RD 2018 August Flashcards
MSK: Typical appearance of gout: Para-articular corticated erosions Juxta-articular osteopaenia Ill defined erosions
*LW:
Para-articular corticated erosions
*SCS
well defined, sclerotic border, punched out with overhanging margins
Normal bone density.
Chronic Recurrent Multifocal OM:
Outer third of clavicle
5 or more lesions on bone scan diagnostic
Tibia most common site
*LW:
Tibia most common Site.
Clavicle involvement is a characteristic finding as is uncommon in haematogenous OM.
Bone scan shows multifocal uptake in keeping with multi focal nature of disease.
*AJL - agree with above.
Tibia is most frequent location (favoured answer).
Other two options are classic descriptors however as stated on RP, imaging findings are suggestive rather than pathognomonic.
*RY
Medial (not lateral) clavicle most characteristic
*SCS: statdx: Multifocal lytic and sclerotic lesions of periphyseal metaphyses, metaphyseal equivalents and MEDIAL clavicle (unusual location strongly suggestive of diagnosis).
Bilateral symmetric.
Idiopathic disorder with multi focal nonpyogenic inflammatory bone lesions and relapsing/remitting course.
Associated w other inflammatory conditions: psoriasis/IBD.
Age: most commonly 9-14, female predominance (2.1:1).
whole body MRI/Bone scan to look for other sites. Nothing about >5 lesions on statdx/radiopaedia.
40yo female, knee pain for 6 weeks. Tender medial tibial plateau
Subchondral fracture
Osteoarthritis
*LW: Favoured answer is OA
Sub chondral fracture; is usually insufficiency, and commonly occurs Females aged 55yrs or older, and although can occur in tibia, is more common in femur..
Regarding Erosive OA, [which is correct?]:
Doesn’t have synovitis
Equal DIP and PIP joint involvement
Doesn’t usually involve MCPs
Has no genetic component
Doesn’t usually involve MCPs
*LW: Erosive oa: - Proliferative synovitis - Distal distribution of DIP, PIP and 1st CMC. DIP > PIP - Multi genetic trait.
MCPJs only if other predisposing factors
e.g., trauma, hemochromatosis
*SCS I have edited the question slightly so it makes sense.
I favour “Doesn’t usually involve MCPJs.
DIPJ>1st CMCJ> PIPJ (from radiopaedia OA hand article)
Primary OA has a strong genetic component
Osteosarcoma medullary or cortical Metaphyseal cortical Metaphyseal medullary Epiphyseal medullary Diaphyseal medullary Diaphyseal cortical
*LW:
Conventional OS:
- Originates in intra medullary space
- Metaphysis 91%.
Paraosteal OS:
- Surface OS
- Metaphyseal (posterior femoral metadipahyseal cortex)
Periosteal osteosarcoma:
- Surface osteosarc.
- Commonly dipahysis or meta diaphsysis of long bones.
High grade surface OS:
- Diaphyseal surface.
Low T1 and low T2 lesion in a Bakers cyst, no calcification:
Synovial sarcoma
PVNS
*LW:
PVNS, low signal implying heamosiderin layering within joint and thus extending out into Bakers cyst.
Low T1 and low T2 lesion in a Bakers cyst, no calcification
Synovial sarcoma
PVNS
*SCS: ? Poor recall. PVNS/ Synovial sarcoma can masquerade as a Bakers cysts clinically and are differentials for popliteal mass.
The “no calcification” implies synovial sarcoma is less likely.
Stay Dx says Bakers cysts are associated with inflammatory conditions ie RA, Gout. Doesn’t specifically mention PVNS but says PVNS and synovial chondromatosis can extend into SM-GM bursa from knee joint mimicking Bakers cyst.
Definition of bakers cyst:
Medial gastric and semimembranosus
*LW:
Baker cysts, or popliteal cysts, are fluid-filled distended synovial-lined lesions arising in the popliteal fossa between the medial head of the gastrocnemius and the semimembranosus tendons via a communication with the knee joint.
