Pathology Flashcards
What process do they arrows likely represent after a stroke?
Wallerian degeneration of cortical spinal fibers.
What are the small oval cells? What is the common stain for them?
Astrocytes: small, no cytoplasm
GFAP
What are the small cells on the very outer layer? They form the arachnoid membrane.
What do they stain with?
Meningothelial cells
Stains positive for epthelial membrane antigen (EMA)
What type of cells are these? What do they produce? What do they stain with?
Choroid Plexus: Large cuboidal epithelium overlying blood vessels, connective tissue and meningothelial cells.
- Produces CSF
- Stains positive for transthyretin
What cell type is circled?
Alive or dead?
When do they appear after ischemia?
Neurons become brightly eosinophilic with loss of the Nisl substance within 6-24 hours of ischemia (“Red neurons”).
What are these cells? What would they stain + for?
When do they appear after ischemia?
Reactive astrocytes. GFAP, as always :)
12-36 hours
What are these cells? When do they invade after a stroke?
Polymorphonuclear cells invade the ischemic territory within hours and peak at 48-72 hours.
When does vascular proliferation occur after a stroke?
What imaging correlate does it have?
After 48 hrs. Should allow for some contrast enhancement due to BBB breakdown.
What is caused the area in the circle? What is the finding the arrow is pointing to?
Cystic cavity surrounded by gliotic tissue with glial strands (circle)
– There is compensatory (ex-vacuo) ventricular enlargement
What type of stroke caused this? What is the underlying vascular problem identified on pathology?
Lacunar infarction
• Infarctions ranging in size from 1 mm to 1.5 cm (arrow)
• Classically, the walls of small arteries become thickened from the formation of hyalinemembranes (lipohyalinosis) (circle)
– Caused by chronic hypertension
- These arteries may also rupture and cause hemorrhage
Old guy found down and brought back to life. Died of inability to feed himself. What was the cause?
Watershed infarction. Couldn’t eat due to man in a barrel like weakness and couldn’t get food to his mouth. So sad.
What cells are killed of by transient global hypoperfusion?
Transient shock or cardiopulmonary arrest causes focal ischemic injury to neurons with high metabolic rates:
– Layer 3 and 5 of cortex
– Hippocampus
– Purkinje cells
What is this pathology? What is the black stain?
Tearing of the endothelial lining of the blood vessel with extravasation of blood
into the vessel wall
Seen in:
– Marfan’s syndrome
– Fibromuscular dysplasia,
– Ehlers-Danlos type IV
– Trauma
I believe that is reticulin staining.
What is this process? How can you differentiate it from viral encephalitis?
Vasculitis
• May be part of a systemic vasculitis or isolated to the CNS.
• Requires transmural vessel wall inflammation
17 year old out parting at Elich’s and then got gastro and is overweight on OCPs. Presents with seizure then rapid decline.
Wa happened?
Venous Sinus Thrombosis
• Venous congestion over the convexities with parietal petechial hemorrhages.
Associated with:
– Post-partum
– Dehydration
– Hypercoagulable states
– Adjacent inflammation
(e.g., mastoiditis).
15 year old presents with first seizure. What is the cause of this pathology? Is there normal tissue?
AVM
Located in cortex
Composed of both large arteries (open arrow) and veins (solid arrow) without
intervening capillaries.
Between vessels there is gliotic nonfunctional hemosiderin stained tissue (circle).
10 year old shows up after seizure and has an MRI with popcorn lesions.
Cavernous Malformation
Located in cortex or less frequently in the brainstem.
• Composed of thinwalled vessels (arrow).
• There is no intervening parenchyma between the vessels (circle).
Name the common vascular malformations, if they have arterial flow, what the vessels in the malformation are, if there is a draining vein, and if the intermixed brain tissue is normal.
What are the most common locations for hypertensive hemorrhages in order of frequency?
Hypertensive Hemorrhage
• Commonly occur in the:
– Putamen (65%)
– Pons (10%)
– Cerebellum (10%)
– Thalamus
• These are the same locations of lacunar infarctions.
