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87 Cards in this Set

  • Front
  • Back
where is the ligament of treitz
between the 4th segment of the duodenum and the jejunum
what is the nml small bowel diameter
2.5 cm
nml wall thickness of small bowel
</ = 3mm
ct appearance of crohn's dz in small bowel
inflammation of bowel wall, mucosa, and mesentary (in skip lesion pattern)
TI often involved
bowel wall enhances with contrast
mesenteric abscess
ct findings of complete small bowel obstruction
bowel diameter >2.5 cm
collapsed bowel distal to obx (= transition zone)
ct findings of small bowel ileus
diffusely dilated bowel loops, no transition zone b/c everything is dilated
what is the most common cause of sbo
adhesions (but not commonly seen on ct)
risk factors for intussusception
seen with lymphoma, lipoma, carcinoma, mets
describe appearance of intussusception on ct
there is a bowel loop inside the lumen of another bowel loop, creating a target appearance, there is cecal mesentary (fat density) surrounding intussuseptum
in sbo, what finding indicates that bowel wall is still viable
contrast enhancement of bowel wall
what is a closed sbo
obstruction on 2 separate ends of bowel wall
what causes closed sbo
usually from adhesions or hernia
on plain film, how to distinguish btwn ileus vs obstruction
if you get an upright film, with an ileus, there will be equal air-fluid lvls at dependent portions of bowel loop
in obstruction, these levels are unequal
(picture a manometer)
how big does appendix have to be for appendicitis to be considered
describe the anatomy of the paracolic gutters
the ascending and descending colon are retroperitoneal. the peritoneum sweeps anteriorly over these portions and extend laterally, forming the paracolic gutter
t or f:
most diverticuli are along mesenteric surface
general findings of colitis
thickening of bowel wall, if total wall width >3mm when distended
mural thickening with homogeneous enhancement or halo appearance
ct findings of ulcerative colitis
wall thickening (7-8 mm) with lumen narrowing +/- inflammatory pseudopolyps
no skip lesions, starts in rectum, which is narrowed
ct findings of general crohn's dz
TI and prox colon most often involved
bowel wall thickened (10-20mm)
irregular outer wall
difference in ct findings btwn acute active crohn's and chronic dz
target/halo sign seen in acute dz
chronic dz = fibrosis and fat prolif
ct findings of c diff
pancoliits or segmental irregular wall thickening </= 30mm
wall has accordian like appearance
what is typhlitis
neutropenic colitis
potentially fatal infx of cecum and ascending colon
toxic megacolon
dilation of colon to 5cm, with thinning of colon wall
--> pneumatosis, perforation
`what are the 4 major causes of pneumatosis intestinalis
bowel necrosis
mucosal disruption (from PUD, endoscopy, tubes, trauma, IBD)
increased mucosal permeability from immunosup
pulmonary causes (copd, cf, asthma, intubation)
cystic pneumatosis
well-defined blebs or grapelike clusters with nml tissue surrounding
what is a volvulus
what do you see on ct
sigmoid colon twists on mesocolon, see "whirl sign"
true or false:
centrolobular bronchioles are not visible in healthy pts
can you see the central artery within each lobule

where do these arteries extend to

they do not make it to the pleura unless there is atelectasis
causes of thickened intralobular septa

describe thickening for each cause
lymphangitic spread of CA (smooth or nodular)
interstitial pulmonary edema (smooth)
alveolar proteinosis (smooth thickening with ground glass opacity)
sarcoidosis (nodular if granulomata are present, irregular in fibrotic or end stage)
findings of pulmonary fibrosis
intralobular interstitial thickening (early, see fine reticular pattern)
traction bronchiectasis
visualization of intralobular bronchioles
describe honeycombing
fibrosis with lung destruction and disorganization of lung architecture
describe traction bronchiectasis
dilated bronchi in region of fibrosis
causes of fibrosis
idiopathic (#1)
collagen vascular dz
drug related
end stage hypersensitivity pneumoniti s
end stage sarcoid
describe the pattern of distribution for multiple pulmonary nodules
describe perilymphatic distribution of pulmonary nodule s
nodules near pleural surfaces
large pulmonary vessels and bronchi
interlobular septa
centrilobular regions
describe pattern of random distribution of pulmonary nodules
involve pleural surfaces
have diffuse, uniform distribution, but are randomly distrubuted throughout the lung structure
describe centrilobular distribution of pulmonary nodules
spares pleural surfaces
nodules surrounding vessels
no nodules will touch the pleural surface
which type of nodular pattern will also have tree in bud
etiology of tree in bud appearance
mycoplasm infx
what can cause centrilobular nodular pattern
small airway dz
endobronchial spread of bronchoalveolar CA
describe pathophys behind tree in bud
mucous, pus in dilated centrilobular bronchioles
what things can cause random nodular distribution
miliary tb
hematogenous mets
what does a consolidation look like on ct
obscured pulmonary vessls
air bronchograms
+/- centrilobular nodules
ddx of consolidation
depends on duration of sx
if acute:
PNA, ARDS, edema, hemorrhage