Regarding discitis:
T1 contrast helps make endplate changes more conspicuous
Staph is the most common organism in a 70yo female
*LW:
Regarding discitis:
T1 contrast helps make endplate changes more conspicuous: seem true
*ESG disagree - StatDx: “Early endplate destruction best seen on T1W images” - “The normal low signal line of the endplate is absent, indicative of endplate destruction.” - the point being that contrast is not required to assess the endplates, but is useful for assessing vertebral marrow, epidural and paravertebral involvement, and abscess vs phlegmon.
Staph is the most common organism in a 70yo female: true.
Which is a stable fracture: Odontoid 1 Odontoid 2 Odontoid 3 Hangmans Extension tear drop
*LW:
Odointoid type 1
Which is a stable fracture:
Odontoid 1: stable (although rare)
Odontoid 2: unstable
Odontoid 3 relatively stable if non displaced.
Hangmans: unstable
Extension tear drop: unstable (in extension as ALL is compromised, stable in flexion).
What injury is not associated with a pivot shift mechanism ACL PCL Medial meniscus LCL
*LW:
Pivot shift ligamentous injuries include:
- ACL
- Posterior capsule and arcuate ligament
- Posterior horn lateral or medial meniscus
- MCL.
Thus from below recalls, either PCL or LCL are not commonly associated with pivot shift.
Which doesn’t cause basilar invagination: Hypoparathyroidism OI Pagets Cleidocranial dysostosis Klipel Feil
*LW:
Which doesn’t cause basilar invagination:
Hypoparathyroidism: false - (Hyper parathyroidism)
OI: true
Pagets: true
Cleidocranial dysostosis: true
Klipel Feil: true
McCune Albright
unilateral ?.
*LW:
McCune Albright:
endocrinopathy: precocious puberty
polyostotic fibrous dysplasia: more severe than in sporadic cases, and tends to be unilateral.
cutaneous pigmentation: coast of Maine ‘cafe au lait’ spots
Colon: Angiodysplasia Right colon antimesenteric Left colon mesenteric Right colon mesenteric Left colon antimesenteric
*LW:
Right colon antimesenteric
Most common ileocolic fistula Adenocarcinoma Diverticulitis Lymphoma Crohns Radiation therapy
A: Crohns
*SCS: I have added extra answers for learning.
All are causes of colo-enteric fistula (Radiopaedia)
Spincteric abscesses, 2 questions one was define 3, one was similar
*LW:
St James’s University Hospital classification 1:
grade 1: simple linear intersphincteric
grade 2: intersphincteric with abscess or secondary tract
grade 3: transsphincteric
grade 4: transsphincteric with abscess or secondary tract within the ischiorectal fossa
grade 5: supralevator and translevator extension
WJI: parks classification -intersphincteric -transspincteric -suprasphincteric -extrasphincteric Causes: diverticulitis, Crohns, tb, childbirth, iatrogenic
Hep bil: 20yo woman, most common pancreatic lesion: SPEN IPMN Mucinous Serous Neuroendocrine
*LW:
SPEN - Solid pseudopapillary Neoplasm.
WJI:
Songs for FRCR rhyme-
My grandma is often serious, a bubbly shining star.
My mum is quite the opposite, we wear coats when we walk far.
Now me I’m growing, spending days at work; blood, sweat and tears.
While grandad feeds his ducks and fish and other animals near.
Serous CA: grandmother, >6cysts, <2cm diameter, hyper vascular with central calcification
Mucinous: mother, <6, >2cm, encapsulated
SPEN: daughter, encapsulated, large, heterogenous
IPMN: grandfather, ductal, fish mouth papilla
40yo women, Large cystic lesion with peripheral calcification in pancreas IPMN Mucinous Serous micro Serous macro SPEN
*LW:
Mucinous “Mother lesion”.
