Strategy Flashcards
T1 Bright
Fat
melanin (melanoma)
blood (subacute)
protein rich fluid
calcification (hyalinized)
slow moving blood
laminar necrosis
T2 Bright
Fat
Water
blood (extracellular methemogloving)
most tumors
T1 and T2 dark
flow void
fibrosis/scar
metal
air
REstricts diffusion
stroke
hypercellular tumor
epidermoid
abscess (bacterial)
acute demyelinations
CJD
T2 shine through
PEDS neck looks cystic
Thyroglossal Duct Cyst Brachial cleft cyst Necrotic Level 2 Node Hemangioma of Infancy Cystic Hygroma Phlebectasia
PEDS neck looks cystic
Thyroglossal Duct Cyst
*MIDLINE Ultrasound in Axial Planes C T / MRI in Sagital Planes Posterior to Tongue Anterior to Hyoid
PEDS neck looks cystic
Brachial Cleft Cyst
‘ LATERAL
Axial Plane Most Likely
Anterior to the
Sternocleidomastoid (type 2)
PEDS neck looks cystic
Necrotic Level 2 Node
Looks Just like BC Cyst - but the kid is too old (late teens / “young adult”)
Thyroid CA, or Nasopharyngeal HPV related CA
C T axial plane - most likely
PEDS neck looks cystic
Hemangioma of Infancy
T2 Bright
Enhances
Will have flow in it on doppler
If you saw it you’d think to yourself “if that doesn’t involute that kid is never getting a date to prom”
PEDS neck looks cystic
Cystic Hygroma
OB Ultrasound - most likely modality Cystic Hygroma . J2 Brjght DOES NOT Enhance Will NOT have flow in it on doppler Turners, Downs.
PEDS neck looks cystic
Phlebectasia
Kinda looks like a big dilated jugular vein (because it is a big dilated jugular vein)
No stenosis or collaterals
PEDS neck looks solid
Septic Thrombophlebitis Ectopic Thyroid Fibromatosis Coli Rhabdomyosarcoma Metastatic Neuroblastoma
PEDS neck looks solid
Septic Thrombophlebitis
Jugular Vein with a clot - they will have to prove that has a clot in it - fprobably with doppler us Lemierre’s Syndrome Septic Emboli to the lungs Recent ENT procedure, or Infection Fusobacterium Necrophorum
PEDS neck looks solid
Ectopic Thyroid
Back of the tongue or in front of the hyoid
Tc-MIBI, or 1-123
PEDS neck looks solid
Fibromatosis Coli
Ultrasound
“Two Heads” of the Sternocleidomastoid
PEDS neck looks solid
Rhabdomyosarcoma
MRI orCT
Seriously pissed off looking mass (probably in the orbit - maybe in the masticator mass)
Enhances heterogenous,
PEDS neck looks solid
Metastatic Neuroblastoma
MRI orCT Soft Tissue Mass, Calcifications, Restricted Diffusion Classic is the orbit
Cyanotic peds
TOF TAPVR Transposition truncus tricuspid atresi
not cyaotic peds
ASD VSD PDA PAPVR AORTIC coarctation (adutl type - post ductul)
Congenital Heart on C X R
cyanotic, right sided arch, incrased pulmonary vasculature
Truncus (types 1-3)
Congenital Heart on C X R
cyanotic, right sided arch,normal pulmonary vasculature
TOF
Congenital Heart on C X R
cyanotic, left arch, massive heart
Ebsteins or
Pulmonary Atresia without VSD
Non-Cardiac (wo n ’t be cyanotic)
- Infantile Hemangioendothelioma
- Vein o f Galen Malformation
Congenital Heart on C X R
cyanotic, left sided arch, normal heart size, increased pulmonary blood flow
- TAPVR (especially type 3)
- D-Transposition -Ebsteins
- Truncus (look for R A rch)
- “Tingle Ventricle”
Congenital Heart on C X R
cyanotic, left sided arch, normal heart size, decreased or normal pulmonary blood flow
- TOF
- Ebsteins
- Tricuspid Atresia
Neonatal Chest
high lung volume symmetric pattern ( looks like pulmonary edema)
Transient Tachypnea
“Pulmonary Edema + Effusions”
Neonatal Chest
high lung volume, less symmetric pattern (perihilar/streaky
Meconium Aspiration
or
Non GB Neonatal Pneumonia
Neonatal chest
low lung volumes, not usually pleural effusions
Surfactant- Deficient Disease (SDD)
“Diffuse Granular”
Neonatal chest
low lung volumes, pleural effusions 25% of the time
Beta Hemolytic Pneumonia
“Diffuse Granular
T H IS vs THAT: Meconium Asp ira tion o r Non Group B Strep Pneumonia
This is su p e r tough without any history, an d b e cau se o f that I f e e l like the te st w rite r has
two o p tion s: (J) Stop being an a ssh o le an d g iv e you some history, (2) not include both as
an sw e r ch o ices - assuming only one is co rre c t. Now, a long those lines i f you saw both as
choices an d the question h ea d e r g iv e s you no h isto ry you c o u ld eliminate them both as
d istra c to rs - b ecause they both c a n ’t be co rre c t.
Prematurity
u e s s in g th at the kid is p rem a tu re can be h e lp fu l fo r e lim in a tin g
ch o ic e s (M e co n ium A sp ira tio n is m o re o f a p o s t te rm th in g ), an d ra isin g y o u r p rete st
p ro b ab ility (SD D , o r N EC in a belly film). T h e re are two main clues:
(1) Humeral H ea d Ossification - T h is ten d s to o c c u r c lo s e r to term . I f th e h um era l
h e ad is N O T ossified y o u can a ssum e (in th e w o rld o f m u ltip le ch o ic e ) th at the kid
is lik e ly p rem a tu re .
