Big path MCQ Flashcards
Alcoholic having treatment for Wernickes has rapid change in heart size over one
week. Change most likely due to ? Rob p839
1.Dehydration
2.Resolution of pericardial effusion
3.Projectional change on CXR
4.Beri-beri heart disease
Beri-beri heart disease this is caused by vit B1 (Thiamine) deficiency
Patient with drug resistant Parkinsons and autonomic neuorpathy ? Rob 844
1.Shy Drager Syndrome
2.Drug resistant Parkinsons
3.Striatnigeral degeneration
4.Olviopontocerebellar atrphy
5.Progressive supranuclear palsy
6.Huntingtons
Shy Drager Syndrome – type of MSA
MSA C – cerebellar. Pons, medulla and cerebellum small. -> hotcross bun (pontine)
MSA P – extrapyramidal. Low T2 + high T1 in putamen
MSA A – autonomic (Shy dragger).
PSP – Atypical parkinsons. Midbrain atrophy -> hummingbird. Midbrain : pons area calculation
Schwannoma versus plexiform neurofibroma ?
Schwannoma - Round or lobulated well delineated encapsulated tumours arising eccentrically from parent nerve and can be separated from it (c/w plexiform neurofibromas)
nf2 not nf1. spinal nerves usually not cutaneous and spinal. no malignant degen.
Child with post paravertebral mass, biopsy shows acute neural elements and schwann
cells not attached to nerve – DIAGNOSIS ?
1.Ganglioneuroma
2.Ganglioglioma
3.Neurofibroma
4.Schwannoma
5.Neuroblastoma
answer: Ganglioneuroma (Neurogenic neoplasm of sympathetic ganglia. Nerve fibres, schwann
cells, mature ganglion cells and mucous matrix)
2.Ganglioglioma
3.Neurofibroma (Each fascicle is infiltrated by neoplasm – not possible to separate lesion
from nerve)
4.Schwannoma (most common in 5th to 6th decade except in NF-2)
5.Neuroblastoma (Malignant tumour of sympathetic chain. Small round blue cells +
schwannian stroma cells)
Periventricular mass in patient with renal transplant
1.Lymphoma – 1°
2.GBM
3.Lymphoma – 2°
Lymphoma – 1° (Most common in immunosuppressed patients)
Cystic tumour in brain LEAST LIKELY is ?
1.Haemangioblastoma
2.JPA
3.PNET
4.Meningioma
5.Schwannoma
6.DNET
answer: Meningioma (Cystic or necrotic change may be present - most often in parasagittal
tumours (3 – 14%))
- Haemangioblastoma (60% are cystic masses with mural nodule that usually abuts pial
surface)
2.JPA (Cerebeallar JPA 30% of total of JPA - Well-circumscribed mass with large cyst, and
small reddish-tan mural nodule)
3.PNET (commonly cystic)
5.Schwannoma (cystic change is common)
6.DNET (Well-defined “pseudocystic” lesion (high water content))
CJD & variant CJD
1.caused by a slow virus
2.CJD patients live for <12 months, vCJD can live for a few years.
3.Associated with frontal atrophy.
CJD patients live for <12 months, vCJD can live for a few years.
Pilocytic Astrocytoma
1.Associated with NF2
2.50% are solid
3.Prognosis is less than 70% 5 year survival rate
4.Rosenthal fibres
Rosenthal fibres often present = eosinophilic bodies within astrocyte processes
up to 100% 5YS
Rosenthal fibers
Pilocytic astrocytoma
glioma
pineal tumor
Alexander’s disease
long-standing gliosis
Least common site for meningioma:
1.adjacent to hippocampus
2.parietal lobes
3.between cerebrum & cerebellum
4.adjacent to nose
adjacent to nose
Most common
Hemispheric convexity (20%)
Parasagittal (25%) → may occlude SSS
Very common
Sphenoid ridge, wing (15 – 20%) → may involve optic canal, wing meningiomas often en plaque –
extensive dural involvement. Usually extra-cranial extension into calvarium, orbit or soft tissue
Olfactory groove (5 – 10%)
Common
Parasellar (5 – 10%) CR p79 Case 63
Cavernous sinus
66% partially or totally encase carotid artery
33% narrow the artery
Less common
CPA, along clivus (posterior fossa – 10%)
Tentorium cerebelli
Foramen magnum
Rare
Optic nerve sheath (<2%)
Extracranial (nose, sinuses, skull (intraosseous))
Intraventricular
usually trigone of (L) lateral ventricle
most common trigonal mass in adults
Spinal canal (M : F = 1:10 )
mostly thoracic region
Sylvian fissure
Paediatric age group
Least likely site for hypertensive bleed in the brain is:
1.hippocampus
2.cerebellum
3.basal ganglia
4.thalamus
hippocampus
Which is least likely to involve the corpus callosum: (GC)
1.GBM
2.Marchifava Bignami
3.DAI
4.Dandy Walker
5.Lymphoma
4.Dandy Walker F - assocd with dysgenesis of the CC in 20-25% (cf. primary involvemt)
1.GBM T - most commonly spread via direct extension along WM tracts, including the CC -
classic butterfly pattern.
2.Marchifava Bignami T - primarily affects the CC - acute form affects the genu &
splenium, chronic form affects the body.
3.DAI T - classic triad of GW junction, dorsolateral brainstem, and CC (most commonly
eccentrically and in the splenium).
5.Lymphoma T - differ from GBM as usually less peritumoral oedema,
Hashimoto’s – FNA findings (TW)
1.Hurthle cells
2.Fibrosing nodules
3.Psammoma bodies
Hurthle cells -T - mononuclear inflammatory infiltrate containing small lymphocytes,
plasma cells, and well-developed germinal centers. The thyroid follicles are small and are
lined in many areas by epithelial cells with abundant eosinophilic, granular cytoplasm,
termed Hurthle cells.
Hurthle cells seen in:
Hashimotos
Follicular adenoma
2.Fibrosing nodules - F - Reidel’s thyroiditis
3.Psammoma bodies - F - in papillary thyroid carcinoma. Concentrically calcified
structures.
Which is not a feature of Alzheimer’s: (GC)
1.Hirano bodies
2.Lewy Bodies
3.Senile Plaques
4.Neurofibrillary tangles
5.Granulovacuolar degeneration
6.Amyloid
Lewy Bodies F - eosinophilic intracytoplasmic inclusions found in some neurones in
Parkinson’s disease.
.PNET, which is the most typical appearance:
1.Cortical
2.Angiogenesis
3.Cystic
4.Vasogenic oedema
5.Astrocytoma
Angiogenesis T - WHO grade IV. Supratentorial PNETs had highly branched capillaries with extensive endothelial cell hyperplasia. Glomeruloid arrays of microvessels extended from the capillaries. Small fragments of endothelial tubes were scattered throughout the tumor.
In HSV I encephalitis, which is least correct (TW)
1.Age 50-70 years
2.Typically involves superior frontal lobes
3.Common presentation is headache
4.May present with seizures,
Typically involves superior frontal lobes - F - abnormal signal and enhancemen t of
medial temporal and inferior frontal lobes. Affects limibic system: temporal lobes, insula,
subfrontal area and cingulate gyri typical.
Age 50-70 years - T - can occur at any age, with highest incidence in adolescents and
young adults. Bimodal distribution by age with 1st peak occurring younger than 20y
(primary infection), and second occuring in those older than 50y (reactivation of latent
infection).
3.Common presentation is headache - T - fever, headache, seizures, +/- viral prodrome.
4.May present with seizures, ataxia and lethargy - T - altered mental status, focal or diffuseneurologic deficit (<30%)
Child with posterior paravertebral mass, biopsy shows mature neural elements and
Schwann cells not attached to nerve – diagnosis is (TW)
1.Ganglioneuroma
2.Ganglioglioma
3.Neurofibroma
4.Schwannoma
5.Neuroblastoma
1.Ganglioneuroma - T - The most well-differentiation lesions (in the neuroblastoma
spectrum) - see ganglion cells and Schwann cells, and neuroblasts are no longer present.
2.Ganglioglioma - F - tumor of neoplastic astrocytes (rarely oligodendrocytes) and ganglioncells.
3.Neurofibroma - F - PNST arise from cells of the peripheral nerve (Schwann cells,
perineural cells, fibroblasts) - attached to nerve, but can be separated from it
4.Schwannoma - F - PNST - see ans 3.
5.Neuroblastoma - F- small, primitive-appearing cells with dark nuclei, scant cytoplasm,and poorly defined cell borders growing in solid sheets. Certain NBs may have some degreeof differentiation with clusters of larger cells resembling ganglion cells.
Child with mass FNA shows small round blue cells- least likely diagnosis is (TW)
1.Neuroblastom
2.Ewing’s sarcoma
3.Rhabdomyosarcoma
4.Wilms tumour
5.Retinoblastoma
Wilms tumour - F - classic Wilms tumor comprised of 3 cell types - Blastemal cells
(undifferentiated cells), Stromal cells (immature spindle cells and heterologous skeletal, cartilage, osteoid, or fat), and epithelial cells (Glomeruli and tubules).
1.Neuroblastoma - T - small, primitive-appearing cells with dark nuclei, scant cytoplasm,and poorly defined cell borders growing in solid sheets.
2.Ewing’s sarcoma - T - monotonous sheets of small round blue cells with hyperchromatic
nuclei and scant cytoplasm.
3.Rhabdomyosarcoma - T - subtypes Botryoid and spindle cell (leiomyomatous / Embryonal
/ Alveolar / Undifferentiated. Histo of embryonal and alveolar types - cells have scant cytoplasm and a centrally placed round nucleus that occupies the majority of the cell.
5.Retinoblastoma - T - sheets, trabeculae and nests of small blue cells with scant cytoplasm.
Ewing’s sarcoma family of tumors (EFT) includes Ewings sarcoma, extraosseous Ewing’s sarcoma,more differentiated neuroectodermal tumors (PNET: previously AKA neuroepithelioma, adultneuroblastoms, Askin’s tumor of chest wall).
Definition of Hamartoma is (TW)
1.Abnormal disorganised tissue in abnormal position
2.Abnormal disorganised tissue in normal position
3.Normal disorganised tissue in normal position
4.Normal disorganised tissue in abnormal position
Normal disorganised tissue in normal position - T - cellular elements are mature and identical to those found in remainder of organ, but do not reproduce the normal
architecture of the surrounding tissue. Tumor-like malformation with tissues of particular part of body arranged haphazardly, usually with excess of one or more of its components.
Pick’s disease, uncommon findings (TW)
1.Asymmetrical atrophy
2.Predominant frontal lobes
3.Cortical atrophy
4.Involvement of post ⅔ superior temporal gyrus & parietal lobe
Involvement of post ⅔ superior temporal gyrus & parietal lobe - F - spared posterior
aspect of superior temporal gyrus and pre- and postcentral gyri. Unremarkable parietal and occipital lobes.
Picks disease / Frontotemporal dementia - nonspecific songioform degneration, with gliosis and neuronal loss, sometimes with Pick cells and bodies. 25-40% of FTD is familial. 10-30% of patients with positive family history have tau mutations (Tauopathy).
1.Asymmetrical atrophy - T - worse atrophy of dominant hemisphere
2.Predominant frontal lobes - T - anterior frontotemporal atrophy.
3.Cortical atrophy - T - thin cortex. Gliosis of corticl gray matter. Soft, retracted subcortical
white matter. Almost complete loss of large pyramidal neurons, diffuse spongiosis and
gliosis.
40 year old female with stroke, underlying cause least likely is (TW)
1.Atherosclerosis
2.Dissection
3.Coarctation of aorta
4.Giant cell arteritis
5.Mitral valve prolapse
.Giant cell arteritis - F - GCA is a chronic vasculitis of large and medium sized vessels.
Mean age at Dx is approx 72yo, and the disease essentially never occurs in individuals
younger than 50yo (UpToDate).
Atypical Scenario (TW)
1.Craniopharyngioma in a 42 year old
2.Anaplastic thyroid cancer in a 29 year old
3.Bowel cancer in a 32 year old
4.Cholangiocarcinoma in a young adult with emphysema
Anaplastic thyroid cancer in a 29 year old - F - older patients, mean age 65yo
1.Craniopharyngioma in a 42 year old - T - Bimodal age distribution (peak 5-15yo;
papillary craniopharyngioma >50y).
3.Bowel cancer in a 32 year old - T - peak incidence for CRC is 60-70yo. CRC in a young
person, preexisting UC or one of teh polyposis syndromes must be suspected.
4.Cholangiocarcinoma in a young adult with emphysema - T - a-1-antitrypsin deficency
predisposes to cholangiocarcinoma.
Pilocytic Astrocytoma, which is true (TW)
1.Associated with NF2
2.50% are solid
3.Prognosis is less than 70% 5year survival rate
4.Multipolar cells with microcysts, and bipolar cells with Rosenthal fibres
4.Multipolar cells with microcysts, and bipolar cells with Rosenthal fibres - T - classic
“biphasic” pattern of two astrocyte populations: compacted biplar cells with Rosenthal fibers (electron dense GFAP staining cytoplasmic inclusions); Loose-textured multipolar cells with microcysts, eosinophilic granular bodies.
1.Associated with NF2 - F - NF1. 15% of NF1 patients develop PAs (most commonly in
optic pathway). Upt o 1/3 of patients with optic pathway PAs have NF1.
2.50% are solid - F - 40% solid with necrotic center, heterogeneous enhancement. 10%
solid, homogeneous. 50% non enhancing cyst with enhancing mural nodule.
3.Prognosis is less than 70% 5year survival rate - F - median survival rates at 20y >70%
Retinoblastoma, which is the least likely ? (TW)
1.Very radio sensitive. Excellent prognosis even if it extends retro-orbitally
2.Carriers of RB gene have a 90% risk
3.Can get extraocular Retinoblastomas
Very radio sensitive. Excellent prognosis even if it extends retro-orbitally - F - enuleation
usually is indicated for large tumors with not visual potential, blind, painful eyes, and/or
tumors that extend into the optic nerve. External beam XRT was original globe-sparing
treatment for Rb. Risk of tumor recurrence following ext XRT 7%, occurring within
40months. Also risk of secondary cancers with XRT.
