, Moraxella
Staph, S Pne, Kleb
compare v/q in bronchitis v emphysema
bronchitis has v/q mismatch bc small airways plugged, emphysema does not
key histol finding in bronchitis
hypertrophy of mucus cells with Reid>0.5
key findings resistance and compliance in emphy and bronchitis
bronchitis-increase resistance
emphy-low elastic recoil
findings histol asthma
s m hyperplasia, excess mucus, inflamm in all airways but no parenchymal damage
which airways COPD affect
is there parenchymal damage in COPD
yes (unlike asthma)
popcorn calcif
hamartoma, <1cm usu benign
slow growth, late met lung ca
para neo seen in lung ca
(metab/endo, neuromsc, direct extension, misc)
-Metab/endo (Cushing, SiADH, incr Ca, gynecomastia)
-neuromusc (Eaton-Lambert, Cb ataxia)
-direct extension-Pancoasts/Horners, SVC syn, hoarse voice
-skel hypertrophic osteo
-derm-acanthosis nigricans
also thrombophlebitis,
tends to necrose-lung ca
large cell
Kulchinsky cells
seen in carcinoid lung cancer
describe present carcinoid lung ca
red/yellow/prpl mass causing prox bronchial obstruct--arise major bronchi
progression carcinoid lung ca
low malig, spread by direct extension
lung ca-
ADH, ACTH-small cell
lung ca most clearly linked to smoking
carcinoid syndrome
flushing, diarrhea, wheezing, salivation
lung ca arise peripherally
adeno (MC), bronchoalveolar, large cell
Pancoast's tumor
ca in apex lung affecting cerv symp plexus causing UE wknss/pain and Horners
engorgement of neck/face veins, CNS HA, N/V, cough, hoarseness
lung ca shows no invasion of stroma, vasc
adeno (pure bronchoalveolar growth)
lung ca-invade around bronchus
general qualities large cell
peripheral necrotic, undifftd
general qualities SCC
arise centrally, linked to smoking, slower growth late met, can see PTH
general qualities small cell
central, very malign (no sx) often already met, assoc paraneo, clear link smoking
symptoms coming from lung ca mets
path fx-bone
general qualities adeno lung ca
peripheral, rapid growth, lung scar in non-smoker,
physio shunt, def? ex? v/q?
blood not oxygenate-thesbian veins and bronchial arteries
name for v/q=infinity
dead space (the conducting airways)
how resistance change w lung volume
increases w volume (asthma COPD breathe higher volume)
resistance of airways exn
8(viscosity)(length)/pi radius^4
major site airway resistance
med sized bronchi
exn surface tension,
which airways diff to keep open
Pressure to keep alveoli open=2(surface tension)/radius
so small alveoli are hard to keep open (atelectasis esp w decr surfactant)
Cl shift
HCO3 leaves the RBC in exch for Cl (enz in RBC carbonic anhydrase)
zones and dz
1=A>a>v hemorrhage, positive pressure ventilation
2=a>A>v no ex
changes pul circulation with exercise
dilation of apical capil, so apical v/q moves from 3 to close to 1.
diff bw bronchoPNA and lobar PNA
lobar PNA-intra alveolar exudate leading to consolidation
bronchoPNA-acute inflamm infiltrates from bronchioles into adj alveoli, patchy w >1 lobe
control breathing
the medullary respir center in the reticular formation
central v peripheral chemoR
central=pH CSF
peripheral=carotid and aortic bodies (incr RR when incr PCO2, H+, or PO2<60)