(2) Lack o f Subcutaneous Fat - P rem a tu re k id s ten d to be very sk in n y , a lth o u g h I th in k
o f th is m o re o f a soft sign th at is u se fu l w h en ab sen t m o re th an p re sen t. I ’ll ju s t
say th a t if the kid a p p e a rs ch u b b y he is p ro b ab ly N O T p rem a tu re .
PEDs thing in the left upper lobe
Think Congenital Lobar Emphysema (CLE) first. But,
remember CCAM has no lobar prevalence, so it can be
anywhere
Peds thing in the lerft lower lobe
Think Sequestration First. Congenital Diaphragmatic
Hernia (CDHs) favors this side too
Intralobar sequestration is seen
older kids
Extralobar sequestration
is seen
in infants with comorbids
CLE is in the
upper lobe
The NG tube stops in the upper thoracic
esophagus:
The NG tube stops in the upper thoracic
esophagus: Think esophageal atresia (probably in
the setting o f VACTERL).
The NG tube curling into the chest
it’s either (1) in the lung, or (2) it’s in a congenital diaphragmatic hernia. If 1 had to pick between the two (and it wasn’t obvious), I’d say left side hernia, right side lung - ju st because those are the more common sides.
T h e C la s s ic C o n g e n ita l L o b a r Em p h y s em a T ric k
They can show you a
series o f CXRs. The first one has an opacity in the lung (the affected lung is fluid filled). The
next x-ray will show the opacity resolved. The following x-ray will show it getting more
lucent, and more lucent. Until it’s actually pushing the heart over. This is the classic way to
show it in case conference, or case books
T h e School Aged CXR: Things to look for
Big Heart - Probably showing you a sickle cell case. Look for bone infarcts in shoulders.
Lucent Lung - Think foreign Body (air trapping). Remember you put the affected side down (if it remains lucent- that confirms it).
THIS vs THAT: Cystic Fibrosis vs Primary Ciliary Dyskinesia
CF
Abnormal Mucus - Cilia c an ’t clear it
Bronchiectasis (upper lobes)
Normal sperm, obliterated vas deferens
PCD
Normal Mucus - Cilia do n ’t work
Bronchiectasis (lower lobes)
Normal vas deferens, sperm cannot swim normally
PEDs mandiible
There are only a few things that a mandible will be shown for with
regards to Peds. Think Caffeys first - especially if the picture looks blurry and old (there
hasn’t been a case o f this in 50 years). If it’s osteonecrosis think about O.I. on
bisphosphonates. If it’s a dwarf case, think wide angled mandible with Pycnodysostosis. A
“floating tooth” could be EG.
The Abdominal Plain Film - on a newborn
Single Bubble:
In a newborn this is Gastric (antral or pyloric atresia). In an older child think gastric volvulus
The Abdominal Plain Film - on a newborn
Double Bubble
duodenal atresia
The Abdominal Plain Film - on a newborn
triple bubble
jejunal atresia
The Abdominal Plain Film - on a newborn
Single Bubble + Distal Gas
+ “Bilious Vomiting
concern for mid gut volvulus
next step = upper gi
The Abdominal Plain Film - on a newborn
Multiple Dilated Loops
concern for lower obstruction
next step = contrast enema
THIS vs THAT: Duodenal Atresia vs Jejunal Atresia
Duodenal Atresia
double bubble
failure to canalize (often isolated atresia)
associated with downs
Jejunal atresia
triple bubble
Vascular Insult * More likely associated with other atresias
THIS vs THAT: In tra lob a r vs E x tra lo b a r S eq u e stra tion
intralobar
No pleural covering
More Common
Presents later with recurrent infection
extralobar
Has its own pleural covering
Less Common
Presents early with other bad congenital things (heart, etc…)
Right sided heterotaxia
Two Fissures in Left Lung
Asplenia
Increased Cardiac Malformations
Reversed Aorta/I VC
Left sided heterotaxia
One Fissure in Right Lung
Polysplenia
Less Cardiac Malformations
Azygous Continuation o f the IVC
orbital calcs less than 3
retinoblastoma
cmv
colomoatous dyst
orbital calcs older than 3
toxo
retinal astrocytoma
Peds Liver Masses
Infantile Hepatic Hemangioma
Hepatoblastoma
Mesenchymal Hamartoma
HCC
Fibrolamellar Subtvpe HCC
Undifferentiated Embryonal Sarcoma
Mets (Neuroblastoma, Wilms)
Peds Liver Masses
Infantile Hepatic
Hemangioma
Age 0-3
Endothelial growth factor is elevated
Progressively Calcify - as they involute
Associated:
High Output CHF
Skin Hemangiomas
Peds Liver Masses
Hepatoblastoma
Age 0-3
AFP is elevated
Calcifications are Common
Risk Factor = Prematurity
Many Association:
Wilms, Beckwith- Weidemann
may cause precocious puberty
Peds Liver Masses
Mesenchymal
Hamartoma
Age 0-3
AFP is negative
Calcification are RARE
CYSTIC MASS
Favors Right Lobe
“Developmental anomaly’’
Peds Liver Masses
HCC
Age > 5
AFP is elevated
Kids with cirrhosis (biliary atresia, Fanconi syndrome, glycogen storage disease)
Peds Liver Masses
Fibrolamellar Subtvpe
HCC
Age > 5
AFP is negative
Calcifies more often than conventional HCC
No Cirrhosis
Central Scar (scar does NOT enhance, and is T2 dark)
Peds Liver Masses