if chronic:
BOOP, bronchoalveolar CA, chronic eosinophilic PNA
what is the difference btwn consolidation and ground glass opacity
with ground glass opacity, you can still see the BV
lungs just look hazy
ddx for ground glass opacity
depends on duration of sx
if acute:
PCP/viral PNA
acute hypersensitivity pneumonitis

if chronic:
bronchoalveolar CA
lipoid PNA
Pulmonary alveolar proteinosis
in a pt with acute sx, what does ground glass opacity indicate

and in chronic dz
active dz

usually means active dz, but sometimes ground glass opacity can develop 2/2 fibrosis
appearance of mets that have lymphangitic spread
interlobular septal thickening
peribronchial cuffing
thickened fissures
thin, patchy unilateral distribution
appearance of mets that have hematogenous spread
randomly distributed small nodules
pleural and fissure thickening
large nodules
bilateral distribution
ct findings of idiopathic pulmonary fibrosis
intralobular thickening
traction bronchiectasis
subpleural, postero/inferior lung involvement
+/- ground glass opacity
non-specific interstitial PNA
ct findings of NSIP
ground glass opacitiyes in posterior lung region
spares immediate subpleural lung
reticular formation
traction bronchiectasis
ct findings of active sarcoid
perilympatic nodules (1-10mm) +/- calcs
pathcy distribution, asymmetric
upper lobe preodominance
ct findings of chronic sarcoid
irregular septal thickenin g
architectural distortion
ectatic bronchi
ct findings of silocosis and coal workers pneumoconiosis
perilymphatic nodule s
symmetric distribution
posterior lung fields
superior lobes
mases of nodules or fibrosis in upper lobes
complication of pulmonary alveolar proteinosis
nocardia or mycobacterial superinfx
describe pathophys of pulmonary alveolar proteinosis
filling of alveolar spaces with lipid rich, proteinaceous material, usually idiopathic, but can be 2/2 silica, malignancy or chemo
ct findings of pulmonary alveolar proteinosis
pathcy or geographic ground glass opacity
smooth interlobular septal thickening in regions of ground glass opacity (= crazy paving)
ct findings of hypersensitivity pneumonitis
patchy or geographic ground glass opaity
poorly defied centrilobular nodules of ground glass opacitiy
mosaic perfuson from bronchiolar abn
air trapping
complications of pulmonary alveolar proteinosis
suprainfection with nocardia or mycobacteria
etiologies of boop
2/2 toxins
drug rxn
clinical course of boop
progressive sob
ct findings of boop
patchy nodular consolication/ground glass opacity
peripheral or peribronchial distribution
ct findings of histiocytosis
centriolobular nodules early in course
cystic lesions late in course
sparing of costophrenic angle
upper lobe predominance
who gets lympahgiomyomatosis
women of child bearing age who have had spont ptx, sob, cylous pleural effusion
ct findings in lymphagiomyomatosis
thin walled rounded cysts with intervening nml lung
variant of lymphangiomyomatosis
women with tuberous sclerosis get the same thing
features of high risk pulm nodules
irregular, spiculated edge
lobulated contour
air bronchograms
cavitation with cavitary wall (>15 m)
diameter >2 cm
presentation of bronchoalveolar carcinoma
can present as ground glass opacities or halo sign
appearance of hamartoma
smooth, rounded
contain either all fat, fat + calcs, or all calcs
where is rounded atelectasis usually found
posterior paravertebral regions
can be bilateral
seen mostly with pleural effusions or asbestosis
describe the comet tail sign
what is it associated with
bending and bowing of adjacent bronchi and arteries towards the edge of atelectasis

will see air-bronchograms, displacement of fissures

seen in rounded atelectasis
4 key criteria that must be present to dx rounded atelectasis
ipsilateral pleural thickening/effusion
contact btwn lung lesion and abnormal pleural surface
comet tail
volume loss in lobe with opacity

if these 4 things not present, do bx
describe appearance of halo sign
soft tissue attenuation nodule surrounded by less dense rim or halo of ground glass opacity
when is halo sign seen
bronchoalveolar ca
lymphoma m
describe air crescent sign
mass within a cavity
when is air crescent sign seen
invasive aspergillosis
clot/neoplasm within cavity
echinococcal cyst
nml length of adrenal glands
4-5 cm long
nml thickness of adrenal glands
<10 mm
what is in a myelolipoma
macroctic extracellular fat with interspersed bone marrow elements
how to dx a myelolipoma
should have same HU as fat
differences btwn an adrenal true cyst and pseudocyst
true cyst:
lined wiht endothelium/epithelium
density same as fat

pseudocyst :
mass with visible wall
higher density than simple fluid
how does adrenocorical ca present most often
as cushing's dz
ct findings of adrenocortical ca
large (>5 cm)
central necrosis and irreg calcs possible
post-contrast shows nodular areas of enancement, central hypoperfusion, delayed washout
complication of adrenocortical ca
thrombus in renal vein or ivc --> pe
differential for adrenal calcifications
(the adrenals are like a HAAT on the kidney)
clinical presentation of conn's syndrome
primary hyperaldo