What study should be ordered on a patient with a similar presentation (before autopsy)?
Angiography.
Subarachnoid Hemorrhage
• Caused by aneurysmal rupture ortrauma
• Overlying the blood is the arachnoid membrane (arrow).
What was the mechanism of injury for this patient?
Area of hemorrhagic necrosis from cerebral contusion.
– Usually affects the crest of gyri.
– Frequently seen in subfrontal and anterior temporal lobes as the base of the brain slides over the irregular skull base
• Blood is removed by macrophages leaving an irregular tan discoloration.
What is the mechanism of the injury seen here?
Diffuse Axonal Injury
• Widespread ruptured axons from trauma.
– Neuroimaging is normal but patients are comatose, may see microhemorrhages in white matter tracts.
- On gross examination, there is white matter atrophy.
- The injured axons dilate (“axon retraction balls”)
Name the herniation and vessel at risk.
Subfalcine: an edematous cingulate gyrus (arrow) compresses the ipsilateral anterior
cerebral artery as it runs in the falx cerebri.
Name the herniation and vessel at risk
Uncal Herniation
• The medial temporal lobe (uncus) herniates across the tentorium cerebelli compressing:
– the ipsilateral 3rd nerve
– the midbrain resulting in compression of the contralateral cerebral peduncle on Kernohan’s notch
– the posterior cerebral arteries resulting in occipital lobe infarcts.
What went for a dip?
What is the brainstemp pathology?
Tonsillar Herniation
• With elevated posterior fossa pressure, the cerebellar tonsils are forced downward into the foramen magnum causing hemorrhage and compression of the medulla.
• Since the blood vessels are fixed by the dura, downward displacement of the brainstem causes rupture of the penetrating arteries resulting in multiple linear hemorrhages (Duret).
Patient presents with fever, neck stiffness and somnolence. Dies two days later. What is causing the appearance of the patholigic specimen?
Bacterial Meningitis
– Purulent material in the subarachnoid space (arrow) from abundant polymorphonuclear cells.
What is the process depicted both on gross and microscopic section? What are common causes of these findings?
Granulomas
• Composed of epitheliod macrophages (closed arrow), multinucleate giant cells (circle), lymphocytes (open arrow)
• Caused by:
– Tuberculosis
– Fungi
– Spirochetes
– Sarcoidosis (noncaseating)
– Foreign body
Patient recently moved from out of country or has AIDs and a wicked cough. Now dead. Presented with chronic headache and altered mental status.
What is the cause?
Tuberculosis Meningitis
• Subacute to chronic course
• Tuberculosis, fungus, and spirochetes have a predilection for the base of the brain.
• Tuberculosis and other mycobacterium are acidfast bacteria (arrow).
Patient is from the southwest and had a bad cough. Now subacute meningitis.
Coccidiodidomycosis
– small yeast
– large spherical endospore (arrow).
Which yeast is it?
Aspergillus
– narrow regular hyphae branching at acute angles (arrow) invading blood vessels.
• Mucormycosis (bottom)
– broad irregular hyphae branching at 90º (circle).
• Both are angioinvasive
Immunecompromised patient with this is a pathologic sample. Name the yeast.
Candidiasis
• Rare CNS pathogen
• This fungi exists as a yeast.
• Multiple yeast may connect to each other mimicking branching hyphae (pseudohypae) (circle).
Patient with HIV presents with multiple ring enchanceing lesions. Unfortunately, dies. What is the cause of ring enchanging lesions?
Toxoplasmosis
• Exists in 2 forms
– Slow-growing round bradyzoite (circle)
– Active-growing comma-shaped tachzoites
• Also see chronic inflammation (lymphocytes and plasma cells)
Patient with seizures and CSF pleocytosis. Biopsy obtained in work up ( I make the clinical scenario up by the way). Please diagnose now with this limited information. Why is it not vasculitis?
Viral encephalitis
• Microglial nodules
– hypercellular cluster containing microglia and reactive astrocytes (circle).
• Perivascular cuffing
– Lymphocytes surrounding blood vessel (arrow).