Undifferentiated Embryonal Sarcoma
Age > 5
AFP is negative
Cystic / Heterogeneously Solid Mass
Known to rupture
Peds Liver Masses
Mets
Neuroblastoma, Wilms
Fetus - 4
6 - Early Teens
Multiple Masses in the Setting of Known Primary
Adult Benign Liver Masses
Hemangioma
FNH
Heptaic adenoma
hepatic angiomyolipoma
Adult Benign Liver Masses
hemangioma
Ultrasound - Hyperechoic
CT - Peripheral Nodular Discontinuous Enhancement
MR - T2 bright
Trivia - rare in cirrhotics
Adult Benign Liver Masses
FNH
Ultrasound - spoke wheel
CT - homogenous arterial enhancement
MR - stelath lesion - iso on t1 and t2
Trivia - central scar, bright on delayed eovist (gd-eob-dtpa)
Adult Benign Liver Masses
hepatic adenoma
Ultrasound - variable
CT - variable
MR - fat containing on in/out phase
Trivia - ocp use, glycogen storage idsease, can explode and bleed
Adult Benign Liver Masses
hepatic angiomyolipoma
Ultrasound - hyperechoic
CT - gross fat
MR - t1/t2 bright
Trivia - unlike renal aml 50% dont have fat, Tuberous sclerosis
Liver Sulfur Colloid HOT or COLD
hepatic adenoma
cold
Liver Sulfur Colloid HOT or COLD
FNH
40% HOT,
30% COLD,
30% Warm
Liver Sulfur Colloid HOT or COLD
cavernous hemangioma
cold
RBC Scan HOT
Liver Sulfur Colloid HOT or COLD
HCC
cold
Liver Sulfur Colloid HOT or COLD
cholangiocarcinoma
cold
Liver Sulfur Colloid HOT or COLD
mets
cold
Liver Sulfur Colloid HOT or COLD
abscess
cold
gallium hot
Liver Sulfur Colloid HOT or COLD
focal fat
cold
xenon hot
regenerative liver nodules
contains iron
t1 dark, t2 dark
dots not enhance
dysplastic liver nodules
contains fat, glycoprotein
ti bright, t2 dark
usually does not enhance
hcc
T2 bright
does enhance
This vs That: HCC vs
Fibrolamellar Subtype HCC
HCC: Cirrhosis Older (50s-60s) Rarely Calcifies Elevated AFP
FL HCC: No Cirrhosis Young (30s) Calcifies Normal AFP
This vs That:
Central Scars of FIN H and Fibrolamellar HCC
FNH: T2 Bright Enhances on Delays Mass is Sulfur Colloid Avid (sometimes)
FL HCC:
T2 Dark (usually)
Does NOT enhance
Mass is Gallium Avid
Multiple Low Density (NOT Cystic) Liver Lesions
METS
Think Colon First
- unless they have a known primary
Multiple Low Density (NOT Cystic) Liver Lesions
HCC
Does the Liver look Cirrhotic?
Multiple Low Density (NOT Cystic) Liver Lesions
Regrnative nodules
Does the Liver look Cirrhotic?
Multiple Low Density (NOT Cystic) Liver Lesions
infections
Low Density Nodes - Think Mycobacterium
Hyperenhancing Nodes - Think Bartonella
Multiple Low Density (NOT Cystic) Liver Lesions
sarcoid
Spleen Should be Involved Also
Gamesmanship - Probably gets some hints in the form of a CXR, or
Labs (elevated ACE)
Multiple Cystic Liver Lesions
AD Polycystic
Kidney
Different Size Cysts
(small and big)
Renal Cystic Disease
Multiple Cystic Liver Lesions
Von
Meyenburg
Complex
Hamatromas
Small ( < 1.5 cm)
Will NOT connect with Ducts
Uniform distribution
Multiple Cystic Liver Lesions
Choledochal Cysts (Caroli)
WILL communicate with duct
Central “dot” Sign
Multiple Cystic Liver Lesions
Abscess
Bacterial and Fungal = Multiple, R > L Amoebic = Single and Subdiaphragmatic Peripheral Enhancement Necrotic center will not enhance
Liver infection buzzwords
Starry Sky (US)
Viral Hepatitis
Liver infection buzzwords
Double Target (CT)
Pyogenic Abscess
Liver infection buzzwords
Bull’s Eye (US)
Candida
Liver infection buzzwords
“Extra Hepatic Extension”
Amoebic Abscess
Liver infection buzzwords
Water Lily (CT, Sand Storm US
Hydatid Disease
Liver infection buzzwords
tortoise shell
Schistosomiasis
Primary Hemochromatosis
Genetic - increased absorption
Liver, P an c re a s
Heart, Thyroid, Pituitary
Secondary Hemochromatosis
Acquired - chronic illness, and multiple
transfusions
Liver, S p le en
This vs That: AIDS Cholangiopathy vs Primary Sclerosing Cholangitis
AIDS:
Focal Strictures o f the extrahepatic duct > 2cm
Absent saccular deformities o f the ducts Papillary Stenosis
PSC:
Extrahepatic strictures rarely > 5mm
Has saccular deformities o f the ducts
Intrahepatic biliary dilation ddx
PSC infection cholangitis pancreatic head mass cbd stone - late biliary stricture
extrahepatic biliary dilation only ddx
post cholecystectoy
sphincter of oddi dysfucntion
type 1 choledochal cyst
cbd stone- early
THIS vs THAT: Chronic Pancreatitis Duct Dilation vs Pancreatic Malignancy Duct Dilation
CP:
Dilation is Irregular
Duct is < 50% o f the AP gland diameter
Cancer:
Dilation is uniform (usually)
Duct is > 50% o f the AP gland diameter (obstructive atrophy)
Uncommon Types and Causes o f Pancreatitis
Autoimmune
Pancreatitis
Groove
Pancreatitis
Tropic
Pancreatitis
Hereditary
Pancreatitis
Ascaris
Induced
Uncommon Types and Causes o f Pancreatitis
Autoimmune
Pancreatitis
Associated with elevated IgG4
Absence of Attack Symptoms
Responds to steroids
Sausage Shaped Pancreas, capsule like delayed rim enhancement around gland (like a scar). No duct dilation. No calcifications.
