pulmon
Terms
undefined, object
copy deck
- 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)
LL=asbestosis
(UIP) - 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
- silicosis
- 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
- T
- 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
centriacinar=smoking - 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
- T
- 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
-
dynein
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
- kallikrein
- 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)
- TLC
- 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
- IC=IRV+TV
- volume can take in on top of normal inspiration
- IRV (IC-TV)
- 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
ex -
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)
ex-CO - formula collapsing pressure in lung
- =2tension/radius
- formular dead space
- VD=VT[(PACO2-PECO2)/PaCO2]
- 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 -
3
0.6
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
- SCC
- 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
- Chlamydia
- 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 - HAP PNA, dx
-
usu gram - PSEUDO, also E coli, Kleb, Enterobacter.
if gram + usu Staph,
dx BAL>10^4CFU - PNA in HIV
- 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
- PNA in ETOH
- S Pneu
- PNA in COPD
- H flu, Moraxella
- PNA in IVDA
- 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
- peripheral
- is there parenchymal damage in COPD
- yes (unlike asthma)
- popcorn calcif
- hamartoma, <1cm usu benign
- slow growth, late met lung ca
- SCC
-
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?
PTH? -
ADH, ACTH-small cell
PTH-SCC - lung ca most clearly linked to smoking
- SCC
- 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
- SVC Syn
- 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
- SCC
- 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
-
sz-brain
path fx-bone
jaundice/hepatomegaly-liver - general qualities adeno lung ca
-
peripheral, rapid growth, lung scar in non-smoker,
common! - physio shunt, def? ex? v/q?
-
blood not oxygenate-thesbian veins and bronchial arteries
(v/q=0) - 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
3=a>v>A - 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)