2.Carriers of RB gene have a 90% risk - T - If a mutant RB allele arises in the germ line, it
can be transmitted as a dominant trait, and carriers are at high risk (>90% risk for most
mutations) for retinoblastoma. Robbins.
3.Can get extraocular Retinoblastomas - T - trilateral RB = bilateral RB with
neuroectodermal pineal tumor. Quadrilateral RB = trilateral RB with 4th focus in
suprasellar cistern. Dahnert 6th.
Paragangliomas, which is false : (TW)
1.paraganglioma, chemodectoma, and carotid body tumors can be used interchangeably
2.carotid body tumors often adherent to vessels resulting in incomplete excision and
recurrence of 10%
3.glomus jugulare and carotid body paragangliomas are the most common head and neck
paragangliomas
4.paragangliomas have bipphasic or biphenotypic pattern and composed of chief cells and sustentacular cells
paraganglioma, chemodectoma, and carotid body tumors can be used interchangeably - F - multiple names: glomus tumor, chemodectoma, endothelioma, perithelioma,
sympathoblastoma, fibroangioma, sympathetic nevi. Paragangliomas are classified based on their location, innervation, and microscopic appearance. Would need to specify location for paraganglioma / chemodectoma to be able to use interchangeably with carotid body
tumor.
2.carotid body tumors often adherent to vessels resulting in incomplete excision and
recurrence of 10% - T - Shamblin classification - Type I are localized and easily removed;
type II adherent and partially surround carotid vessels; type III adherent and completely surround carotid vesels and extremely difficult to resect often requiring resection of ICA and vein graft interposition. Prevalence of local recurrence and local invasion - 40-50% of glomus jugulare tumors, 17% for vagal paragangliomas, and about 10% for carotid body tumors.
3.glomus jugulare and carotid body paragangliomas are the most common head and neck paragangliomas - T - conflicting reports regarding the prevalence of these 2 subtypes some saying one is more prevalent, some saying the other is.
4.paragangliomas have bipphasic or biphenotypic pattern and composed of chief cells and sustentacular cells
CMV encephalitis: which is false? (TW)
1.characteristic inclusions
2.ependymal & subependymal involvement
3.may cause haemorrhage
4.majority of newborns have systemic signs of disease, of which about half have CNS
involvement
majority of newborns have systemic signs of disease, of which about half have CNS
involvement - F - most infected newborns appear normal. 10% have systemic signs of
disease (hepatosplenomegaly, petechiae, chorioretinitis, jaundice, and IUGR). 55% with
systemic disease have CNS involvement (microcephaly, parenchymal Ca+, SNHL, seizures, hypotonia or hypertonia).
1.characteristic inclusions - T - CMV inclusion-bearing cells. Prominent cytomegatic cells
with intranuclear and intracytoplasmic inclusions can be readily identified. Hallmark is cytomegaly with viral nuclear and cytoplasmic inclusions.
2.ependymal & subependymal involvement - T - may affect any cell type by striking
tendency for virus to localise in teh epehdymal and subependymal regions of brain. Replicates in ependyma, germinal matrix, and capillary endothelia.
3.may cause haemorrhage - T - results in severe necrotising ventriculo-encephalitis with massive necrosis, haemorrhage, ventriculitis and choroid plexusitis
IV contrast, 4 -12 hrs afterwards, it results in skin necrosis. It’s a repeatable
response. What type of reaction is it? (TW)
1.Type 1
2.Type 2
3.Type 3
4.Type 4
5.Non-immune reaction
Type 3 - T - Immunocomplex disease. Induced by antigen-antibody complexes that
produce tissue damage as a result of their capacity to active the complement system. Can be generalized (immune complexes formed in circulation adn deposited in many organs etc), or localized to particular organs such as kidney (GN), joints (arthritis) or the small blood vessels of the skin if the complexes are formed an deposited locally (the local Arthus reaction). See below. Eg SLE, serum sickness.
Local immune complex disease (Arthus reaction) - type III hypersensitivity reaction. Localized area of tissue necrosis resulting from acute immune complex vasculitis, usually elicited in the skin.Reaction can be produced by intracutaneous injection of antigen in an immune patient having
circulating antibodies against the antigen. Unlike IgE mediated type I reactions, which appearimmediately, the Arthus lesion develops over a few hours and reaches a peak 4-10hrs after injection, when it can be seen as an area of visible oedema with severe hemorrhage followed
occasionally by ulceration.
Type 1 hypersensitivity - F- Anaphylactic type. Rapidly developing immunologic reaction
developing within minutes after combination of antigen with antibody bound to mast cells or
basophils in individuals previously sensitized to antigen
2.Type 2 - F - Cytotoxic type. Mediated by antibodies directed toward antigens present on
surface of cells or other tissue component (subtypes: complement-dependent reactions;
antibody-dependent cell mediated cytotoxicity; antibody mediated cellular dysfunction. Eg
ABO)
Type 4 - F - Cell mediated (delayed). Initiated by specifically sensitized T lymphocytes.
.Bowen Disease (TW)
1.associated with BCC in 5% of cases if left untreated
2.may have a penile cutaneous horn
3.results from chronic irritation and/or inflammation with development of scaly palques
often involving the meatus
4.carcinoma in situ occurring within follicle-bearing epithelium
carcinoma in situ occurring within follicle-bearing epithelium – T - Usually appears as a
solitary, dull-red plaque with areas of crusting and oozing.
HIV positive patient with CD4 count less than 100 has a mass on CT brain. What is the
likely diagnosis? (TW)
1.Lymphoma
2.Toxoplasmosis
3.Cryptosporidium
4.TB
5.PML
Toxoplasmosis - T- most common cause of focal lesion in HIV+.
1.Lymphoma - F - less likely, although increased risk with immunosuppression (35x).
3.Cryptosporidium - F - less likely cf toxoplasmosis
4.TB - F - less likely
5.PML - F - diffuse/patchy WM abnormalities.
Neuroblastoma, which is associated with a better prognosis: (GC)
1.Age > 1 year
2.Stage 4B
3.Abdominal primary
4.Decreased N-myc amplification
5.Metastases to bone only
4.Decreased N-myc amplification T - less copies of gene is better
1.Age > 1 year F - age < 1yr has a better prognosis
2.Stage 4B F - stage 4S has a near 100% survival
3.Abdominal primary F - thoracic primary has a better prognosis
5.Metastases to bone only F - mets to liver and skin is associated with better prognosis
Evans anatomic staging: (prognosis - % survival)
1: confined to organ of interest (90%)
2: extension beyond organ but not crossing midline (75%)
3: extension crossing midline (30%)
4: distal mets (10%)
4S: age < 1yr, mets confined to liver, skin and bone marrow.
[Paeds pocket rad]
Commonest sites for ependymoma, which is least likely: (GC)
1.Periventricular areas
2.Lateral and third ventricle in infants
3.Fourth ventricle in children
4.Spine in adults
2.Lateral and third ventricle in infants - anaplastic ependymoma (rare), usually in infants and children.
In children: infratentorial 70%; supratentorial 30%, of which frontal > parietal > temporoparietal
juxtaventricular region (uncommonly intraventricular), lateral ventricle, 3rd ventricle. [Dahnert]
- Periventricular areas T - supratentorial ependymoma is more commonly seated in the brain parenchyma, typically arising near the trigone of the lateral ventricle. Thought to
arise from embryonic rests of ependymal tissue trapped in the developing cerebral
hemispheres. Tend to be larger in size, more often cystic components cf. infratentorial. [RG
2005, eMedicine]
3.Fourth ventricle in children T - most commonly arises from floor of 4th ventricle.
4.Spine in adults T - common site, better able to excise completely and generally better
prognosis. Most common intramedullary spinal neoplasm in adults.
.Huntington’s disease, which is true: (GC)
1.Autosomal recessive
2.Affects the putamen and caudate
3.Presents in the second decade
4.Chorea due to striatal excitation
Affects the putamen and caudate T - degeneration of the striatum (C&P).
1.Autosomal recessive F - autosomal dominant disorder
3.Presents in the second decade F - age of onset most commonly in 4th and 5th decades,
related to the length of the CAG repeat.
4.Chorea due to striatal excitation F - loss of striatal inhibitory output, from the
degeneration of GABA-containing neurons. This leads to disregulation of the basal ganglia that normally modulate motor output.
In drug resistant Parkinsons and autonomic neuropathy an MRI would look for all the
following except? (TW) (MSA a)
1.Striatonigral degeneration
2.Decreased putaminal ADC values
3.Cerebellar atrophy
4.Cruciform pontine hyperintensity
2.Decreased putaminal ADC values - F - DWI appears to differentiate Parkinsons Disease
from progressive supranuclear palsy and the Parkinsons variant of multiple system atropy
MSA - striatonigral degeneration: clinically similar to idiopathic PD in presentation but is
relatively resistant to L-dopa treatment (due to pattern of neuronal degeneration - ie both
dopaminergic projections and its target neurons are absent, therefore L-dopa cannot bulster neurotransmission as occurs in parkinsons disease). Also have gross atrophy of caudat nucleus and putamen. Some patients also show evidence of pontocerebellar degeneration.
DWI - appears to differentiate PD from progressive supranuclear palsy and Parkinson variant of MSA. in MSA-Pv get increased putaminal ADC values. In PSP have increased ADC in putamen,
GP, and caudate nucleus.
1.Striatonigral degeneration - T - predominant degeneration of substantia nigra and
striatum, with putamen > caudate nucleus.
3.Cerebellar atrophy - T - hemispheres > vermis
4.Cruciform pontine hyperintensity - T - hot cross bun sign (but not pathognomonic of MSA)
Patient with possible ADEM. Which clinical setting least likely? (TW)
1.2 week history of viral illness
2.female
3.headache and confusion progressing to coma in 48 hrs
4.HIV positive
5.Age less than 40
4.HIV positive - F - this is probably rare, however ADEM has been assoc with HIVseroconversion illness. Probably getting you to Dx from PML.
1.2 week history of viral illness - T - monophasic (usually) demyelinating disease following
either a viral infection, or, rarely, a viral immunisation. Typically develops a week or two
after anticedent infection.
2.female - T - common finding. Male predominance reported in some series 1.3 : 1
3.headache and confusion progressing to coma in 48 hrs - T - usually fever, malasie,
myalgia as prodromal phase. Then headache, fever, drowsiness. Can have cranial nerve
palsies, seizures, hemiparesis, decreased consciousness (from lethargy to coma).
5.Age less than 40 - T - peak age 3-5yo, but can occur at anytime
A new Nuc Med agent can attach to the amyloid in neuritic plaques. Which is most
correct? (TW)
1.Should help exclude congophilic angiopathy in the elderly
2.Uptake would allow distinction between Alzheimers and age matched Parkinsons disease
3.Alzheimers patients should have greater uptake in the medial temporal lobe than age
matched control patients
4.Cerebellar uptake would suggest ataxic telangiectasia
5.Deep cerebral uptake would suggest multi-infarct dementia or MS
Alzheimers patients should have greater uptake in the medial temporal lobe than age
matched control patients - T - degenerative process starts in medial temporal lobe, spreads to parahippocampal gyrus, temporal and frontal lobes, and finally involves motor and visual cortex. Get parietal and temporal cortical atrophy with disproportionate
hippocampal volume loss. Predominates ijn medial temporal and pareital lobes.
34/40 fetus with large mass protruding posteriorly from sacrum. No evidence of Chiari malformation. Most likely is (TW)
1.Benign sacrococcygeal teratoma
2.Malignant sacrococcygeal teratoma
3.Congenital neuroblastoma
4.Imperforate cloacal membrane
5.Mature ganglioneuroma
Benign sacrococcygeal teratoma - T - sacrococcygeal region is the most frequent tumor
site of teratomas. SCTs occur most commonly in infants and may be Dx in utero, or at birth
with the majority in females. Frequence of malignancy in this location varies from less than
10% when younger than 2mo, to more than 50% when older than 4mo (Nelson’s pediatrics).
Prevalence 1 in 35000 to 40000 births (Donnelly).
16 year old with Friedrichs ataxia has a poor quality MRI. Most likely cause is (TW)
1.Intention tremor
2.Recurrent facial tic
3.Orthopnoea
4.Salaam spasms
5.Hemiballismus
Orthopnoea
Friedrich ataxia - AR degenerative disorder. Most common hereditary ataxia. Most cases caused by loss of function in frataxin gene (frataxin is a mitochondrial protein whose prescise function is
unknown).
Neuropathology - degeneration of posterior columns and the spinocerebellar tracts of the spinal cord and loss of the larger sensory cells of the dorsal root ganglia.
Major clinical manifestations of FQ - neurologic dysfunction, cardiomyopathy, and diabetes mellitus. Neuro - ataxia of limbs, absence of lower limb reflexes, and presence of pyramidial signs.
Early loss of position and vibration sense.
Cardiomyopathy - concentric LVH, asymmetric septal hypertrophy, and globally decreased LVF
patterns of disease.
Major causes of death are complications related to the cardiomyopathy or bulbar dysfunction,
leading to an inability to protect the airway.
.Hemorrhagic areas in cerebrum on CT. Least likely (TW & GC)
1.Recent pelvic fracture
2.Past rheumatic fever
3.Active mastoiditis
4.Recent neck manipulation
5.Recent placental abruption
Recent neck manipulation - F - vert dissection, but probably least likely option.
Population-based, case-control study found pts under 45yo, those with vertebrobasilar
dissection or occlusion were 5x more likely than controls to have visited a chiropractor in
the previous week. Actual incidence reports vary (1 per 400 000 manipulations, to 2 per
million).