Uncommon Types and Causes o f Pancreatitis
Groove
Pancreatitis
Looks like a pancreatic head Cancer - but with little or no biliary obstruction.
Less likely to cause obstructive jaundice (relative to pancreatic CA)
Duodenal stenosis and /or strictures of the CBD in 50% of the cases
Soft tissue within the pancreaticoduodenal groove, with or without delayed enhancement
Uncommon Types and Causes o f Pancreatitis
Tropic
Pancreatitis
Young Age at onset, associated with malnutrition
Increased risk of adenocarcinoma
Multiple large calculi within a dilated pancreatic duct
Uncommon Types and Causes o f Pancreatitis
hereditary pancreatitis
Young Age at Onset
Increased risk of adenocarcinoma
SPINK-1 gene
Similar to Tropic Pancreatitis
Uncommon Types and Causes o f Pancreatitis
Ascaris
Induced
Most commonly implicated parasite in pancreatitis
Worm may be seen within the bile ducts
I Say Autoimmune Pancreatitis
You Say IgG4
I Say IgG4
Autoimmune Pancreatitis Retroperitoneal Fibrosis Sclerosing Cholangitis Inflammatory Pseudotumor Riedel’s Thyroiditis
THIS vs THAT:
Autoimmune Pancreatitis vs Chronic Pancreatitis
Autoimmune pacreatitis:
no ductal dilation
no calcs
chroic pancreatitis:
ductal dilation
ductal calcifications
Cystic Pancreatic Lesions
Main Branch
IPMN
Side Branch
IPMN
Serous Cystic
Mucinous
Cystic
Solid Pseudo-
Papillarv
Cystic Pancreatic Lesions
Main Branch
IPMN
40s - 50s
Main Duct
High Malignant Potential (60%)
Cystic Pancreatic Lesions
Side Branch
IPMN
50s - 60s
Favor head, Uncinate
Typically Benign
(maybe 5% will develop malignancy)
Communicates with duct
Cystic Pancreatic Lesions
serous cystic
Grandma F > M >60
Favor Head
Does NOT Communicate with Main Duct Central Calcifications “Micro-Cystic” - “Honeycomb” Benign Glycogen Rich Associated with von Hippel Lindau
Cystic Pancreatic Lesions
Mucinous
Cystic
Mother F > M 40s
Favor Body / Tail
Does NOT Communicate with Main Duct
Peripheral Calcifications
Larger Cysts (sometimes uni-locular)
Premalignant
Cystic Pancreatic Lesions
Solid Pseudo-
Papillarv
Daughter F > M 20s
Favor Tail
Large (5-10 cms) Solid with Cystic Parts Enhances like a Hemangioma Has a Capsule Asian or Black Female
Malignant Ulcer
Width > Depth Located within Lumen Nodular, Irregular Edges Folds adjacent to ulcer Aunt Minnie: Carmen Meniscus Sign
Benign Ulcer
Depth > Width Project behind the expected lumen Sharp Contour Folds radiate to ulcer Aunt Minnie: Hampton’s Line
Direct Hernia
Less common
Medial to inferior Epigastric
Defect in Hesselbach triangle
NOT covered by internal spermatic fascia
Indirect Hernia
more common
lateral to inferio epigastric
failure of processus vaginalisu to close
coverved by internal spermatic fascia
Sigmoid volvulus
old person (constipated)
points to the RUQ
cecal volvulus
Younger Person (mass, prior surgery, or 3rd Trimester Pregnancy)
Points to the LUQ
Crohns
Slightly less common in the USA Discontinuous “Skips” Terminal Ileum - String Sign Ileocecal Valve “Stenosed” Mesenteric Fat Increased "creeping fat ” Lymph nodes are usually enlarged Makes Fistulae
Ulcerative Colitis
Slightly more common in the USA Continuous Rectum Ileocecal Valve “Open” Perirectal fat Increased Lymph nodes are NOT usually enlarged Doesn’t Usually Make Fistulae
Tumor markers
cholangio
CEA and CA19-9 increased
Tumor markers
pancreatic CA
CA19-9 increased
Tumor markers
Colon CA
CEA increased
More Common In :
Crohns vs UC
gallstones
crohns
More Common In :
Crohns vs UC
PSC
UC
More Common In :
Crohns vs UC
Hepatic abscess
Chrohns
More Common In :
Crohns vs UC
pancreatitis
crohns
Multicystic Dysplastic Kidney
unilateral
- Neonate, No Renal Function (MAG 3)
- Associated with congenital UPJ obstruction
- Associated with reflux (VUR) -
Multilocular Cystic Nephroma
unilateral
- “Micheal Jackson - Young Boy, Older Woman”
- Multiple Cysts - Herniates into the Renal Pelvis”
cystic wilms
peds renal cyst mass, unilateral
AR- Polycystic Kidney Disease
bilateral
- enlarged, hyperechoic
- microcystic
Peds Tumor / Mass kidney
Mesoblastic
Nephroma
Nephroblastomatosis
wilms
Clear Cell - Wilms
Rhabdoid - Wilms
Multi-Cystic
Nephroma
RCC
Renal Lymphoma
Peds Tumor / Mass kidney
Mesoblastic
Nephroma
“Solid Tumor o f Infancy” (you can be born with it)
Peds Tumor / Mass kidney
Nephroblastomatosis
“Nephrogenic Rests” - left over embryologic crap that didn’t go away
Might turn into wilms (bilateral wilms especially)
“Next Step” - f/u ultrasound till 7-8 years old
Variable appearance
Peds Tumor / Mass kidney
wilms
90% + Renal Tumors
“Solid Tumor o f Childhood” - Never born with it
Grows like a solid ball (will invade rather than incase)
Met to the lung (most common)
Peds Tumor / Mass kidney
Clear Cell - Wilms
Met to Bone
Peds Tumor / Mass kidney
Rhabdoid - Wilms
Brain Tumors
It fucks you up, it takes the money (it believes in nothing Lcbowski)
Peds Tumor / Mass kidney
Multi-Cystic
Nephroma
Micheal Jackson Tumor (Young Boys, Middle Age Women)
Big cysts that don’t communicate
Septal Enhancement
Can’t Tell it is not Cystic Wilms (next step = resection)
Peds Tumor / Mass kidney
RCC
“Solid Tumor o f Adolescent ”
Syndromes - VHL, TS
Peds Tumor / Mass kidney
Renal Lymphoma
Non-Hodgkin
Multifocal
Neuroblastoma v wilms
Neuroblastoma: Age: usually less than 2 (can occur in utero) Calcifies 90% Encases Vessels (doesn’t invade) Poorly Marginated Mets to Bones
Wilms: Age: Usually around age 4 (never before 2 months) Calcifies Rarely (<10%) Invades Vessels (doesn’t encase) Well Circumscribed Doesn’t usually met to bones (unless clear cell Wilms variant). Prefers lung.