– Similar findings in demyelinating disease and CNS lymphoma
These are 2 different types of inclusion bodies. What viral processes are they most typical for in each case?
Cowdry A
– Single, large inclusion surrounded by a halo that efface the nucleus (circle).
– Seen in HSV, CMV, VZV, and SSPE.
Cowdry B
– Multiple, small inclusions without a halo that do not efface the nucleus (arrows).
– Seen in Polio or normally in the substantia nigra (Marinesco body), but also in normal aging.
Patient presents with fever, headache, AMS and seizures.
For extra points (Adam will by you dinner, he promised): If the patient survives, but then starts acting like Gary Busey what disorder do they have, what structures are involved. What are the main clinical findings?
HSV Encephalitis
• HSV has a predilection for the temporal lobes/ basal forebrain (circle).
• Classically presents as a hemorrhagic encephalitis
Kluver-bucy syndrome (bilateral lesions of mesial temporal lobes & Amygdala)=
“HIP HIP”
H = Hypermetamorphosis (old visual stimuli approached as if they are new)
I = Increased oral exploratory behavior
P = Placidity (Docility- dimished fear)
H = Hypersexuality + Hyperphagia
I = Impaired memory (Anterograde Amnesia)
P = Psychic Blindness (objects in visual field treated inappropriately)
Patient is bit by a bat and is now afaid of water. What are the inclusions?
Rabies
• Characterized by eosinophilic intracytoplasmic inclusions within pyramidal cell neurons (Negri bodies) (circles).
• Carried by:
– Raccoons
– Skunks
– Bats
– Foxes
– Coyotes
Patient with MS, presents with headache, difficulty with math, oh and is on Tysabri, once got rituximab, too.
Would you A) do plasmapheresis B) give more tysabri C) do nothing?
Progressive Multifocal Leukoencephalopathy (PML)
• Necrotic demyelination beginning in the white matter within a cortical gyrus (circle).
• Characterized by:
– Ground glass inclusions in oligodendroglia nuclei (blue arrow)
– Bizzarre astrocytes (black arrow)
Please, plasmapheresis.
Old guy with memory problems. What are they inclusions? What is the protein involved?
Neurofibrillary tangles
– intracytoplasmic neuronal aggregates of tau protein that take the shape of the neuron’s cell body. In pyramidal cells, they appear flame shaped (arrow).
Same old guy with memory problems. What is this patholgical finding? What is the protein involved?
Neuritic plaques (circle)
– extracellular accumulation of an amyloid core surrounded by swollen neuritic
processes (look like burntout camp fires).
In Alzheimer’s both of these can be found. What are they?
• Granulovacuolar degeneration (top and bottom)
– Small cytoplasmic vacuoles that contain a single granule (circles)
• Hirano bodies
– Rod-shaped eosinophilic inclusions that appear adjacent to neurons in the neuropil (arrow).
50 year old, previously did not have a sweet tooth. Now also disinhibited.
What is the disease? What chromosome has it been associated with?
Frontotemporal Dementia
• Severe focal atrophy of the frontal and temporal lobe
• with sparing of the posterior 2/3 of the superior temporal gyrus (knife-edge)
Chromosome 17
In FTD some with have these inclusions. What are they made out of?
• Pick bodies
– Intracytoplasmic neuronal oval aggregates (circle) of tau (arrow).
• May also see
– neuronal loss with gliosis
– ballooned neurons with achromatic cytoplasmic inclusions
Patient presents with rigidity, falls and limited up gaze. Pathology obtained.
Do they have retrocollis or anterocollis?
Progressive Supranuclear Palsy (PSP)
• Intracytoplasmic neuronal aggregates of tau throughout the brainstem
– These aggregates take the shape of the neuron’s cell body appearing globose” (arrow).
PSP- retrocollis
MSA- anterocollis
What area of the brain is this? What does it project to? What disease is this most likely?
Midbrain (Substantia Nigra Pars Compacta). Caudate. Parkinson’s disease.
There is loss of pigmentation of the substantia nigra (arrows) and locus ceruleus.