Panc: Calcification centrally, lots of cysts <2cm, old. Macrocystic serous adenoma Microcystic serous adenoma Mucinous SPEN IPMN
*LW:
Microcystic serous adenoma
Todani for multiple saccular intrahepatic 1 2 3 4 5
5
*LW:
Todani for multiple saccular intrahepatic
Todani type I: Fusiform dilation of the extrahepatic bile duct. this is the most common form of choledochal cyst.
Todani type II: Diverticulum of the extrahepatic bile duct. This is a rare type of choledochal cyst.
Todani type III: A diverticular expansion of the distal bile duct within the duodenal wall, termed a choledochocele. This is a rare type of choledochal cyst.
Todani type IVa: Cystic dilation of the intrahepatic and extrahepatic bile ducts. This is the second most common type of choledochal cyst.
Todani type IVb: Cystic dilation of the cystic duct and extrahepatic bile ducts.
Todani type V: Cystic dilation of the intrahepatic bile ducts. This is synonymous with Caroli disease.
Neuro: Aneurysm 3mm High risk – needs to be expedited Unlikely to cause symptoms If enlarges, could cause cranial nerve symptoms Should talk to a neurosurgeon
*LW:
Favoured answer is unlikely to cause symptoms currently.
Aneurysm 3mm:
High risk – needs to be expedited: False: low risk of rupture until > 7mm
Unlikely to cause symptoms: correct, as vast majority are assymptomatic, especially small lesions.
If enlarges, could cause cranial nerve symptoms: unlikely, cranial neuropathy is uncommon, but possible, so would dependent on lesion location and size.
Should talk to a neurosurgeon: not immediately.
Autoimmune encephalitis: VGKC encephalitis Mesial temporal Habenulae Others
*LW: favoured answer is - VGKC encephalitis.
Autoimmune encephalitis:
VGKC encephalitis:
Voltage gated potassium channel (VGKC) antibody encephalitis is an autoimmune encephalitis with antibodies against the voltage gated potassium channel. It is one of the most common forms of autoimmune limbic encephalitis in the absence of primary extra-CNS tumours.
Mesial temporal: commonly due to reactivation of HSV encephalitis.
Habenulae: part of the epithalamus,.
Others
Diffuse midbrain glioma
Usually pontine without enhancement or dwi
Medulla most common site
Avid enhancement
DWI restriction
*LW: Favoured answer: Usually pontine without enhancement or dwi
`mm - agree
Diffuse intrinstic pontine glioma:
- Expansile mass centered in pons with indistinct margins & no enhancement
- Tumor often extends into brainstem/medulla or middle cerebellar peduncle
- Diffusion restriction uncommon; ADC signal usually much brighter than adjacent brain
- Fibrillary tumors: Variable enhancement, usually none or minimal
- Focal areas of enhancement → worse prognosis (higher grade).
- majority are found in young children and are located in the pons.
Glioblastoma: Often has focal areas of enhancement with central necrosis
WJI: agree with answer but note statdx says 67% enhance. Also it’s called a diffuse MIDLINE glioma
Varicella
Spinal cord lesions
Various other ones
*LW:
Varicella-zoster virus (VZV):
Varicella: May affect multifocal areas of cortex
Zoster: Brainstem/cortical GM, cranial nerves
VZ can result in viral myelitis also.
WJI: statdx:
Cortex and cerebellum > rarely spinal cord GM, brainstem.
DAI sensitivities and adc
MRI is 90% sensitive to non-haemorrhagic
CT is 60% sensitive
Whole brain ADC is not useful in prognosis
Corpus callosum rarely involved
*LW: MRI is 90% sensitive to non-haemorrhagic: TRUE, Radiopedia states T2 weighted sequences has a 92% sensitivity for non haemorrhagic lesions.
Dai sensitivities and adc:
MRI is 90% sensitive to non-haemorrhagic: TRUE, Radiopedia states T2 weighted sequences has a 92% sensitivity for non haemorrhagic lesions.