Neuroblastoma vs Adrenal Hemorrhage
Neuroblastoma:
Heterogenous and vascular
High on T2 , Iso-Low on T1
Will grow on followup
Adrenal Hemorrhage
Centrally Hypoechoic and Avascular
High on T1 (7 days - 7 weeks)
Should shrink on followup
Adult RCC Associations
clear cell
Von Hippel-Lindau
Adult RCC Associations
papillary
Hereditary papillary renal.
carcinoma
Adult RCC Associations
chromophobe
birt hogg dube
Adult RCC Associations
medullary
sickle cell trait
Bladder Cancer
Transitional Cell
CA
The “normal” kind Bladder CA » > Ureter CA
Bladder Cancer
Squamous Cell
CA
Calcifications
Chronic Catheter
Schistosomiasis (worm)
Bladder Cancer
adenocarcinoma
Midline
Urachus Association
Bladder Exstrophy
Urethra cancer
Prostatic Urethra
TCC
Urethra cancer
Bulbar / Penile Urethra
SCC
Urethra cancer
Urethral
Diverticulum
Adenocarcinoma
Renal Cyst Associations
ADPCKD
Cysts in Liver
Kidneys are BIG
Renal Cyst Associations
VHL
cysts in pancreas
Renal Cyst Associations
Acquired (uremic)
kidneys are small
Big Kidney with Lots o f Cysts
Liver Cysts
AD Polycystic Kidney
Normal Sized Kidneys with Lots o f Cysts Solid Renal Masses (RCCs) Pancreatic Cysts (simple and serous cystic) Pancreatic Masses Adrenal Masses (paragangliomas)
von Hippel - Lindau
Renal Cysts
Multiple Fat Containing Renal Masses
(AMLs) - maybe bleeding
Lungs Cysts (LAM)
Tuberous Sclerosis
Small / Calcified Spleen
Gallstones (or absent GB)
Bone Infarcts
sickle cell
Severe Pancreatic Fatty Atrophy
Small bowel stool
Fatty Liver
CF
Big Liver, Big Spleen
Bone Infarcts
Extramedullary Hematopoiesis
Gaucher
Bilateral Adrenal Masses
(Pheochromocytoma - not adenoma)
Thyroid Cancer
MEN 2
Islet Cell Tumors
Pituitary Adenoma
MEN 1
Renal Masses (Wilms, AML)
Adrenal Masses (Pheochromocytoma)
Skin Nodules
Scoliosis
NF-1
Vascular Malformation in the Liver Bowel Angiodysplasia Enlarged Hepatic Artery Pulmonary AVM Brain Abscess
Osier Weber Rendu
Hereditary Hemorrhagic Telangiectasia
Cyst Morphology Trivia:
- ADPCKD - Round and Distributed Throughout Kidney
* ARPCKD - Tubular Cysts which Spare Cortex
Anterior Mediastinal Mass
normal htymus
- Age < 10
- Homogenous
- No Mass Effect
Anterior Mediastinal Mass
lymphoma
- Age > 1 0
- Mass Effect
- Lymph Nodes
- SV C Compression
- Hodkin> NHL
Anterior Mediastinal Mass
teratoma
- Fat
- Cystic
- Calcifications
Anterior Mediastinal Mass
NS - Germ cell tumore
- Big
- Aggressive
- Hemorrhage
- Klinefelter
- Necrosis
Anterior Mediastinal Mass
Seminoma
- Straddle Midline
- Bulky
- Lobulated
DIP
- Apical Emphysema (smoking related) - Basilar Ground Glass - Peripheral Basilar Reticulation - Smoker - Severe end of RB-ILD
NSIP
Basilar Ground Glass
(sub-pleural sparing)
Traction Bronchiectasis
Scleroderma Association
(dilated esophagus)
UIP
Honeycombing - basilar
predominant
LAM
- Thin walled cysts -
distributed evenly
‘ Tuberous sclerosis
LCH
■ Nodules with cavitation (early) * Apical - “B izarre” Cysts (late) ' Smoker -20s-30s ' Sparing of the costophrenic recesses
LIP
■ Thin walled c ysts (less than LAM) " Ground Glass - clears with treatment " Sjogrens, RA, HIV
Eosinophilic pneumonia
Reverse Pulmonary
Edema Pattern
(peripheral)
Ground glass and
consolidation
COP
- Atoll / Reverse Halo Sign - Consolidation around Ground Glass - Patchy, Peripheral Consolidation
Aspergillosis
■ Halo Sign - Ground Glass
around consolidation
* Air Crescent - “invas ive”
Upper Lobe Predominant
Most inhaled stuff (not asbestosis). Coal
Workers, and Silicosis. This includes
progressive massive fibrosis.