65 year old, 3rd yearly follow up scan for sCJD. Which is most correct? (TW)
1.This is expected as CJD is slowly progressive
2.Incorrect diagnosis
3.Patient most likely has variant CJD
4.CJD has variable progression with 10-15% having a long term survival of > 10 years
5.Patient more likely to have the more indolent familial form
Incorrect DX
1.This is expected as CJD is slowly progressive - F - rapidly progressive mental
deterioration and myoclonus (sCJD). Mean duration of illness for sCJD 4-5months
(howevers urvival range varies depending on subtype of sCJD).
3.Patient most likely has variant CJD - F - mean duration of illness 14months.
4.CJD has variable progression with 10-15% having a long term survival of > 10 years - F -
both vCJD and sCJD are progressive and uniformly fatal. Occasional case reports of
survival to 40-50months, but rare.
5.Patient more likely to have the more indolent familial form - F - fCJD accounts for 10- 15% cases. Longer survival - mean duration 26 months. Age little younger than sCJD (~60yo).
Least likely sites for Toxo in the brain (TW)
1.GW junction
2.Pons
3.Cerebellum
4.Spinal cord
5.Putamen
Spinal cord - F - toxoplasmosis of the spinal cord is less frequent than in the brain (in
HIV), and has become even less common cause of myelopathy after the introduction of
HAART )
Most at risk for cerebral venous infarction false (TW)
1.diabetic in renal failure
2.post obstetric patient
3.young girl on progesterone only pill
4.young girl with SLE
3.young girl on progesterone only pill - F - oestrogen is major prothrombotic component.
Progesterone much lower risk. Most frequent reisk factor for cerebral venous sinus
thrombosis is the OCP (but this is presumably the oestrogen containing one).
Solitary 3cm cystic lesion in the brain containing an opaque gel-like substance (TW)
1.Hydatid / echinococcus
2.Cysticercosis
3.Amoebiasis
4.Strongyloides
5.Ascaris
1.Hydatid / echinococcus - T - large uni- or multilocular cyst +/- detached germinal
membraine. Cyst fluid is opalescent. Cyst is 3cm.
2.Cysticercosis - F - although most common parasitic infection world wide, cyst size is
variable and typically 1cm, with range of 4-20mm. Parenchymal cysts 1cm or less, however
subarachnoid systs may be larger, up to 9cm reported (and recemose). Cysts are ovoid and
white-to-opalescnet, rarely exceeding 1.5cm. Contain an invaginated scolex with hooklets
that are bathed in clear cyst fluid. Fluid can be opalescent in the vesicular – colloidal stage,
but question says cyst is 3cm.
3.Amoebiasis - F - cerebral amebiasis is a rare cause of brain abscess. Amebic encephalitits
NF1 – which is not/least associated (TW)
1.Wilms -
2.Rhabdomyosarcoma
3.CML
4.phaeochromocytoma
5.osteosarcoma
osteosarcoma - F - couple of case reports of NF1 and osteosarc, but not indicated that is
associated. Note however that NF1 is assoc with sarcomas.
wilms also a little shakey but more assoc.
Children with Ependymoma, which is false: (GC)
1.Prognosis poor
2.Less common than medulloblastoma
3.Does not metastasize as frequently as medulloblastoma
4.Myxopapillary variant in filum terminale
5.4 year survival 50%
4 year survival 50% F - current 5YS rate for patients with intracranial ependymomas is
approximately 50%, when rates from children and adults are combined. Stratification based
on age reveals 5YS rates of 76% in adults and only 14% in children.
1.Prognosis poor – T - Despite the survival advantage of gross total resection, lesions of the
posterior fossa are in close proximity to cranial nerves with a significant risk of long-term
neurologic dysfunction and disability. Hence, most tumors of the posterior fossa cannot be
fully resected and are likely to recur without postoperative radiation. Osborn: “cannot
remove completely”
2.Less common than medulloblastoma T - third most common paediatric brain tumour,
after medulloblastoma & JPA.
3.Does not metastasize as frequently as medulloblastoma T - subarachnoid dissemination
via CSF rare, observed in <10% of patients at diagnosis when ependymoblastomas are
excluded. The incidence is higher with infratentorial ependymomas than with supratentorial
tumors (9% vs 1.6%).
4.Myxopapillary variant in filum terminale T - considered a biologically and
morphologically distinct variant of ependymoma, occurring almost exclusively in the region
of the cauda equina and behaving in a more benign fashion than grade II ependymoma.
Huntington’s chorea, what does it show: (GC)
1.Various locations including basal ganglia
2.Caudate nucleus + putamen
3.Cerebellum
4.Locus ceruleus
Caudate nucleus + putamen T - striking atrophy (heart or box-shaped frontal horns), less
.Pilocytic Astrocytoma, most common location: (GC)
1.Cerebrum
2.CPA
3.Brainstem
4.Hypothalamus
5.Pituitary
Hypothalamus
Most lesions occur in or near the midline. Commonest locations: cerebellum, hypothalamus
(around 3rd ventricle), optic n./chiasm
Peripheral MCA aneurysm, most likely history: (GC)
1.SLE
2.Past history of irradiation for fibrous dysplasia
3.Hypertension
4.History of rheumatic fever and tooth extraction
History of rheumatic fever and tooth extraction T - Aneurysms that develop at distal sites
in the intracranial circulation are often caused by trauma or infection. Mycotic aneurysms
are most commonly due to infected arterial embolus, occurring in subacute bacterial endocarditis. In such cases, they are often multiple, being situated in small
corticomeningeal branches of the cerebral artery.
1.SLE F - Commonly reported CNS vascular lesions with SLE include infarcts and
transient ischemic attacks. Intracranial hemorrhages are present in approximately 10% of
patients with CNS symptoms. Although uncommon, arteritic and nonvasculitic aneurysms
occur in SLE. These can be saccular, fusiform, or a bizarre-looking mixture of both.
2.Past history of irradiation for fibrous dysplasia F - Radiation is contraindicated as it has
been found to increase the rate of secondary malignancy by 400 times. If in the remote
past… intracranial aneurysms may develop (and rupture) post irradiation.
3.Hypertension F - Charcot-Bouchard microaneurysms secondary to segmental
lipohyalinosis of the walls of long penetrating arteries.
Dying of presumed Alzheimer’s disease, which is NOT suggested in the diagnosis: (GC)
1.Parietal atrophy
2.Silver-staining dystrophic neurites surrounding a central amyloid core
3.Amyloid
4.Neurofibrillary tangles in occipital region
5.Intracellular changes in hippocampal pyramidal cells
Neurofibrillary tangles in occipital region - NFT’s are commonly found in the entorhinal
cortex, as well as in pyramidal cells of hippocampus, amygdala, basal forebrain, raphe
nuclei. Perhaps in advanced dementia there may be occipital cortex involvement (?).
Posterior cortical atrophy (Benson’s syndrome) and Balint’s syndrome may be regarded as
variants of AD, whereby deposition of neuritic plaques and NFT’s are specifically revealed
in the posterior cerebral areas (occipital cortex, visual cortex). [Acta Neuropathologica
1993]
1.Parietal atrophy - gross examination of brain shows a variable degree of cortical atrophy
with widening of the cerebral sulci, most pronounced in the frontal, temporal and parietal
lobes with compensatory ventricular enlargement. Parietal involvement helps differentiate
from Pick’s disease - asymmetric frontal & temporal lobe atrophy, with sparing of the
posterior 2/3 of superior temporal gyrus and only rare involvement of the parietal or
occipital lobes.
2.Silver-staining dystrophic neurites surrounding a central amyloid core - neuritic (senile)
plaques are a Dx feature.
3.Amyloid - almost invariable accompaniment of AD.
5.Intracellular changes in hippocampal pyramidal cells - these include Hirano bodies,
NFT’s, granulovacuolar degeneration.
Subependymoma, which is true (TW)
1.Usually slow growing and asymptomatic
2.Associated with TS
3.5-10 yo
4.Commonly in lateral ventricle
Commonly in lateral ventricle - T - inferior fourth ventricle, frontal horn of lateral
ventricle most common sites.
1.Usually slow growing and asymptomatic - F - slow growing, however, although can be
asymptomatic, 50% become symptomatic. WHO grade I.
2.Associated with TS - F - TS assoc with cortical / subcortical tubers, subependymal
hamartomas, subependymal GCA. Zits, fits, nitwits (facial angiofibroma, epileptic seizures,
mental retardation).
3.5-10 yo - F - middle-aged / elderly adult (typically 40-50yo). Rare in children (unlike
ependymoma).
TB Meningitis, which is most correct: (GC) see August 2007
1.Endarteritis causes ischaemia.
2.Small multiple miliary nodules in brain
3.Cannot be seen macroscopically
4.Can be asymptomatic
1.Endarteritis causes ischaemia. T - ischaemic infarcts of BG + internal capsule in 20-40%,
due to vascular compression and/or occlusion of small perforating vessels in basal cisterns.
.Juvenile pilocystic astrocytoma, which is false: (GC) see August 2007
1.Even without surgery rarely fatal
2.Well circumscribed, easy to cut out
3.Commonly cortical
4.More benign behaviour when it occurs in patient with NF1
5.Abundant Rosenthal fibres
3.Commonly cortical F - most lesions occur in or near the midline, usually arising from the
cerebellum, optic n/chiasm, hypothalamic-thalamic region.
Leighs, which is incorrect… (TW)
1.Increased T2 signal in peri-aqueductal gray matter
2.Enhancement is uncommon
3.Lysosomal storage disorder
4.May be x-linked inheritance
5.Most present by 2y age
Lysosomal storage disorder – F – mitochondrial disorder characterised by
neurodegeneration. Brain and striated muscle highly dependent on oxidative
phosphorylation which are moste severely affected in mitochondrial disorders.
1.Increased T2 signal in peri-aqueductal gray matter – T – best diagnostic clue = bilateral,
symmetric increased T2/FLAIR in putamina and peri-aqueductal gray matter
2.Enhancement is uncommon - T
4.May be x-linked inheritance – Autosomal recessive, X-linked, and maternal inheritance of
mutated proteins involved in mitochondrial energy production underlie Leigh syndrome.
5.Most present by 2y age – T – majority by 2yo
Which is not a feature of Alzheimer’s: (GC) see April 2007
1.Hirano bodies
2.Lewy bodies
3.Senile plaques
4.Neurofibrillary tangles
5.Amyloid
2.Lewy bodies F - eosinophilic intracytoplasmic inclusions found in some neurones in parkinsons
Regarding vestibular schwannomas: (TW)
1.Bilateral tumours are associated with NF1
2.Haemorrhage is uncommon
3.About 70% are cystic
4.Meningeal reaction is typical
5.A melanotic variant is a recognized entity –
Haemorrhage is uncommon – T – rare to get haemorrhagic foci (0.5%).
1.Bilateral tumours are associated with NF1 – F – NF2 = MISME, multiple inherited
schwannomas, meningiomas, and Ependymomas.
3.About 70% are cystic – F – 15% have intramural cysts (Harnsberger)
4.Meningeal reaction is typical – F – this is a differentiating factor to Dx from meningioma.
5.A melanotic variant is a recognized entity – F - CME says F. However there are a handful
of cases reported (so very, very rare). Melanotic schwannoma is a rare melanin-producing
nerve sheat tumor. MSs are of neural crest origin, prob from neoplastic proliferation of a
common precursor cell for both Schwann cells and melanocytes. Most involve cranial or
spinal nerve roots (esp spinal Cx and thoracic nerves). 10% involve symp chain. There have
been reports of MSs of vestibular nerves. MSs may be component of Carney complex.
.Mesial temporal sclerosis, which is false (TW)
1.contrast enhancement of the para hippocampal gyrus
2.atrophy hippoc gyrus
3.may see fornix and/or mamillary body atrophy
4.dilatation of temporal horn may be evident
1.contrast enhancement of the para hippocampal gyrus - F – no enhancement.
2.atrophy hippoc gyrus – T – decreased size of hippocampus
3.may see fornix and/or mamillary body atrophy – T – location: mesial temporal lobe –
hippocampus > amygdale > fornix > mamillary bodies. Bilateral in 20% cases.
4.dilatation of temporal horn may be evident - T
The following statements regarding agenesis of the corpus callosum, false?: (TW)
1.Ventriculomegaly predominantly affects the occipital horns
2.Is associated with Down’s syndrome
3.The lateral ventricles are widely placed
4.There is an association with heterotopic gray matter
5.It is associated with colpocephaly
Is associated with Down’s syndrome – F – Assoc with abnormal karyotype (T13, 15, 18 –
not typically assoc with T21, however there are some case reports). Multiple other assoc:
Dandy-Walker cyst, interhemispheric arachnoid cyst, hydrocephalus, intracerebral lipoma
of CC, AC II malformation, porencephaly, Holoprosencephaly, polymicrogyria.
1.Ventriculomegaly predominantly affects the occipital horns – T – occipital horns often
dilated (colpocephaly). Pointed frontal horns. Can get dilation of the posterior temporal
horns in the absence of splenium.
3.The lateral ventricles are widely placed – T- “bat-wing” appearance of lateral ventricles
(= wide separation of lateral ventricles with straight parallel parasagittal orientation with
absent callosal body)
4.There is an association with heterotopic gray matter – T – polymicrogyria, gray-matter
heterotopia
5.It is associated with colpocephaly - T
Sellar lesions, which is true (TW)
1.normal sella favours meningioma rather than macroadenoma
2.squamous variant of craniopharyngioma is more likely cystic
3.intrasellar arachnoid cyst will displace stalk anteriorly
4.17mm pituitary is normal for pregnant female
5.macroadenoma more likely to compress ICA than meningioma
normal sella favours meningioma rather than macroadenoma - T - as pituitary MAs grow
they first expand sella and then grow upwards. Aggresive adenomas extend inveriorly,
invade sphenoid, and may destroy upper clivus. As they are soft - often are indented by
diaphragma sellae giving them a ‘snowman’ configuration which can help Dx from
meningoma.