CT is 60% sensitive: False, CT head normal in upto 80% of cases.
Whole brain ADC is not useful in prognosis: unsure but dont think so. (Stat Dx - May show foci of restricted diffusion. IVM)
Corpus callosum rarely involved: FALSE - 20% involvement
Dwi abscess and methaem:
- intracellular methaem May cause low dwi.
- dwi around the abscess - is it normal ?
- Normal diffusion restriction around an abscess
- High ADC in infarct
Methaemoglobin causes something…
*LW:
Dwi abscess and methaem:
intracellular methaem May cause low dwi:
- early subacute (3 to 7 days)
- intracellular methaemoglobin
- T1 signal gradually increases (T1 shortening) to
- become hyperintense
- low signal on isotropic DWI and reduced ADC values
dwi around the abscess - is it normal ?
- peripheral or patchy restricted diffusion may also be seen; however not that constant with up to half of rim-enhancing lesions demonstrating some restriction not proving to be abscesses.
High ADC in infarct:
- Low in the first 7 days, with pseudonormalisation in 2nd week.
- Becomes high after 3 weeks.
Methaemoglobin causes something:
- Late subacute (7 to 14-28 days)
- extracellular methaemoglobin: over the next few weeks, as cells break down, extracellular methaemoglobin leads to an increase in T2 signal
- high signal on isotropic DWI and reduced ADC values
Petrous apex lesion. Bony destruction. Low T1, T2, enhancing. No DWI. Diagnosis: Petrous apicitis Metastases Chondrosarcoma Cholesterol granuloma Cholesteatoma
*LW: unsure given low signals….
Petrous apex lesion. Bony destruction. Low T1, T2, enhancing. No DWI.
Diagnosis:
Petrous apicitis: boney destruction, enhancing thick dura, non enhancing pus which would be DWI bright.
Metastases: bone destruction, intermediate T1 and T2, enhances, may restrict diffusion.
Chondrosarcoma: invasive bony margins, should have chondroid matrix, high T2 signal, mixed enhancement.
Cholesterol granuloma: Smooth expansile bone remodelling, High T1 and T2.
Cholesteatoma: smooth expansile, low T1 and high T2, non enhancing, DWI bright.
(seems odd as low on both..)
Painless proptosis, preseptal swelling and lacrimal swelling.
TED
Idiopathic
Mets
*LW:
Favour thyroid eye disease given proptosis and lacrimal gland swelling. Unsure of pre septal swelling.
*ESG
Favour orbital sarcoidosis (maybe not recalled as an option)
Multiple sites of orbital involvement
Diffuse lacrimal gland infiltration
Optic nerve-sheath thickening, enhancement
Asymmetric extraocular muscle infiltration
Intraorbital enhancing soft tissue masses
Eyelid and periorbital preseptal infiltration
Uveitis, especially anterior, but also posterior
SCS: Radiopaedia. Lacimal gland swelling is seen in TED (lymphocytic infiltration). No mention of pre-septal swelling however.
Face: Where will pterygopalatine lesion least likely spread Anterior into sinus Posterior into middle cranial fossa Medial into nose Lateral into subtemporal fossa Suprior into orbit
*LW:
Answer: Anterior into sinus - this is favoured option being least likely spread.
medially:
- nasal cavity via the sphenopalatine foramen
laterally:
- masticator space (or infratemporal fossa) via the pterygomaxillary fissure
anteriorly:
- orbit via the inferior orbital fissure (superiorly)
posteriorly and superiorly:
- Meckel cave and cavernous sinus (of the middle cranial fossa) via the foramen rotundum
posteriorly and inferiorly:
- middle cranial fossa via the vidian canal
posteriorly and medially:
- palatovaginal canal to the nasopharynx.
inferiorly:
- palate via the greater and lesser palatine canals
Where will pterygopalatine lesion least likely spread
Posterior into middle cranial fossa
Medial into nose
Lateral into subtemporal fossa
Suprior into orbit