CF
RB-ILD
Centrilobular emphysema
AS
SArcoid
Lower Lobe Predominant
asbestosis
primary cilia dyskinesia
Most Interstitial Lung Diseases
(UIP, NSIP, DIP)
Panlobular Emphysema (Alpha 1)
Rheumatoid Lung
Scleroderma (associated with NSIP)
Collagen Vascular Disease Pulmonary Manifestations
lupus
More pleural effusions and
pericardial effusions than
with other connective tissue
disease
Fibrosis is uncommon. Can
get a “shrinking lung.”
Collagen Vascular Disease Pulmonary Manifestations
RA
Looks like UIP and COP. Lower lobes are favored. Reticulations with or without honeycombing, and consolidative opacities which are organizing pneumonia
Collagen Vascular Disease Pulmonary Manifestations
scleroderma
NSIP> UIP; lower lobe
predominant findings.
Look for the dilated fluid filled
esophagus.
Collagen Vascular Disease Pulmonary Manifestations
sjogrens
LIP
Extensive ground glass
attenuation with scattered thin
walled cysts.
Collagen Vascular Disease Pulmonary Manifestations
ankylosing spondylitis
Upper lobe fibrobullous
disease
Usually unilateral first, then
progresses to bilateral.
Infections in AIDS by CD4
> 200 Bacterial Infections, TB
<200 PCP, Atypical Mycobacterial
< 100 CMV, Disseminated Fungal, Mycobacterial
ACR Appropriateness Criteria
First Line for Suspected Metastatic Disease
= CXR
Recommendation for patients on
mechanical ventilation = Daily CXR
First Line for Chest Pain and High
Suspicion for Aortic Dissection = CXR
Which Sequence(s) most useful?
Cardiac Myxoma
Low T l , High T2 (high myxoid content)
Which Sequence(s) most useful?
Acute vs Chronic MI
Look at T2 - Bright on Acute ; Dark on Chronic
fibrous scar
Which Sequence(s) most useful?
Arrhythmogenic Right Ventricular
Dysplasia (ARVD)
T l Bright
Which Sequence(s) most useful?
Microvascular Obstruction
First Pass Perfusion (25 seconds post Gad)
Which Sequence(s) most useful?
infarct
Delayed Enhancement (10-12 mins post Gad)
Cardiac MRI Enhancement Patterns
subendocardial
infarct
Cardiac MRI Enhancement Patterns
transmural
infarct
Cardiac MRI Enhancement Patterns
Subendocardial Circumferential:
Amyloidosis *can also be transmural
Cardiac MRI Enhancement Patterns
midwall focal
HCM
Cardiac MRI Enhancement Patterns
Midwall septal linear
mycoraditis, idiopathic dilated cm
Cardiac MRI Enhancement Patterns
midwall outer linear
myocraditis, sarcoidosis
Cardiac MRI Enhancement Patterns
epicardial
myocarditis, sarcoidosis
C a rd ia c S u rg e ry T y p e s / In d ic a tio n s
CHF in Infancy, Single Ventricle
Pulmonary Artery Banding
C a rd ia c S u rg e ry T y p e s / In d ic a tio n s
Transposition, Pulmonary Outflow Obstruction
Rastelli (RV Baffle)
C a rd ia c S u rg e ry T y p e s / In d ic a tio n s
Transposition
Jatene (a type o f arterial switch)
C a rd ia c S u rg e ry T y p e s / In d ic a tio n s
Diseased Aortic Valves in Children
Ross
C a rd ia c S u rg e ry T y p e s / In d ic a tio n s
Aortic Root / Valve Replacement in Marfan
Bentall
Cardiac surgery
Glenn
Vein to Artery
(SV C to Pulmonary Artery)
Primary Purpose: Take
systemic blood directly to the
pulmonary circulation (it
bypasses the right heart).
Most Testable Complications:
- SVC Syndrome
- PA Aneurysms
Cardiac surgery
Blalock Taussig
Artery to Artery
(Subclavian Artery to Pulmonary
Artery)
Primary Purpose: Increase
pulmonary blood flow
Most Testable Complications:
-Stenosis at the sh u n t’s
pulmonary insertion site
Cardiac surgery
Fotan
It’s complicated with multiple
versions - steps are unlikely to
be tested
Primary Purpose: Bypass the
right ventricle / direct systemic
circulation into the PAs.
Most Testable Complications:
-Enlarged Right Artium causing
arrhythmia
-Plastic Bronchitis
Large Vessel Vasulitis
Takayasu
giant cell
cogan syndrome
Takayasu
Large Vessel Vasulitis
Young Asian Female - thickened aneurysmal aorta
giant cell
Large Vessel Vasulitis
Old Person with involvement o f the “crutches” / armpit region
(Subclavian, axillary, brachial).
cogan syndrome
Large Vessel Vasulitis
Kid with eye and ear symptoms + Aortitis
Medium Vessel vasculitis
PAN
Kawasaki
PAN
Medium Vessel vasculitis
PAN is more common in a MAN (M > F). Renal Microaneurysm
(similar to speed kidney). Associated with Hep B.
KAwasaki
Medium Vessel vasculitis
Coronary Artery Aneurysm
Small Vessel (ANCA +) vasculitis
Wegeners
Churg Strauss
Microscopic Polyangiitis
Wegeners
Small Vessel (ANCA +) vasculitis
Nasal Septum Erosions, Cavitary Lung Lesions
Churg Strauss
Small Vessel (ANCA +) vasculitis
Transient peripheral lung consolidations.