2.squamous variant of craniopharyngioma is more likely cystic - F - squamous papillary
type (more common in adults) rarely calcifies, oftsn solid, isodense. Both
adamantinomatous and squamous papillary types enhance.
3.intrasellar arachnoid cyst will displace stalk anteriorly - F - 10% arachnoid cysts are
suprasellar & would push stalk back.
4.17mm pituitary is normal for pregnant female - F - normal pituitary measurements:
children 6mm, males and post-menopausal females 8mm, young menstruating females
10mm, pregnant/lactating females 12mm.
5.macroadenoma more likely to compress ICA than meningioma
Sensorineural hearing loss, which is true (TW)
1.destruction of ossicular chain from otitis media
2.cochlear SNHL is more common than retrocochlear SNHL
3.sudden loss after minor trauma is typical for vestibular aqueduct synd
sudden loss after minor trauma is typical for vestibular aqueduct synd - T
1.destruction of ossicular chain from otitis media - F - conductive
2.cochlear SNHL is more common than retrocochlear SNHL - F - other way around.
retrocochlear SNHL (abnormalities of neurons of the spiral ganglion) more common than
cochlear SNHL (damage to cochlea / organ or Corti). Dahnert 6th.
MS (TW)
1.juxta cortical favours MS vs age
2.enhancement lasts 3 months
3.usually thoracic spinal lesion
4.perpendicular to long axis if cord
enhancement lasts 3 months - T - Dahnert says Gd-DTPA enhancement of lesions on
T1WI up to 8weeks following acute demyelination. Osborn says >90% of enhancing lesions
disappear within 6 months.
1.juxta cortical favours MS vs age - F - calloseptal favors MS, plus infratentorial.
2.enhancement lasts 3 months - T - Dahnert says Gd-DTPA enhancement of lesions on
T1WI up to 8weeks following acute demyelination. Osborn says >90% of enhancing lesions
disappear within 6 months.
3.usually thoracic spinal lesion - F - predilection for cervical cord
4.perpendicular to long axis - F - parallell to long axis of spinal cord / perpendicular to the
axis of CC, ventricles.
.CC dysgenesis, false (TW)
1.genu always present in partial
2.cingulate gyrus normal
3.foramen monro enlarged
4.assoc with AC II
2.cingulate gyrus normal - F - dysgenesis of cingulate gyrus / persistent eversion of
cingulate gyrus medial parietal sulci affected - T - radial array pattern of medial cerebral
sulci, gyri “point to” 3rd ventricle
1.genu always present in partial - T - depending on time of arrested growth (anteroposterior
development of genu, body, splenium, however, rostrum forming last). Can have: genu only,
genu + part of body, genu + entire body, genu + body + splenium (without rostrum).
3.foramen monro enlarged - T - enlarged / elongated foramina of Munro
4.assoc with AC II - T - 7%. Also assoc with DW cyst, interhemispheric arachnoid cyst,
hydrocephalus, lipoma of CC, porencephaly, holoprosencephaly, polymicrogyria.
Congenital CNS infections, which is least likely:
Chicken pox
Rubella
CMV
Toxo
Herpes
Herpes
Macroscopic features of de Quervains Thyroiditis (AKA subacute). (TW)
1.Diffuse smooth symmetrical goiter
2.Multiple nodules
3.Bilateral or unilateral enlarged lobes
Bilateral or unilateral enlarged lobes - T - gland may be unilaterally or bilaterally
enlarged and firm, with an intact capsule. Both thyroid lobes are involved from the
beginning in most patients.
1.Diffuse smooth symmetrical goiter - F - only mild-moderate enlargement (Dahnert,
UptToDate), patchy with occasionally distinctly focal inlvolvement. On cut section -
involved areas are firm and yellow-white and stand out from the more rubbery, normal
brown thyroid substance.
2.Multiple nodules - F - early scattered follicles may be entirely disrupted and replaced by PMN forming microabscesses. Later the characteristic changes: aggregates of cells around damaged follicles.
.55 yr old man with oncocytes from biopsy of a solitary parotid cyst? (TW)
1.Benign pleomorphic adenoma
2.Warthins tumour
3.HIV.
4.Type 1 Branchial cleft cyst
5.Mucoepidermoid
Warthins tumour - T - benign neoplasm. Distinctive double layer of lining cells with
surface palisade of columnar cells having abundant, finely granular, eosinophilic
cytoplasm, imparting an oncocytic appearance, resting on a layer of cuboidal to polygonal cells.
1.Benign pleomorphic adenoma - F - heterogeneity. Epithelial elements resembling ductal cells or myoepithelial cells disposed in duct formations, acini, irregular tubules, strands, or sheets of cells.
3.HIV.
4.Type 1 Branchial cleft cyst - F - fibrous walls usually lined by stratified squamous or
pseudostratified columnar epithelium underlaid by an intense lymphcytic infiltrate or, more
often, well-developed lymphoid tissue with reactive follicles.
5.Mucoepidermoid - F - mucus secreting cells, often forming glandular spaces. Higher
grade tumors are composed of squamous cells with only a scatterin gof mucus-secreting
cells.
Oncocytes are epithelial cells stuffed with mitochondria that impart the granular
appearance to the cytoplasm.
Least likely to cause Hyperthyroidism? (TW)
1.Graves disease
2.Toxic adenoma
3.Hashimotos thyroiditis
4.Riedels Thyroiditis
5.Subacute thyroiditis
Riedels Thyroiditis - F - rare, chronic inflammatory disease of thyroid gland
characterized by a dense fibrosis that replaces normal thyroid capsule. Morbidity is most frequently related to local compressive symptoms. Most patients are euthyroid, and
hypothyroidism can be seen in 30% cases.
1.Graves disease - T - thyroid stimulating antibodies. Elevated T3 and T4.
2.Toxic adenoma - T - AKA Plummer disease / toxic autonomous nodule. Hyperthyroidism
caused by one / two hyperfunctioning nodules independent of normal pituitary-thyroid control.
3.Hashimotos thyroiditis - T - thyrotoxicosis in early stage 4%. Hypothyroid at presentation
20%. Chronic lymphocytic thyroidits. Autoimmune process with marked familial
predisposition.
5.Subacute thyroiditis - T - AKA subacute thyroiditis. Hyperthyrodisim 50% secondary to severe destruction. Short-lived hypothyroidism (25%) due to hormone depletion of gland.
Probably viral aetiology. Lymphocytic infiltration, granulomatous and foreign body giant cells
Which of the following is least correct? (TW)
1.Chordomas arise from physaliphorous cells
2.Paragangliomas are parasympathetic tumours
3.Cholestrol granulomas need an aerated pterous apex for formation
4.Cholestatomas arise from epithelial rests
1.Chordomas arise from physaliphorous cells - F - arise from embryonic remnants of the
primitive notochord. Microscopically, cordomas are composed of characteristic mucoid, fluid-containing, translucent cells of variable size with a large, intracytoplasmic vacuole, and they are rich in mucin and glycogen (physaliphorous cells)
2.Paragangliomas are parasympathetic tumours - T - rare neuroendocrine tumors arising from paraganglionic tissue found between base of skull and floor of pelvis. Adrenal
paraganglioma = phaeochromocytoma, extraadrenal paraganglioma sympathetic /
parasympath
3.Cholestrol granulomas need an aerated pterous apex for formation - T - results from
obsturction of the normal aeration of petrous air cells.
4.Cholestatomas arise from epithelial rests - T - derived from aberrant embryonic
ectodermal rests in temporal bone (primary, AKA epidermoid cyst). Ingrowth of squamous
epithelium throught tympanic membrane secondary to repeated inflammation / marginal perforation of ear drum.
Which of the following are true in regards to choristomas and hamartomas? (TW)
1.A hamartoma is an ectopic rest of tissue
2.A choristoma is abnormal tissue in a normal location
3.An adenoma is a typical hamartoma -
4.Adrenal tissue under the renal capsule is an example of a choristoma
5.Hamartomas predispose to an increased risk of malignant transformation
Adrenal tissue under the renal capsule is an example of a choristoma- T - normal cells or
tissues in an abnormal location.
1.A hamartoma is an ectopic rest of tissue- F - Tumor-like malformation with tissues of a
particular part of the body arranged haphazardly, usually with excess of one or more of its components. Excessive but focal overgrowth of cells and tissues native to the organ in which it occurs (cf teratoma - tissues NOT specific to the part)
2.A choristoma is abnormal tissue in a normal location - F - AKA heterotopia. Normal cells
or tissues that are present in abnormal locations. eg rest of pancreatic tissue found in the wall of the somtach or small intestine, or small mass of adrenal cells found in the kidney, lungs, ovaries, or elsewhere. The heterotopic rests ore usually of little significance, but can be confused clinically with neoplasms.
4.Adrenal tissue under the renal capsule is an example of a choristoma- T - normal cells or
tissues in an abnormal location.
5.Hamartomas predispose to an increased risk of malignant transformation - F - not
neoplastic. No tendency to excessive growth, being co-ordinated with surrounding tissues
and stops after adolescence.
Which is not a mixed neural/glial tumour? (TW)
1.Ganglioglioma
2.DNET
3.Lhermitte Duclos
4.Pleomorphic xanthoastrocytoma
5.Neurocytoma
Pleomorphic xanthoastrocytoma - F - rare distinct astrocytoma subtype tumor of children and young adults. Astrocytic tumor.
Neuroglial tumors - nerve cells and glial cells of the brain come from a primitive neuroepithelial precur cell and germinal matrix. Pure neurons = ganglion cells (gangliocytoma, neurocytoma).
Tumors of oligodendrocytes and astrocytes may be combined with ganglion cells and calledgangliogliomas. If abnormalities which are considered to incorporate all these tumor types - can be called neuroepithelial tumors (DNET).
1.Ganglioglioma - T - benign tumor composed ofneoplastic astrocytes and ganglion cells.
2.DNET - T - mixed neuronal-glial neoplasm of infancey with a distinct desmoplastic
component.
3.Lhermitte Duclos - T - dysplastic gangliocytoma of cerebellum - very rare, tumor-like neuronal lesion of the cerebellum, with distincet dysplastic features.
4.Pleomorphic xanthoastrocytoma - F - rare distinct astrocytoma subtype tumor of children and young adults. Astrocytic tumor.
5.Neurocytoma - T - Interventricular tumor composed of uniform round cells with
immunihistochem an ultrastructural features of neuronal differentiation. Arises from septum pellucidum.
Which of the following is least correct regarding fat embolism? (GC)
1.Symptoms of irritability and confusion
2.Petechial rash
3.Hypovolaemic shock
4.Passive flow of adipose tissue through the vascular system
Hypovolaemic shock - F - tachycardic, SOB and hypoxic (but not hypotensive) in fat
embolism syndrome, which occurs 1-3 days after injury. Hypovolaemic shock may have
been an issue at the time of injury.
1.Symptoms of irritability and confusion - T - systemic hypoxaemia and dyspnoea,
mentation changes (headaches, confusion), petechiae in 50% from coagulopathy (release of tissue thromboplastin), fever.
2.Petechial rash - T - see ans (1).
4.Passive flow of adipose tissue through the vascular system - T - fat enters circulation after fractures of long bones (ie. rupture of marrow vascular sinusoids), or after soft tissue injury (rupture of venules). Pathogenesis involves obstruction of pulmonary vessels by fat globules,
followed by chemical pneumonitis from unsaturated plasma fatty acids, producing
haemorrhage/oedema.
VHL is associated with all of the following except… (TW)
1.Clear cell RCC
2.Papillary cell RCC
3.Retinal angiomas
4.Pheochromocytomas
5.3p deletions
2.Papillary cell RCC - F - RCCs of predominant papillary, chromophobe, or oncocytic
histology are not associated with vHL disease (UTD). pRCC is the 2nd most common
subtype, and most common multifocal or bilateral renal tumor. Most pRCCs are sporadic.
1.Clear cell RCC - T - all vHL-associated RCCs are clear cell tumors, although these clear
cell tumors may contain minor papillary components (usually <25% of the lesion).
3.Retinal angiomas - T - see below
4.Pheochromocytomas - T - vHL phenotype: pheochromocytoma (frequently bilateral),
paraganglioma (rarely), retinal angioma, cerebellar hemangioblastoma, epididymal
cystadenoma, renal and pancreatic cysts, pancreatic neuroendocrine tumors, and renal cell carcinoma.
5.3p deletions - T - vHL gene Ch 3p25. Specific germline mutations or deletions of the vHL
gene can influence the clinical manifestations of vHL disease
70 year old man with a 5 year history of a slowly enlarging, painless parotid mass which has markedly increased in size over the last 3 mths. The most likely cause is: (–)
5.Pleomorphic adenoma with malignant transformation to adenocarcinoma
6.Infected first branchial cleft cyst
7.Warthin’s Tumour with cystic change
8.Haemorrhage into a pleomorphic adenoma
9.Erosion and fistula
Pleomorphic adenoma with malignant transformation to adenocarcinoma
A carcinoma infrequently arises in a pleomorphic adenoma, referred to variously as a carcinoma ex pleomorphic adenoma or a malignant mixed tumor.
The incidence of malignant transformation increases with the duration of the tumor, being about
2% for tumors present less than 5 years
10% for those of more than 15 years’ duration
The cancer usually takes the form of an adenocarcinoma or undifferentiated carcinoma, and often it virtually completely overgrows the last vestiges of the preexisting pleomorphic adenoma; but to substantiate the diagnosis of carcinoma ex pleomorphic adenoma, recognizable traces of the latter must be found.
Regrettably, these cancers, when they appear, are among the most aggressive of all salivary gland malignant neoplasms, accounting for a 30% to 50% mortality in 5 years
Nasal polyps which is TRUE? Big Rob p762
1.By definition < 2cm
2.Mostly associated with atopy
3.Ulcerate in chronic disease and not secondary to bacterial infection
4.30% have history of atopy
5.Histology is orderly mucosa with stromal
Ulcerate in chronic disease and not secondary to bacterial infection
1-4cm
most not atopy
not orderly; oedematous, loose stroma, hyperplastic or cystic mucus flands, infiltrated inflammatory
Cholestatoma which is TRUE? Big Rob p767
1.Contains cholestrol crystals
2.Stratified Squamous epithelium and keratinous material
3.Causes destructive lesion in inner ear
Stratified Squamous epithelium and keratinous material
Cholesteatomas associated with chronic otitis media are not neoplasms, nor do they always contain cholesterol.
Rather, they are cystic lesions 1 to 4 cm in diameter, lined by keratinizing squamous epithelium or metaplastic mucus-secreting epithelium, and filled with amorphous debris (derived largely from desquamated squames)
Sometimes they contain spicules of cholesterol
Tracheo-oesophageal fistula, MOST COMMON ? Rob p549 (TW)
1.Proximal fistula, distal blind pouch
2.“H” type
3.Distal fistula, proximal pouch
4.Misnomer because no atresia
5.Misnomer because no fistula
Distal fistula, proximal pouch - T - oesophageal atresia and tracheo oesophageal fistula
not in communication with proximal oesophagus (82%)
Classic appearance of Malloy Weiss tear is ? Rob p550 (–)
1.Linear at gastro-oesphageal junction
2.Linear with hiatus hernia
3.Undermined proximal mucosa
4.Circular at GOJ
Linear at gastro-oesphageal junction (linear lacerations in axis of oesophagus lumen, at or
below the G-E junction)
boerhaaves = rupture
What are risk factors for malignancy in a stomach ulcer ?
1.pernicious anaemia
2.Crohn’s disease
3.coeliac disease
4.H. Pylori
pernicious anaemia (Pernicious anaemia + gastritis- 3x risk only)
H. Pylori (H.P associated chronic gastritis is assoc. with 5x increased risk
Long-term risk of gastric cancer in Autoimmune gastritis = 2 – 4%
Even in heavily colonized stomachs, the organisms are absent from areas with intestinal metaplasia
As such, they probably account for the increased incidence of gastric cancer in atrophic forms of
gastritis, particularly in association with pernicious anemia
2004 QUESTION SAID OCCURS IN AREAS OF ATROPHY
Malignant gastric ulcer. What would be the most concerning for malignancy? Rob p561
(TW)
1.> 4cm diameter
2.single ulcer of greater curvature
3.heaped edges
heaped edges - heaping up of the margins is rare in the benign ulcer but is characteristic
of the malignant lesion.
1.> 4cm diameter - size does not diffentiate a benign from malignant ulcer, usually less than 2cm)
2.single ulcer of greater curvature - location of gastric carcinoma within stomach is: pylorus and antrum 50-60%; cardia 25%; remainder in body an fundus. The lesser curvature is involved in about 40% and the greater curvature in 12%. Thus, a favored location is the lesser curvature of the antropyloric region. Although less frequent, an ulcerative lesion on the greater curvature is more likely to be malignant.
Stomach cancer, which is NOT TRUE? Rob p561 (TW)
1.Benign ulcers on lesser curvature at antrum
2.Alcohol is not a risk factor
3.Most common is adenocarcinoma/ then lymphoma/ then carcinoid/then GIST
4.Early gastric cancer is confined to the mucosa/submucosa with negative perigastric nodes
5.Morphological types – excavated, exophytic or flat
Early gastric cancer is confined to the mucosa/submucosa with negative perigastric nodes - F - regardless (ie not influenced by) of presence of perigastric nodes (Robbins).
Ulcerated carcinomas usually have nodular raised margins with “dirty” necrotic bases, and lack surrounding radiating folds
Early gastric carcinoma: lesion confined to mucosa and submucosa, regardless of presence or absence of perigastric lymph node metastases.
Advanced gastric carcinoma: neoplasm that has extendd below the submucos into the muscular wall.
1.Benign ulcers on lesser curvature at antrum - T - gastric ulcers are predominantly located
along the lesser curvature, in or around the border zone between the corpus and the antral mucosa.
2.Alcohol is not a risk factor - T
3.Most common is adenocarcinoma/ then lymphoma/ then carcinoid/then GIST - T -
Adeono 90-95%, Lymphoma 4%, Carcinoids 3%, malignant stromal cell tumours (2%).
5.Morphological types – excavated, exophytic or flat (true)
Which of the following statements concerning GIT diseases IS INCORRECT: (JS)
1.Most gut lymphomas are T-cell type
2.Villous adenomas are most common in the rectum
3.In Hirshsprung’s Disease, the rectum is always involved
4.Angiodysplasia is most common in the proximal colon
5.Necrotising enterocolitis is most common in neonates
Most gut lymphomas are T-cell type - F - most are B cell lymphomas (90%)
Coeliac diseasease What is the least likely? (JS)
1.anti-gliadin antibodies
2.treatment prevents development of lymphoma
2.treatment prevents development of lymphoma - F - there is a long term risk of malignant disease at 2 times the usual rate - intestinal lymphomas (including disproportionately high number of T-cell lymphomas) and GIT and breast cancers.
1.anti-gliadin antibodies - T - due to a sensitivity to gluten (gliadin)
Coeliac disease associated with? Rob p571 (JS)
1.2x risk of malignancy
2.Bowel wall thinning
1.2x risk of malignancy - T - there is a long term risk of malignant disease at 2 times the
usual rate - intestinal lymphomas (including disproportionately high number of T-cell
lymphomas) and GIT and breast cancers.
2.Bowel wall thinning - F - crypts are elongated, hypoplastic and tortuous but the overall mucosal thickness remains the same
.Coeliac disease, T/F (JS)
1.definitive diagnosis is shown by showing histological total villous atrophy
2.10-20% have anti-gliadin Ab’s without having the disease
1.definitive diagnosis is shown by showing histological total villous atrophy - T - diagnosis
requires documentation of malabsorption, demonstration of intestinal lesion by small bowel biopsy and improvement in symptoms with gluten free diet.
2.10-20% have anti-gliadin Ab’s without having the disease - T - 90% of patients with
coeliac disease will have a positive IgA AGA before treatment but 10-20% of people will
have a false positive IgA AGA and a normal small bowel biopsy. IgG EMA (Endomysial
antibodies) has a much lower false positive rate (1%) and is found in 95-100% of patients
with the disease.
Which of the following statements concerning gastrointestinal diseases is most correct?
(JS)
1.The colon is the most common site for GIT lymphoma -
2.Pseudomembranous colitis is due to toxins of clostridium difficile
3.Inflammatory pseudo-polyps are a characteristic feature of Crohn’s colitis
4.Apthous ulcers are a characteristic feature of ulcerative colitis
5.Juvenile polyps typically occur in the ascending colon.
3.Inflammatory pseudo-polyps are a characteristic feature of Crohn’s colitis - F - associated
with UC but can occur in Crohns
4.Apthous ulcers are a characteristic feature
1.The colon is the most common site for GIT lymphoma - F - Stomach (55-60%), small
intestine (25-30%), proximal colon (10-15%) and distal colon (10%) with appendix and
oesophagus rarely involved.
2.Pseudomembranous colitis is due to toxins of clostridium difficile - T - Caused by
exotoxins A and B of C. difficle after antibiotic therapy of ulcerative colitis - F - associated with Crohns
5.Juvenile polyps typically occur in the ascending colon. - F - hamartomatous
malformations of mucosa, typically in the rectum
In which one of the following are granulomas NOT a characteristic feature? (JS)
1.Crohn’s disease
2.Sarcoidosis
3.Foreign body response
4.Ulcerative colitis
5.Tuberculosis
Ulcerative colitis
Which of the following IS NOT a recognised feature of diverticular disease of the colon:
(JS)
1.Hypertrophy of the circular muscle layer of the bowel
2.Dissection into the appendices epiploicae
3.Crypt abscesses
4.Fistulae
5.Haemorrhage
3.Crypt abscesses - F - Typical lesion of UC - collections of neutrophils within crypt
Concerning carcinoid tumours of the gastro-intestinal tract, which of the following
statements IS LEAST correct: (JS)
1.The appendix is the most common site
2.They have a characteristic desmoplastic reaction
3.They are benign tumours -
4.A characteristic feature is a solid, yellow-tan appearance on transactions
5.They are a more common small bowel neoplasm than primary adenocarcinoma
3.They are benign tumours - F - all are potentially malignant
1.The appendix is the most common site - T - Appendix most common, followed by terminal ileum, stomach, rectum & colon
2.They have a characteristic desmoplastic reaction - T
4.A characteristic feature is a solid, yellow-tan appearance on transactions - T - Solid,
yellow-tan appearance on cut section
5.They are a more common small bowel neoplasm than primary adenocarcinomas - T - most common lesion of small bowel – about the same incidence (both about half)
Amebiasis which is TRUE ?
1.Organism is Ngareri Fowleri
2.Invasion through mucosa and into peyers patches
3.10% of infected people have dysentery
4.Cysts release trophozoites secondary to pancreatic enzymes.
5.Release exotoxin and denude epithelium
3.10% of infected people have dysentery - T
1.Organism is Ngareri Fowleri - F - Entamoeba histolytica
2.Invasion through mucosa and into peyers patches - F - invade the crypts of the colonic
glands and burrow through the tunica propria and are halted by the muscularis mucosae.
4.Cysts release trophozoites secondary to pancreatic enzymes. - F - release trophozoites
under anaerobic conditions
5.Release exotoxin and denude epithelium - F - This is referring to C difficle in
pseudomembranous colitis. Amoebae produce proteins involved in tissue invasion including proteinases, lectin and amebapore, resulting in ulcers and sloughing of the mucosa
Crohn’s disease in counselling a sibling of risk (JS)
1.1% risk
2.No increased risk
3.10% risk
10% risk - T - lifetime risk if either a parent or sibling is affected is 9% (Robbins)
Crohns diease is NOT ASSOCIATED with ? Rob p573 (JS)
1.Hydronephrosis
2.Carcinoma
3.Hip arthopathy
4.Sclerosing cholangitis
5.Sclerosing peritonitis
Sclerosing peritonitis - T - associated with peritoneal dialysis
Patient with ulcerative colitis with elevated CEA (Carcinoembryonic antigen)? Rob p574,
208,585 (JS)
1.Likely colon cancer
2.May be colon cancer but also raised in UC active inflammation
3.Active ulcerative Colitis
May be colon cancer but also raised in UC active inflammation - T - produced in
embryonic tissue of the gut, pancreas and liver. Elevated in 60-90% of colorectal, 50-80%
of pancreatic and 25-50% of gastric and breast cancer. Also elevated in cirrhosis, hepatitis, UC, Crohns and in smokers. Lacks specificity and sensitivity for early cancer detection but can be used in prognosis and detection of recurrence.
Which does not cause bowel obstruction? mRob p578 (–)
1.Tuberous Sclerosis
2.GVHD
3.Collagen vascular disorders
4.Viral infections
5.Ingested toxins
Collagen vascular disorders (scleroderma, dermatomyositis – muscle dysfunction –
marked dilatation of small bowel simulating small bowel obstruction)
In colonic polyps which is TRUE ? Rob p579 (JS)
1.Peutz Jeger is sporadic hamartomatous polyps
2.HNPCC (Hereditary Nonpolyposis Colorectal Cancer) not associated with adenoma
3.Most common type in adults is villous
4.Juvenille polyps occur in ileum
HNPCC (Hereditary Nonpolyposis Colorectal Cancer) not associated with adenoma - T -
HNPCC is characterised by familial carcinoma of the colon, affecting predominantly
caecum and proximal colon, which DON’T arise within adenomatous polyps.
1 Peutz Jeger is sporadic hamartomatous polyps - F - Autosomal dominant syndrome (not sporadic) characterised by multiple hamartomatous polyps
3.Most common type in adults is villous - F - Tubular adenomas are the most common
(90%) followed by tubulovillous (5-10%) then villous (1%)
4.Juvenille polyps occur in ileum F - Focal hamartomatous polyps found most frequently in the rectum in children younger than 5y
Adenomatous polyps are NOT a feature of ? (JS)
1.Gardners Syndrome
2.Familial Polyposis
3.Turcot’s Syndrome
4.Peutz-Jeghers Syndrome
5.Sessile Villous lesions
Peutz-Jeghers Syndrome - T - hamartomatous lesions which don’t have malignant
potential themselves, but patients have an increased risk of other cancers (pancreas, breast, lung, ovary and uterus)
1.Gardners Syndrome - F - AD variant of FAP with intestinal polyps, osteomas and soft
tissue tumours
2.Familial Polyposis - F - AD disorder with innumerable adenomatous polyps with
progression to adenocarcinoma in 100%
3.Turcot’s Syndrome - F - rare variant of Gardners syndrome with colonic polyposis and tumours of the CNS
5.Sessile Villous lesions - F - type of adenomatous polyps
Following associated with increased risk of bowel malignancy EXCEPT? Rob p579 (JS)
1.Obesity
2.Diabetes
3.Crohns
4.Meat/low fibre diet
diabetes
Risk factors for colorectal cancer include diet (low fibre, high intake of refined carbs, intake of red meat, reduced intake of protective micronutrients such as vitamins A, C and E), obesity, physical inactivity, family history, IBD, previous XRT, FAP, HNPCC.
60 year old male has colonic carcinoma which involves muscularis mucosa. No regional lymph nodes, no distant metastasis. What is prognosis? Rob p582 (–) (GC & TW)
1.100% 5 year survival
2.95% 5 year survival
3.67% 5 year survival
4.40% 5 year survival
5.10% 5 year survival
3.67% 5 year survival B1 = 67% (path notes); TNM staging is 90%
STAGING
Single most important prognostic indicator = extent of tumour at time of diagnosis
Modified Dukes Classification / Astler-Coller Staging:
A Limited to the mucosa (TNM – ‘T is’ (in situ))
B1 Extending into but not through muscularis propria, no nodal spread (TNM – T1)
B2 Through muscularis propria, no nodal spread (TNM – T2)
C1 Into muscularis propria + nodal spread (ie B1 + nodes)
C2 Through muscularis propria + nodal spread (ie B2 + nodes)
D Distant metastases
Staging can only be applied after resection of neoplasm and surgical exploration
Recurrences most common (10%):
at operation site, near anastomoses
in peritoneal cavity
in liver and distant organs
PROGNOSIS
Related to stage:
A = ~100% 5YS
B1 = 67% MR says for TNM staging prognosis is 90%
B2 = 54% MR says for TNM is 78%
C1 = 43%
C2 = 23%
Overall 5 year survival 40 – 50%
Commonest site for adenocarcinoma colon commonest to rarest are ?