Microscopic Polyangiitis
Small Vessel (ANCA +) vasculitis
Diffuse pulmonary hemorrhage
Small Vessel (ANCA -) vasculitis
HSP
Bechcets
buergers
HSP
Small Vessel (ANCA -) vasculitis
Kids. Intussusception. Massive scrotal edema.
behcets
Small Vessel (ANCA -) vasculitis
Pulmonary artery aneurysm
buergers
Small Vessel (ANCA -) vasculitis
Male smoker. Hand angiogram shows finger occlusions.
Tc-99m
Energy - “Low” - 140
Physical half life - 6 hours
Iodine - 123
Analog - iodine
Energy - low 159
Physical half life - 13 hours
Xenon - 133
Energy - low 81
Physical half life - 125 hours (biologic t l /2
30 seconds)
Thallium -201
Analog - Potassium
Energy - “Low” - 135 (2%), 167
(8%), use 71 ^01Hg
daughter x-rays
Physical half life -73 hours
Indium - 111
Energy - “Medium” - 173 (89%),
247 (94%)
Physical half life -67 hours
Gallium - 67
Analog - iron
Energy - Multiple; 93 (40%), 184
(20%), 300 (20%), 393
(5%)
Physical half life - 78 hours
Iodine -131
Analog - iodine
Energy - high 365
Physical half life - 8 days
Fluorine - 18
Analog - sugar
Energy - high 511
Physical half life - 110 mins
Strontium 89
physical half - life - 50.5 DAYS
14 days in bone
Samarium 153
physical half - life - 46 hours
Radium
physical half - life - 11 days
Yttrium 90
physical half - life - 64 hours
Rubidium 82
physical half - life - 75 seconds
Nitrogen 13
physical half - life - 10 mins
Probable Critical Organ
Tc - MDP
Bladder (some sources say bone)
Probable Critical Organ
Tc - Sulfur Colloid (IV)
Liver
Probable Critical Organ
Tc - Sulfur Colloid (Oral)
Proximal Colon
Probable Critical Organ
Tc - Pertechnetate
Stomach > Thyroid (some sources say colon)
Probable Critical Organ
Tc - Sestamibi
Proximal Colon
Probable Critical Organ
Tc - Heat Treated RBC
Spleen > Heart
Probable Critical Organ
Tagged RBC - MUGA
Heart
Probable Critical Organ
Tc - MAA
Lung
Probable Critical Organ
Tc - DMSA
Renal Cortex
Probable Critical Organ
Tc - MAG 3
Bladder
Probable Critical Organ
DTPA
Bladder
Probable Critical Organ
1-123 M1BG
Bladder (some sources say adrenal medulla)
Probable Critical Organ
1-131 M1BG
Liver (some sources say adrenal medulla)
Probable Critical Organ
1-131,1-123
Thyroid
Probable Critical Organ
In-111 WBC
Spleen
Probable Critical Organ
In-111 ProstaScint
Liver
Probable Critical Organ
In-111 Octreoscan
Spleen
Probable Critical Organ
Thallium 201
Renal Cortex
Probable Critical Organ
F I8 FDG
Bladder
Probable Critical Organ
Gallium
Distal Colon
Probable Critical Organ
HIDA
Gallbladder Wall
Mechanism o f Localization
Tc - Sestamibi
Passive Diffusion
Cross the cell membrane via lipophilic
diffusion
Mechanism o f Localization
Tc - Tetrofosmin
Passive Diffusion
Cross the cell membrane via lipophilic
diffusion
Mechanism o f Localization
Tc - HMPAO
Passive Diffusion
Delivery is flow related - then diffuse into
brain
Mechanism o f Localization
Tc - ECD
Passive Diffusion
Delivery is flow related - then diffuse into
brain
Mechanism o f Localization
DTPA
Filtration
Mechanism o f Localization
F18-FDG
Facilitated Diffusion
Carrier mediated transport across membrane
via GLUT
Mechanism o f Localization
1-123,1-131
Active Transport
Use ATP to move AGAINST concentration gradient
Mechanism o f Localization
Thallium
Active Transport (Na/K Pump)
Mechanism o f Localization
Rubidium
Active Transport (Na/K Pump)
Mechanism o f Localization
M1BG
Active Transport (Na facilitated norepinephrine uptake system)
Mechanism o f Localization
DMSA
Active Transport
Mechanism o f Localization
Pertechnatate
Secretion
Active transport OUT of a gland or tissue
Mechanism o f Localization
MAG-3
Secretion
Secreted by peritubular capillaries
Mechanism o f Localization
Tc-99m IDA
Secretion
Secreted by hepatocytes
Mechanism o f Localization
Sulfur Colloid
Phagocytosis
RES eats the colloid particles
Mechanism o f Localization
Heat Treated RBCs
Sequestration
Mechanism o f Localization
MAA
Capillary Blockade
Lung Perfusion
Mechanism o f Localization
MDP
Chemisorption
Chemical Covalent + Hydrogen Bonding
Mechanism o f Localization
SM -153
Chemisorption
Mechanism o f Localization
Indium WBC
Cellular Migration
Cells migrate to the response of stimuli
Mechanism o f Localization
Octreotide
Receptor Binding
Mechanism o f Localization
DAT Scan
1-123 Isoflupane
Receptor Binding
Tumors that are PET COLD
BAC (Adeno In Situ) - Lung Cancer
carcinoid
rcc
peritoeal bowlel/liver implants
anything mucinous
prostate
Not Cancer but PET HOT
infection
inflammation
ovaries in follicular phase
muscles
brown fat
thymus
FDG PET - Brain
alzheimer
Low posterior
temporoparietal cortical
activity
Identical to Parkinson
Dementia
FDG PET - Brain
multi infarct
Scattered areas o f decreased
activity
FDG PET - Brain
dementia with lewy bodies
Low in lateral occipital
cortex
Preservation o f the mid
posterior cingulate gyrus
(Cingulate Island Sign)
FDG PET - Brain
picks/frontotemporal
low in frontal lobe
FDG PET - Brain
huntingtons
low activity in caudate nucleus and putamen
Tc DTPA
overview
Filtered (GFR)
Good For Native Kidneys with
Normal Renal Function
Critical Organ Bladder
Tc MAG 3
overview
Secreted (ERPF)
Concentrated better by kidneys
with poor renal function
Critical Organ Bladder
Tc GH
overview
filtered
Good for dynamic and cortical
imaging.