Caecum and ascending colon (38%) > Sigmoid (35%)> transverse (18%)> descending
(8%) > multiple sites (1%)
Histologically appendicitis characterised by ? Rob p588 (JS)
1.Neutrophils in the mucosa
2.Neutrophils in the the muscularis propria
3.Plasma cells/lymphocytes in muscularis
4.Serosal hyperaemia
Neutrophils in the the muscularis propria - T - Histologic criterion is neutrophilic
infiltration of muscularis. Usually neutrophils and ulceration is also present within the
mucosa but other conditions can cause mucosal infiltrate (ie spread from GIT infection elsewhere)
HNPCC – barium enema is performed to look for (TW)
1.Colonic carcinoma
2.polyps
3.detect colonic hamartoma
Colonic carcinoma - T - HNPCC (Lynch syndrome) an AD condition, characterised by
familial carcinomas of the colon, predominantly affecting the caecum and proximal colon.
These don’t arise in adenomatous polyps.
HNPCC / Lynch sydrome is the most common of the inherited colon susceptibility syndromes.
Significantly increase risk of colon cancer and endometrial cancer as well as small risk of sever other associated cancers (ovariian, upper GUT, gastric, small bowel, biliary/pancreatic, skin, brain).
Lifetime risk of developing CRC in Lynch = 70%. Like most sporadic CRCs, Lynch cancers appear to evolve from adenomas, but when detected the adenomas tend to be larger, flatter, and are oftenmore proximal.
Accelerated adenoma-carcinoma sequence, dysplasia in flat mucosa of colon.
There are several types of DNA damage, and, correspondingly, there are many forms of DNA repair.
HNPCC results from defects in genes involved in DNA mismatch repair.
DNA repair genes themselves are not oncogenic, but they allow mutations in other genes during the process of normal cell division
Historically
this is true, however, now shown to be due to a DNA mismatch repair gene, where there is
either accelerated adenoma-Ca sequence or dysplasia in an area of flat mucosa.
Patient with suspected mononucleosis, which would be atypical? (JS)
1.Abnormal LFT
2.Proteinuria with viral inclusions in epithelial cells in urine
3.Groin lymphadenopathy
4.Mononuclear meningitis
5.Atypical lymphocytes on FNA
2.Proteinuria with viral inclusions in epithelial cells in urine - T - this occurs in CMV
infection
Echinococcus Granulosus, which is true? (JS)
1.20% infected have liver lesions
2.Myocardial involvement is by antigen cross reaction rather than direct invasion
3.Entry is by breach in skin and mucosal membranes
4.Initially cysts begin at microscopic leve
Initially cysts begin at microscopic level - T - Cysts begin at microscopic size and
progressively increase in size (can reach 10cm in 5 years)
1.20% infected have liver lesions - F - liver is the most common organ of involvement
(73%), followed by lung (14%), peritoneum (12%), kidney (6%). Can also involve spleen,
CNS, orbit, bone, bladder, thyroid, prostate and heart.
2.Myocardial involvement is by antigen cross reaction rather than direct invasion - F -
3.Entry is by breach in skin and mucosal membranes - F - caused by ingestion of tapeworm eggs in dog faeces which hatch in the duodenum
Acute acalculous cholecystitis which is unlikely (JS)
1.Post partum
2.HIV positive
3.TPN
4.Amyloid
5.Post surgical
Amyloid - F - can cause features of a low grade chronic acalculous cholecystitis due to
infiltration of gallbladder wall
Staging hepatocellular carcinoma, portal nodes negative, next most likely site is (JS)
1.Bone
2.Lungs
3.Adrenal
4.Brain
5.Spleen
2.Lungs - T - most common site of mets (followed by adrenal, lymph nodes and bone)
(Dahnert)
Patient with elevated CA 125 (JS)
1.Colon cancer
2.Ovarian cancer
3.Any ovarian pathology
Any ovarian pathology- T - elevated in ovarian cancer, endometrial, cervical, pancreatic,
bronchial and breast cancer. Also with hepatoma, benign ovarian disease, PID,
endometriosis, hepatitis, pancreatitis and pregnancy.
Amyloid, which is false (JS)
1.In TB is AA type
2.Causes Sago spleen and Lardaceous spleen
3.Seen in x% of patients with renal failure
Seen in x% of patients with renal failure - F - although renal involvement is common,
renal function compromise is rare (RG 2004;24(2):405-416). Get amyloid (joint deposition) if on hemodialysis (incidence 21% 2yr dialysis, 50% 4-7y, 90% 7-13y, 100% >13y).
1.In TB is AA type - T - AA type is secondary amyloidosis - Crohns, JRA, Reiter syndrome,
ank spond, familial Mediterranean fever, Sjogren, dermatomyositis, vasculitis, chronic
osteomyelitis, TB, bronchiectasis, CF, SLE etc
2.Causes Sago spleen and Lardaceous spleen - T - Sago spleen refers to deposits of amyloid
within splenic follicles producing tapioca-like granules. Lardaceous spleen is seen with
fusion of the deposits giving rise to large maplike areas of amyloidosis
Megaloblastic anaemia is not caused by : (JS)
1.Pernicious anaemia
2.Crohn’s disease
3.Coeliac disease
4.Pancreatic calcification
Pancreatic calcification – F - CME
1.Pernicious anaemia - T - results in Intrinsic factor deficiency and therefore Vitamin B12
deficiency
2.Crohn’s disease - T - Ileitis can cause impaired absorption of Vit B12
3.Coeliac disease - T - Causes malabsorption
Sickle cell anaemia. An unusual feature would be (JS)
1.splenomegaly
2.splenic atrophy/ absent
3.fungal dacralitis
4.aplastic crises
.fungal dacralitis - F - dacrylitis is caused by vaso-occlusive crisis (hypoxic injury and
infarction caused by sickling), which can be precipitated by infection
1.splenomegaly - T - splenomegaly is seen in children in the early phase of the disease
2.splenic atrophy/ absent - T - continued scarring causes progressive shrinkage -
autosplenectomy
4.aplastic crises - T - refers to temporary cessation of bone marrow activity, usually
triggered by parvovirus infection, with a rapid worsening of anaemia
PRV and splenomagaly —least likely (TW)
1.CML
2.ALL
3.Budd-Chiari
4.Cirrhosis
Cirrhosis - F – however secondary polycythemia can be caused by HCC and EPO
secretion.
1.CML - T - certain features are common to each of the four chronic myeloproliferative
disorders (CML, PCV, essential thrombocytosis, myelofibrosis).
2.ALL - T - polycythemia rubra vera can transform into ALL
3.Budd-Chiari - T - common sites for thromboses in PRV include hepatic veins, protal and
mesenteri cveins, and the venous sinuses of the brain.
T/F Barretts has x40 increased association of SCC
falase, adenocarcinoma x40 with>2cm barretts
Crohn’s colitis is not associated with (JS)
1.Fat wrapping
2.Aphthous ulcer
3.Cobblestone
4.Backwash ileitis
5.Fistulas
Backwash ileitis - T - ulcerative colitis
H.Pylori which is least correct
1.Gram negative spiral
2.Attaches to epithelium in the small and large intestine
3.Role in gastric cancers
4.Associated with MALT lymphoma
Attaches to epithelium in the small and large intestine – F - adheres to gastric epithelium.
1.Gram negative spiral – T – spiral shaped, microaerophilic, gram negative bacterium.
3.Role in gastric cancers – T – HP can cause chronic active gastritis and atrophic gastritis,
early steps in the carcinogenesis sequence. Studies have shown a clear link between HP and gastric adenocarcinoma. Source of gastric cancer may not be from gastric epithelial cells themselves, but rather from bone-marrow derived cells that differentiate into gastric epithelial cells in the presence of HP (UTD).
4.Associated with MALT lymphoma – T – multiple studies have shown association, and
MALToma remission following eradication of HP.
Which is most correct? (JS)
1.Angiodysplasia most commonly affects the sigmoid colon
2.short segment Hirschsprung most common in females
3.Meckel’s diverticulum is present on the mesenteric side
4.complications of necrotising enterocolitis include a stricture
5.pseudopolyps are a feature of Crohn’s disease
4.complications of necrotising enterocolitis include a stricture - T - complications of NEC
include short bowel syndrome, malabsorption, strictures and recurrence of disease
1.Angiodysplasia most commonly affects the sigmoid colon - F - most often seen in the
caecum or right colon
2.short segment Hirschsprung most common in females - F - more common in boys
3.Meckel’s diverticulum is present on the mesenteric side - F - form on the antimesenteric side of the small bowel
5.pseudopolyps are a feature of Crohn’s disease - F - can occur in Crohns but more typical of UC
Patient has a peptic ulcer with increased serum gastrin levels, what would you scan for:
(TW, GC, JS)
1.Pancreas and duodenum
2.Pancreas, duodenum and lymph nodes
3.Mass in duodenum
Pancreas, duodenum and lymph nodes – T – although the majority of gastrinomas in ZES
and MEN-1 are in the 1st part of the duodenum, would presumably still search remainder of gastrinoma triangle, then nodes to assess for metastatic deposits.
gastrinoma triangle – region bounded by confluence of the cystic and common bile ducts superiorly, the 2nd and 3rd portions of the duodenum inferiorly, and the neck and body of the pancreas medially – 85% of gastrinomas.
In contrast to sporatic gastrinomas, which are usually solitary lesions, gastrinomas that occur in patients with ZES and MEN-1 are usually multiple, less than 5mm in size, and located in the proximal duodenum. In ZES most (75%) are in the 1st portion of the duodenum, 14% in the distal duodenum, 11% in jejunum
Which of the following statements concerning gastrointestinal diseases is most correct:
(GC)
1.The colon is the most common site for GIT lymphoma
2.Inflammatory pseudopolyps are a characteristic of Crohn’colitis
3.Aphthous ulcers are a characteristic feature of ulcerative colitis
4.Juvenile polyps typically occur in the rectum
Juvenile polyps typically occur in the rectum T - hamartomatous proliferations; in
general they occur singly and in the rectum. Usually large in kids under 5yo. (1-3cm),
smaller in adults (called retention polyps). No malignant potential.
1.The colon is the most common site for GIT lymphoma F - stomach 50% > SB > colon >
oesophagus; multicentric in 10-50%.
2.Inflammatory pseudopolyps are a characteristic of Crohn’colitis F - of UC; represent islands of regenerating mucosa.
3.Aphthous ulcers are a characteristic feature of ulcerative colitis - false, crohsn
Benign gastric ulcer, which feature is MOST likely: (JS)
1.Greater curvature
2.Heaped up edges
3.Radiating folds
4.Chronic atrophic gastritis
Chronic atrophic gastritis - T - almost universal in patients with peptic ulcer disease,
occuring in 85-100% of patients with duodenal ulcers and 65% with gastric ulcers
1.Greater curvature - F - predominantly located along the lesser curvature around the
border between the body and antrum, less commonly along the greater curvature
2.Heaped up edges - F - rare in benign ulcers, but characteristic of malignant lesions
3.Radiating folds - F - may have scarring that involves the entire thickness of the stomach
with puckering of the surrounding mucosa, causing mucosal folds which radiate from the
crater in spokelike fashion
Achalasia of the oesophagus, which is false: (JS)
1.Dilated vestibule
2).25% have a dilated oesophagus and colon with Chagas
3.Oesophageal perforation is a complication
4.Most oesophageal perforations are iatrogenic
1.Dilated vestibule - F - vestibule is in the region of the LOS which fails to relax in
achalasia - beaked tapering at GOJ
2.25% have a dilated oesophagus and colon with Chagas – T -The digestive forms of the
disease lead to megaesophagus and/or megacolon in approximately one third of chronic
cases, of which 20-50% also present with an associated cardiopathy.
3.Oesophageal perforation is a complication – T - Pneumatic dilatation for achalasia
carries a significant and recognized risk of esophageal perforation (5%). Obtain from
patients prior to the dilatation an informed consent emphasizing this risk of perforation.
4.Most oesophageal perforations are iatrogenic T – treatment as above.
Features of scleroderma include: (JS)
1.Upper third of oesophagus is preserved
2.Colon involvement rare
3.GIT involvement is rare
4.Oesophageal perforation is common
1.Upper third of oesophagus is preserved T - causes atony and aperistalsis of the lower 2/3
of oesophagus with patulous LOS and GOR
2.Colon involvement rare –F - colon is involved in 40-50% with pseudosacculations,
eventual loss of haustra, marked dilatation and stercoral ulceration from retained faecal
material
3.GIT involvement is rare – F - third most common manifestation (after skin and
Raynaud’s), occurs in 40-45%
4.Oesophageal perforation is common - F - not mentioned in Dahnert, Primer or Mayo
clinic book
Elderly man with large bowel narrowing, biopsy showed segmental fibrosis and chronicinflammation, most likely: (TW)
1.Ischemia
2.Vasculitis
3.Carcinoma
1.Ischemia - T - submucosal chronic inflammation and fibrosis can lead to stricture (in chronic ischemia).
Angiodysplasia, most likely: (JS)
1.Most common in sigmoid
2.Can’t be seen macroscopically because covered mucosa
3.Cause of 20% of significant lower GI bleeding, either as massive blood loss of chronic loss
4.Not associated with other GIT lesions or CVS abnormalities
3.Cause of 20% of significant lower GI bleeding, either as massive blood loss of chronicloss - T - account for 20% of significant lower intestinal bleeding
1.Most common in sigmoid - F - most common in caecum and right colon
2.Can’t be seen macroscopically because covered mucosa - F - tortuous dilations of
submucosal and mucosal blood vessels, separated from the intestinal lumen by only the vascular wall and a layer of attenuated epithelial cells
4.Not associated with other GIT lesions or CVS abnormalities - F - associated with aortic
stenosis (20%)
Known (or previous) strongyloides infection with oedema of the mucosa of ascending
colon, what does it mean: (TW)
1.Autoinfection in the immunocompromised
2.Not related – only infects duodenum and SB
3.Ischaemia due to vascular invasion
.Autoinfection in the immunocompromised - T - in contrast to other helminthic parasites,
can complete life cycle entirely within human host. Autoinfection limited by intact immune
respone, however in immunocompromised - can give rise to potentially fatal infection.
During autoinfection, the rhabditiform (non-infectious) mature into filariform larvae
(infectious) within the GIT - these can then penetrate the perianal skin or colonic mucosa to complete the cycle of autoinfection
2.Not related – only infects duodenum and SB - F, but prob true in immunocompetent host -
filariform larvae of Strongyloides stercoralia found in soil or in other materials
contaminated with human faeces. Larvae penetrate skin and migrate hematogenously to lungs where they penetrate the alveolar air sacs. Larvae then ascent tracheobronchial tree and are swallowed. Then mature into adult worms and burrow into mucosa of duodenum and jejunum. Adult worms may life for up to 5y. Female adulte produces eggs, from which develop non-infectious larvae within the lumen of the GIT (which then pass into your turds).
3.Ischaemia due to vascular invasion - F - oedema and inflammation secondary to invasion
Endoscopy can show: duodenum - oedema, brown discoloration of mucosa, erythrmatous spots, subepithelial haemorrhage, and megaduodenum; colon - loss of vascular pattern, oedema, apthous ulcers, erosions, serpiginous ulcerations, and xanthoma-like lesions; stomach - thickened folds and
mucosal erosions.
0 yo with 20 colonic polyps, suspect FAP, which is most likely: (TW)
1.Need >100 polyps
2.Attenuated FAP
3.Polyps in Peutz Jegher restricted to SB
4.Normal patients…inheritance, sporadic mutations are rare
5.Thyroid cancer and mastoid osteoma in Gardners
Attenuated FAP - T - (UTD) attenuated from of FAP - affected patients have fewer than
100 colorectal adenomas and a delayed onset of colorectal cancer. Polyposis typically
develops in 2nd or 3rd decate of life. Similarly high risk, but with older average age of
cancer (54yo).
1.Need >100 polyps - F - attenuated FAP can have <100.
3.Polyps in Peutz Jegher restricted to SB - F - small intestine 64%, colon 64%, stomach
49%, rectum 32%.
5.Thyroid cancer and mastoid osteoma in Gardners - F - 20 colonic polyps. Gardners = FAP + benign manifestations: osteomas and dental abnormalities; cutenous lesions; desmoid tumors; congenital hypertrophy of th retinal pigment; adrenal adenomas; nasal
angiofibromas. And malignant manifestations: extra-colonic malignancies duodenal; thyroid; pancreatic; gastric; CNS; hepatoblastoma; small bowel distal to duodenum; possibly adrenal.
Giardia Diagnosis (TW)
1.Stomach / Proximal bowel
2.Helminth
3.Normal commensal in colon
4.Common in neonatal ICU
Stomach / Proximal bowel – T – probably best answer – G. lamblia attach to mucosal
surface of duodenum and jejunum.
2.Helminth – F – flagellated protozoan parasite.
3.Normal commensal in colon - F
4.Common in neonatal ICU – F – especially common in areas where there are poor sanitary conditions and insufficient water treatment facilities. Hopefully not in NICU, unless feeing the bubs infected turds.
Alcoholic and cachetic patients with Bacteroides (TW)
1.Aspiration from mouth organism
2.Commensal from mouth
3.Aspiration from stomach bug
4.Bowel diverticulitis
5.Osteomyelitis
Aspiration from mouth organism - T - major anaerobic bacteria implicated in human
disease include organisms from genus Bacteroides, Fusobacterium, Porphyromonas, and Prevotella (all gram-neg bacilli), clostridium, actinomyces, eubacterium (gram positive bacilli), peptostreptococcus and peptococcus (gram pos cocci), and veillonella (gram neg coccus). Thes organisms are normally found in oral cavity and they may result in disease when aspirated. Therefore, conditions that favor the occurance of aspiration, eg impaired consciousness, seizure, stroke, drug ingestion, and alcoholism, or conditions that impair ability to clear aspirated secrtions favor development of pulmonary anaerobic infections.
Mid oesophageal stricture 40 yo female, most likely: (JS)
1.If adeno ca likely long segment Barretts
2.SCC only in <5% here
3.SCC there are 4 patterns: multifocal, luminal, polypoid, ulcer
1.If adeno ca likely long segment Barretts - T - Barretts is a cause of mid-oesophageal
strictures and results in adenocarcinoma (although it is usually distal)
2.SCC only in <5% here - F - for SCC, 20% in upper third, 50% middle third, 30% lower
third
3.SCC there are 4 patterns: multifocal, luminal, polypoid, ulcer - F - three patterns -
protruded (polypoid exophytic), flat (diffuse infiltrative) and excavated (ulceration)
bowel cancer risks (TW)
1.Peutz Jeghers
2.FAP nephew
3.5 villous polpys excised previously
Peutz Jeghers – F – non-neoplastic polyp (hamartoma). Has increased risk of pancreatic, breast, lung, ovary and uterine cancer, but not colon cancer (path notes). UTD says increased risk.
2.FAP nephew – T – Autosomal dominant. Polyposis typically develops in 10-30yo. 100%
malignant transformation by 20y after Dx; age at carcinomatous development usually 20- 40yo. This option would be only be true if accounting for appropriate age spread (between siblings [parent of nephew] + age difference with nephew).
3.5 villous polpys excised previously – T – as is seen in colon cancer, increasing size of
adenomas and the presence of villous features are both risk factors for the development of invasive carcinoma within an adenoma.
how to DX Giardia (? False) (TW)
1.total villous atrophy in jejunum
2.oocyst in stool
3.subtotal villous atropy
4.something about aspirate
1.total villous atrophy in jejunum – F – spectrum of findings ranging from none to mild to moderate to subtotal villous atrophy in severe cases (UTD). Although the intestinal
morphology may range from virtually normal to markedly abnormal, most commonly
Giardia causes clubbing of villi, a decreased villus-crypt ratio, and a mixed inflammatory
infiltrate of the lamina propria (Robbins).
Giardia lamblia is a flagellated protozoan parasite. Ingest cysts, excystation occurs in upper small bowel releasing trophozoites. These have adhesive disc for attachment to mucosal surface of duodenum and jejunum – does not invade or cause necrosis of mucosal epithelium – just a ‘resident’. Causes diarrhoea and malabsorption by mechanisms unknown. For the organism to persist in the infectious form, trophozoites must revert to cysts, which occurs in the large intestine.
If you can only do a sigmoidoscope % cancers missed are (TW)
1.5-15%
2.15-25%
3.40-60%
4.80-90%
40-60% - T – best answer.
H. Pylori (TW)
1.Associated with gastritis but most are asymptomatic
2.Causes a duodenitis more than a gastritis
3.Affects 1-2 % of adults
Associated with gastritis but most are asymptomatic – T – majority of infected individual are asymptomatic.
2.Causes a duodenitis more than a gastritis – F – in the duodenum H Pylori are confined to
foci of gastric metaplasia. Gastric metaplasia refers to the presence of gastric epithelium in
the 1st portion of the duodenum. Metaplastic foci provide areas for HP colonization, and
probably have a role in the development of duodenitis. HP is almost always accompanied by gastritis and the diagnosis should be suspect in its absence.
3.Affects 1-2 % of adults – F – Conservative estimates suggest 50% of the worlds
population is affected. In developing nations – majority of kids infected before 10yo,
prevalence of adults peaks at more than 80% before 50yo. Developed countries: infection in kids is usual, but becomes more common in adulthood, 50% in those >60yo.
.No meconium, complete micro colon, which is least correct? (TW)
1.Long segment hirschsrpungs
2.CF
3.Functional immaturity of the colon
4.Ilieal atresia
3.Functional immaturity of the colon – F – AKA meconium plug syndrome / small left colon
syndrome. Functional immaturity of ganglion cells in colon causing functional obstruction
of newborn colon. No microcolon.
1.Long segment hirschsrpungs – T – total colonic Hirschsprung – entire colon may be
small.
2.CF – F – meconium ileus is presenting finding in 10% of CF and is virtually
pathognomonic of the disease. Essentially all patients with MI have CF. Microcolon present
due to non-use. Ileal meconium plugs.
4.Ilieal atresia – T – Often no findings to Dx ileal atresia from other causes of distal bowel
obstruction, so require contrast enema. Get microcolon (however if atresia occurred late in fetal life, microcolon may not be present and colon may contain some meconium).
.GIST tumour – which is correct: (TW)
1.Malignant > benign
2.Histological subtype most important in prognosis
3.Occur mainly in stomach and small bowel
4.Grow as an epithelial tumour
Occur mainly in stomach and small bowel - T- stomach most common site (2/3). Small
bowel (esp duodenum) next most common site. Can occur anywhere in GI tract, and rarely occurs in oesophagus (where leiomyoma is more common).
1.Malignant > benign - F - No GIST can truly be labelled as benign. Most common
mesenchymal tumor of GIT. It is widely accepted that terms “benign” or “malignant” should not be applied to GIST, since these terms are not clinically useful for patient management (UTD). Clinical behaviour of GISTs is variable. Approximately 50% of completely resected GISTs can be expected to recur within 5y of follow up. All GISTs are now regarded as potentially malignant.
2.Histological subtype most important in prognosis - F - histo falls into 3 categories: spindle cell type 70%; epithelioid type 20%; mixed type 10%. Prognosis however is influenced by tumor size, mitotic rate, tumor site (sm intesting worse than stomach), and the completeness of resection
4.Grow as an epithelial tumour - F - GISTs are the most common nonepithelial tumors of the GIT. Submucosal tumor of GIT derived from interstitial cells of Cajal (which normally
regulate peristaltic activity) & express CD117 (KIT) and 2/3 also express CD34. GISTs are
of mesenchymal origin and are not related to leiomyomas or leiomyosarcomas.
Leiomyoma, least common site: (TW)
1.Heart
2.Myocardium
3.Blood vessels, vascular smooth muscle
4.Oesophagus
5.Stomach
6.Uterus
Myocardium – F – smooth muscle is found in the walls of all the hollow organs of the
body except the heart.
Heart – T – leiomyomas can be intravascular and extend to the heart. Primary IVC
leiomomyoma / uterine leiomyoma with intravascular extension.
Blood vessels, vascular smooth muscle – T – see answer 1. Leiomyomas of the head and
neck probably arise from vascular smooth muscle.
Leiomyomas represent the most common gynecologic and uterine neoplasms. Occusionally occur with unusual growth patterns or in unusual locations (eg diffuse periotenal leiomyomatosis, intravenous leiomyomatosis, benign metastasizing leiomyomas, retroperitoneal leiomyomas,
parasitic leiomyomas).
Which is not associated with Hamartoma? (JS)
1.Peutz-jeghers.
2.Cronkhite-canada.
3.Cowdens syndrome.
4.Turcots.
Turcots. - T - rare variant of FAP with colonic polyposis (adenomas not hamartomas) and
tumours of the CNS
.Associations with Gardners syndrome, which is false? (JS)
1.Desmoid tumour
2.Retinal anomalies
3.Brain tumours
4.Polyps
3.Brain tumours. - F - Turcot syndrome is a variant of FAP/Gardner syndrome with
polyposis and tumours of the CNS
1.Desmoid tumour. - T - Soft tissue tumours including sebaceous/epidermoid inclusion
cysts, fibromas, desmoid tumours, mammary fibromatosis, keloid formation
2.Retinal anomalies. - T - hypertrophy of retinal pigment epithelium (doesn’t affect vision) (Path outlines)
4.Polyps. - T - multiple colonic polyps
.Which is not a feature of Zollinger-Ellison syndrome? (GC)
1.Hypervascular GI mass.
2.Gastrinoma.
3.Increased ulcers.
4.Increased lymphoma in Gastric wall.
5.Atrophic Gastritis.
Increased lymphoma in Gastric wall. F - complications include: malignant islet cell
tumour (in 60%), liver mets with continued gastric secretion, perforated DU/jejunal ulcer,
oesoph stricture with reflux, obstruction, GI bleeding, gastric carcinoids (esp. in MEN1).
Gastric carcnoid tumours may be classified as:
Type I: ECL cell hyperplasia, hypergastrinaemia, chronic atrophic gastritis +/- pernicious anaemia; generally benign disease. ie. suspect if polyps found in a pt with chronic atrophic gastritis.
Type II: seen in the hypergastrinaemic state of ZES in assocn with MEN1; also arise from ECL
cells in the setting of hyperplasia; multicentric. ie. multiple masses in setting of diffuse gastric wall thickening.
Type III: sporadic tumours not assocd with hypergastrinaemia; large solitary, may show
ulceration; more likely to metastasise.
Which is most true of Carcinoid? (GC)
1.Need liver mets for carcinoid syndrome.
2.10% occur in terminal ileum.
3.Arise from enterochromaffin and Kulchitsky cells.
4.Hypervascular mass on CT in arterial phase
Arise from enterochromaffin and Kulchitsky cells. T - GIT carcinoids arise from
enterochromaffin cells in crypts of Lieberkuhn (= argentaffinomma due to affinity for silver stain). Kulchitsky cells are generally seen in the lung and give rise to KCC1-3 carcinoid tumours.