critical organ bladder
ATN
Immediate Post OP
(3-4 days post op)
Perfusion Normal
Excretion Delayed
Cyclosporin Toxicity
Long Standing
Perfusion Normal
Excretion Delayed
Acute Rejection - renal
immediate post op
poor perfusion
excretion delayed
Tc WBC vs In WBC
Tc WBC: renal and GI
ln WBC: no renal or gi
Localization indium wbc
spleen
Localization indium wbc damaged
liver and bone marrow
Localization rbc tagged
heart
Localization rbc damaged
spleen
Tc WBC 4 hours
lung
Tc WBC 24 hours
lunc clear
bowel starting
Indium is BETTER than Gallium
for Evaluating
Suspected abdominal-pelvic abscess due
to the lack o f a normal bowel excretory
pathway
Gallium is BETTER than Indium
for Evaluating
• Spine • Diffuse Pulmonary Processes: Gallium is probably the agent o f choice for the evaluation o f pulmonary inflammatory abnormalities. • Lymphocyte mediated infection
Tc HMPAO is BETTER than In WBC
for Evaluating
• Children (lower Dose) • Inflammatory Bowel - *but you have to image early - like around an hour {or 30 mins - depending on who you ask). • Osteomyelitis in Extremity
In WBC is BETTER than Tc HMPAO
for Evaluating
fouo
Neuro toxo
ring enhancing
hemorrhage more common after treatment
thallium cold
pet cold
mr perfusion: decreased CBV
Lymphoma neuro
ring enhancing
hemorrhage less common after treatment
thallium hot
pet hot
mr perfusion: increased or decreased CBV
MR
AIDS
Encephalitis
Symmetric T2
Bright
MR
PML
Asymmetric T2
Bright
T1 dark
MR
CMV
periventricular t2 bright
ependymal enhancement
MR
Toxo
ring enhancement
thallium cold
MR
Cryptococcus
dilated perivascular spaces
basilar meninginitis
Neuro Trivia
nf1
Optic Nerve Gliomas
Neuro Trivia
nf2
MSME; Multiple Schwannomas, Meningiomas, Ependymomas
Neuro Trivia
vhl
Hemangioblastoma (brain and retina)
Neuro Trivia
ts
Subependymal Giant Cell Astrocytoma, Cortical Tubers
Neuro Trivia
nevoid basal cell syndrome (gorlin)
Medulloblastoma
Neuro Trivia
turcot
GBM, Medulloblastoma
Neuro Trivia
cowdens
Lhermitte-Dulcos (Dysplastic cerebellar gangliocytoma)
Maximum B le ed in g -A n eu r y sm Location
ACOM
Interhemispheric Fissure
Maximum B le ed in g -A n eu r y sm Location
PCOM
Ipsilateral Basal Cistern
Maximum B le ed in g -A n eu r y sm Location
MCA trifurcation
Sylvian Fissure
Maximum B le ed in g -A n eu r y sm Location
Basilar Tip
Interpeduncular Cistern, or Intraventricular
Maximum B le ed in g -A n eu r y sm Location
PICA
Posterior Fossa or Intraventricular
Neuro
Inverting Papilloma
Demographics: 40-70
M>F (4:1)
Typical Location: Lateral nasal wall centered at the middle meatus, with occasional extension into the antrum
Trivia: 40% show "entrapped bone" Cerebriform Pattern 10% Harbor a Squamous Cell CA
Imaging Characteristics: Cerebriform Pattern
May have focal
hyperostosis on CT
Neuro
Esthesioneuroblastoma
Demographics: Bimodal 20s &
60s
Typical Location: Dumbbell shaped with
waist at the cribiform
plate
Imaging Characteristics: AVID homogeneous
enhancement
Neuro
SNUC
Demographics: Broad Range
(30s-90s)
Typical Location: Ethmoid origin more
common than
maxillary
Trivia: Large, typically >
4cm on
presentation
Imaging Characteristics: Fungating and Poorly defined Heterogeneous enhancement with necrosis
Neuro
Squamous Cell CA
Demographics: 95% > 40 years
old
Typical Location: Maxillary Antrum is
involved in 80%
Trivia: Most Common
Malignancy of
Sino-Nasal track
Imaging Characteristics: Aggressive Antral Soft Tissue Mass, with destruction of sinus walls Low signal on T2 (highly cellular) Enhances less than some other sinus malignancies
Neuro
JNA
(Juvenile
Nasopharyngeal
Angiofibroma)
Demographics: Nearly Exclusively Male Rare < 8 or > 25
Typical Location: Origin in the
Spenopalantine
Foramen (SPF)
Trivia: Radiation alone
cures in 80%
Imaging Characteristics: Enhancing mass arising from the SPF in adolescent male Dark Flow Voids on Tl Avidly Enhances
Neuro
Sinonasal Lymphoma
Demographics: Usually older,
peak is 60s
Typical Location: Nasal Cavity >
Sinuses
Trivia: Highly variable
appearance
Imaging Characteristics: Homogeneous mass in nasal cavity with bony destruction Low Signal on T2 (highly cellular)