Hypervascular mass on CT in arterial phase. T - although small solitary or multifocal carcinoids are typically not identified on CT scans, and may be hard to see on MRI (best visualized on T1 post gad + fat sat, where they manifest as nodules or focal areas of mural thickening with moderately intense gadolinium enhancement.
1.Need liver mets for carcinoid syndrome. F - Elevated levels of 5-HIAA, a metabolite, are
found in blood and urine. Normally liver deactivates vasoactive amines (serotonin,
histamine, bradykinin, others) released from carcinoid tumors; clinical symptoms occur if liver metastases are present or if tumor venous blood flow bypasses the liver (ie. primary pulmonary or ovarian carcinoids). CS occurs in 1% with carcinoid tumors, 20% with
widespread metastases. Symptoms: vasomotor disturbances (cutaneous flushes, cyanosis of face and anterior chest, intermittent hypertension), palpitations, intestinal hypermotility (nausea, vomiting, diarrhea, cramps); also asthmatic attacks with bronchospasm, fibrosclerosis of AV and tricuspid valves, elastotic sclerosis of mesenteric vessels causing ischemia, dermal sclerosis, hepatomegaly
2.10% occur in terminal ileum. F - 25-35% occur in small bowel, of these, 91% occur in
distal ileum.
.Features of diverticular disease include (TW)
1.Multiple true diverticulae
2.Circular muscular hypertrophy
3.Sacro-ilieitis
4.Increased risk of colonic cancer
2.Circular muscular hypertrophy - T - important feature of colonic diverticula =
hypertrophy of the circular of the muscularis propria.
1.Multiple true diverticulae - F - acquired diverticula lack or have an attenuated muscularis propria (cf congenital diverticula / true diverticula which have all three layers of bowel wall). Tend to occur alon gthe taeniae coli. Colonic diverticula are thin walled and are composed of a flattened or atrophic mucosa, compressed submucosa and attenuated or totally absent muscularis propria.
3.Sacro-ilieitis - F - IBD, seronegative arthritis.
4.Increased risk of colonic cancer - ?F - the natural Hx of diverticulosis: 70%
asymptomatic; 5-15% diverticular bleeding; 15-25% diverticulitis (of this 15-25%, 3/4 are
simple, and 1/4 are complicated ie. abscess, obstruction, perforation, fistula). UTD says
there may be a relation between diverticulosis and colon cancer. One series of 7000 patients found an excess number of colon and rectal cancers in the first 2 yrs after the Dx of diverticular disease, but not with more prolonged follow-up. There was, however, a longterm excess of left-sided colon cancers, suggesting a possible relation between these tumors and diverticular disease
Which of the following is not associated with ulcerative colitis: (GC)
1.crypt abscess
2.continuity
3.cobblestone pattern
4.primary sclerosing cholangitis
5.uveitis
3.cobblestone pattern F - characteristic of Crohn’s (linear ulcers, relatively spared
intervening mucosa develops a coarse cobbletstone appearance). UC: pseudopolyps
(islands of regenerating mucosa), usually normal wall thickness & normal serosa.
Diffuse disease limited to colon, rectal involvement with continuous proximal involvement; no skip
lesions; no deep fissural ulcers; no transmural sinus tracts, no transmural lymphoid aggregates or
granulomas.
Extraintestinal manifestations: migratory polyarthritis, sacroiliitis, ankylosing spondylitis,
pyoderma gangrenosum, clubbing of fingertips, primary sclerosing cholangitis, pericholangitis,
uveitis, cholangiocarcinoma (rare).
1.crypt abscess T - neutrophils in glandular lumen. Image: crypt abscess causing mucosal
stippling.
2.continuity T - diffuse distribution, cf. skip lesions in Crohn’s.
4.primary sclerosing cholangitis T - feature of UC (50-74%) and CD (13%).
5.uveitis T - feature of both UC and CD.
Which of the following is not a feature of Zollinger-Ellison syndrome:
1.Hypervascular pancreatic mass
2.gastrinoma
3.multiple peptic ulcers
4.atrophic gastritis
5.lymphoma of gastric mucosa
5.lymphoma of gastric mucosa F - complications include: malignant islet cell tumour (in 60%), liver mets with continued gastric secretion, perforated DU/jejunal ulcer, oesoph stricture with reflux, obstruction, GI bleeding, gastric carcinoids (esp. in MEN1).
Gastric carcnoid tumours may be classified as:
Type I: ECL cell hyperplasia, hypergastrinaemia, chronic atrophic gastritis +/- pernicious anaemia; generally benign disease. ie. suspect if polyps found in a pt with chronic atrophic gastritis.
Type II: seen in the hypergastrinaemic state of ZES in assocn with MEN1; also arise from ECL
cells in the setting of hyperplasia; multicentric. ie. multiple masses in setting of diffuse gastric wall thickening.
Type III: sporadic tumours not assocd with hypergastrinaemia; large solitary, may show
ulceration; more likely to metastasise.
Which of the following is least frequently associated with malignancy: (GC)
1.Tubular adenoma
2.Peutz-Jegher syndrome
3.Villous adenoma
4.Gardner’s syndrome
5.Turcot’s syndrome
1.Tubular adenoma F - all degrees of dysplasia may be encountered; risk of subsequent adenomas or CRC is related to size; higher risk if 6-10mm or larger, multiple adenomas or family history.
2.Peutz-Jegher syndrome T - AD disease with incomplete penetrance (instestinal polyposis
+ mucocutaneous pigmentation); increased risk of developing cancer of GIT, pancreas,
breast, ovary, endometrium, testis; risk approaches 40% by 40yo.
3.Villous adenoma T - all degrees of dysplasia may be encountered; higher risk of
malignancy than tubular adenoma; 40% risk if sessile and >4cm. Synchronous Ca is found
in as many as 40% of these, the frequency being related to the size of the polyp.
4.Gardner’s syndrome T - AD disease (variant of FAP) with osteomas + soft tissue tumours.
Malignant transformation of colonic polyps in 100%.
5.Turcot’s syndrome T - AR disease with colonic polyposis and CNS tumours (esp.
supratentorial GBM, occ. medulloblastoma). Malignant transformation of colonic polyps in
100%; death from brain tumour in 2nd/3rd decade.
Which is not a feature of scleroderma (TW)
1.Dilated atonic oesophagus with distal stricture
2.Multiple SB sacculation
3.Barrett’s oesophagus in 30-40%
4.Raynaud’s
5.Sclerodactyly
1.Dilated atonic oesophagus with distal stricture - F - probably least correct. B&H: stiff
dilated oesophagus that does not collapse with emptying, and wide gaping LES with free
FOR. Despite free refulx, tight strictures of distal oesophagus are uncommon. Danhert says ‘fusiform stricture 4-5cm above GOJ from reflux oesophagitis”.
2.Multiple SB sacculation - T - pseudodiverticula in small bowel - asymmetric sacculations with squared tops and broad bases on mesenteric side (due to eccentric smooth muscle atrophy).
3.Barrett’s oesophagus in 30-40% - T - 30% incidence. UTD says prevalence of Barrett’s
metaplasia in PPI-treated systemic sclerosis patients is similar to that in other patients with GOR (13% in one study).
4.Raynaud’s - T - Raynaud may precede other symptoms by months/years
5.Sclerodactyly - T - “tapered fingers” = atrophy + resorption of soft tissues of fingertips + soft tissue calcifications
Which is not a non-neoplastic polyp? (JS)
1.Hamartoma
2.Juvenile polyp
3.Hyperplastic polyp
4.Tubular adenoma
Tubular adenoma - T - a form of adenomatous polyp which result from epithelial proliferative dysplasia ie neoplastic epithelial lesion
2.Which of the following has the lowest risk of malignant transformation? (JS)
1.Peutz Jegher hamartoma
2.Villous adenoma
3.Polyp in Gardner’s syndrome
4.Tubular adenoma
5.Polyp in Turcot’s syndrome
1.Peutz Jegher hamartoma - T - don’t have malignant potential themselves, but the patients are at increased risk of developing other cancers (pancreas, breast, lung, ovary and uterus)
2.Villous adenoma - F - all adenomas arise due to epithelial dysplasia and therefore have
malignant potential. Risk of cancer in villous adenomas >4cm is 40%
3.Polyp in Gardner’s syndrome - F - as for FAP, 100% progression to adenocarcinoma
4.Tubular adenoma - F - cancer is rare in tubular adenomas less than 1cm but there is still a risk
5.Polyp in Turcot’s syndrome - F - as for FAP, 100% progression to adenocarcinoma
Which is false regarding acute pancreatitis? (TW)
1.15% of people with gallstones will develop acute pancreatitis
2.Associated with the SPINK 1 gene
3.Associated with trypsinogen activation
4.Coxsackie virus
5.Macroscopic chalky white due to fat necrosis
1.15% of people with gallstones will develop acute pancreatitis - F - UTD: gallstones
(including microlithiasis) account for 35-40% of cases of pancreatitis. However, only 3-7%
of patients with gallstones develop pancreatitis.
2.Associated with the SPINK 1 gene - T - serine protease inhibitor Kazal type 1 (SPINK1)
which may act as a disease modifier has a low penetrance. Other genetic causes: CFTR
(CF), mutations at codons 29 and 122 of cationic trypsiongen gene, PRSS1.
3.Associated with trypsinogen activation - T - see ans 2.
4.Coxsackie virus - T - numerous infectious agents can cause pancreatitis. Viruses: mumps, coxsackievirus, hep B, CMV, VZV, HSV. Bacteria: mycoplasma, legionella, leptospira, salmonella. Fungi: aspergillus. Parasites: toxo, crypto, ascarias.
5.Macroscopic chalky white due to fat necrosis - T - fat necrosis. Released fatty acids
combine with calcium to form insuluble salts that precipitae in situ. Pancreatic substance
exhibits areas of blue-black haemorrhage interspersed with foci of yellow-white chalky fat necrosis
Diverticular disease causes partial bowel obstruction due to… (TW)
1.Diverticulitis
2.Hypertrophy of the circular layer of muscularis propria
3.Vesicocolic fistula
2.Hypertrophy of the circular layer of muscularis propria - T - taeniae coli are also usually prominent. Constipation and diarrhoea can result from the hypertrophy.
18 year old girl presents with a large mixed solid and cystic pancreatic mass, what is most
likely: (TW)
1.Neuroblastoma
2.Solid cystic papillary tumour
3.Mucinous cystadenoma
4.Mucinous cystadenocarcinoma
5.Microcystic adenoma
2.Solid cystic papillary tumour - T - Pancreatic mass of low malignant potential with solid
and cystic features. Well-demarcated large mass. Commonly in body and/or tail. <35yo.
F>M 9.5x. African-Americans or other non-Caucasian groups.
3.Mucinous cystadenoma - F - mucinous cystic pancreatic tumor (mucinous macrocystic neoplasm, macrocystic adenoma, mucinous cystadenoma or cysadenocarcinoma). Thickwalled, uni-/multilocular low grade malignant tumor composed of large, mucin-containing
cysts. Likes the body or tail of pancreas.F>M 9x. Mean age 50yo (20-95yo). 50% occur
between ages 40-60yo.
4.Mucinous cystadenocarcinoma - F - see option 3.
5.Microcystic adenoma - F - serous cystadenoma (glycogen-rich or micro-/macrocystic serious adenoma). Benign pancreatic tumor that arises from acinar cells. Honeycomb or sponge-like mass in pancreatic head (microcystic cystadenoma). Or as Steve Drew says “like the surface of a cut orange”. Mean age 65yo. Middle and elderly age groups. F>M 4x.
Ectopic pancreas least likely location (TW)
1.Stomach
2.Colon
3.Ileum
4.Jejunum
5.Duodenum
colon
May occur anywhere in the GIT. Most frequent locations are the stomach, duodenum or proximal
part of small intestine.
1.Which is least correct regarding scleroderma? (TW) - but dubious.
1.Involves lower oesophagus
2.Sacculations on anti-mesenteric side of small bowel
3.Associated with Barrett’s oesophagus
4.Sclerodactyly
Sacculations on anti-mesenteric side of small bowel - F - pseudodiverticula = asymmetric
sacculations with squared tops and broad bases on mesenteric side (due to eccentric smooth muscle atrophy)
1.Involves lower oesophagus - T - normal peristalsis above aortic arch (where striatued
muscle is present), hypotonia / atony and hypokinesia / aperistalsis in lower 2/3rd.
3.Associated with Barrett’s oesophagus - T - Barretts is a complication of chronic GOR
70%. Erosions and superficial ulcers (from asymptomatic reflux oesophagitis: No protective oesophageal contraction). Complications peptic stricture, aspiration, Barrett oesohagus, adenocarcinoma. Barretts occurs in about 30% of patients.
4.Sclerodactyly - T - “tapered fingers” = sclerodactyly = atrophy and resorption of soft
tissues of fingertips and soft-tissue calcifications.
Scleroderma encompasses a spectrum of related disorders, most of which share a characteristic clinical feature of skin thickening due to an excess of collagen fibers. Classification system takes into account the different potential complications, prognoses, and management strategies for these
disorders.
Simplest division:
Localised scleroderma - Linear scleroderma (abnormalities of skin and subcut tissue often
following dermatomal distribution and are found predominantly on 1 side of body; En coup de sabre (type of linear scleroderma = lesions look like sabre blow); Morphea (localized or genarlized - patches of sclerotic skin).
Systemic scleroderma - “Systemic sclerosis” (emphasizes frequent involvement of internal organs is generally the most important manifestation of these conditions) - Diffuse cutaneous SSc; Limited cutaneous SSc; SSc sine scleroderma (only internal organ involvement); Environmentally induced
scleroderma; Overlap syndrome where SSc coexist with elements ofther rheumatic disorders.
Fibrolamellar HCC, which is False (JS)
1.Female>Male
3.No association with hepatitis B
4.Hard scirrhous tumour
5.No cirrhosis
Female>Male - F - M=F
2.20-40 yo - T - occurs in young adults 20-40y (Robbins)
