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Pathology Post Midterm > Module 7 CNS: Stroke, Encephalopathy, Abscess, Meningitis > Flashcards

Module 7 CNS: Stroke, Encephalopathy, Abscess, Meningitis Flashcards

1
Q

Next topic for CNS is Ischemic Stroke/Cerebral Infarction. there are three types each card will go through the types. What is the first?

A

Thrombotic/Ischemic Stroke (more common)
HTN — atherosclerosis — unstable plaque —thrombosis —bland infarct (white infarct due to 100% occlusion of lumen)
Risk factors for atherosclerosis:
-smoking, DM, hypercholesterolemia (most common under 40) , HTN (most common over 40)

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2
Q

The second etiology for an ischemic stroke is embolic stroke. What are some features?

A

Embolic Stroke: (less common but more serious)
–atrial fibrillation + mural thrombus in left heart — legs (DVT) or brain (Red infarct bc lumen not completely occluded)

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3
Q

The third etiology for an ischemic stroke is carotid artery dissection. What are some features?

A

Carotid Artery Dissection: young and middle aged

  • mild trauma — occludes lumen and causes stroke
  • -extension to the adventitia may cause subarachnoid hemorrhage
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4
Q

What is the most common affected vessel?

A

Middle cerebral artery

–watershed between MCA and ACA

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5
Q

What is the presentation of a patient with an Ischemic stroke?

A 
Contralateral hemiparesis and sensory loss (again for any stroke) 
Aphasia if Broca's Affected 
Cerebellum affected:
D (dysmetria)
D (Dysdiadokinesia) 
A (ataxia)
N (nystagmus)
I (intention tremor) 
S (Slurred speech) 
H (hypotonia)
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6
Q

In an ischemic stroke what does the CT show?

A

Non contrast CT: shows no abnormalities so that rules out hemorrhage but does not rule out ischemic
MRI: much more sensitive

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7
Q

What changes are seen in the brain for an ischemic stroke?

A

0-12 hrs: nothing
12-24 hrs: coagulative necrosis
24 hours: PMNs
–stroke is a permanent neurological deficit after 24 hours (legs recover before arms)
–before 24 hours (transient ischemic attack but can still have perm neuro damages)
over 48 hours: microglia – liquefactive necrosis
2 weeks: astrocytes — glosis

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8
Q

Moving on to Hypoxic-Ischemic Encephalopathy, what is this?

A

Widespread injury to neurons

  • -neurons are more vulnerable to hypoxia/ischemia than other cells (4 minute rule on CPR)
  • -usually due to cardiorespiratory arrest with resuscitation
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9
Q

What are the pathological changes in order of severity for Hypoxic-Ischemic Encephalopathy?

A
  1. Selective Neuronal Necrosis (unpredictable distribution)
  2. Laminar Necrosis: necrosis of all neurons in a given neocortical layer
  3. Pseudolaminar Necrosis: necrosis of all cytological elements in neocortical layers 2 thru 6
  4. Watershed Infarcts
  5. Multifocal grey matter infarcts
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10
Q

What CNS changes are expected in a patient that is dead at a scene?

A

Massive craniocerebral trauma
Vertebrospinal trauma
Diffuse post traumatic vascular injury
Idiopathic cardiorespiratory dysfunction following milder head injury

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11
Q

What CNS changes are expected in a patient that is in a persistent coma/vegetative state (often with disproportionately mild imaging findings)

A

Diffuse axonal injury

Post traumatic hypoxic-ischemic encephalopathy (thalamic involvement)

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12
Q

What CNS changes are expected in a patient with a lucid interval (patients who talk and die)?

A

Acute peridural hemorrhage (epidural hemorrhage)

Post traumatic brain swelling

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13
Q

What CNS changes are expected in a patient with a post traumatic epilepsy, cognitive and/or motor dysfunction?

A

Contusion
Mild diffuse axonal injury
Chronic Subdural
Residual effects of evacuated peridural hematomas

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14
Q

The next topic will be brain abscess, what is the etiology?

A

Two routes of spread:

  1. Hematogenous spread: usually due to sepsis or septic emboli from left sided endocarditis (IV drug users that has tetralogy of fallot)
  2. Direct/Contigual Spread (more common): sinusitis, mastoiditis, otitis media and dental infections
    - -example: Chrug Strauss – CANCA positive with chronic sinusitis
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15
Q

What is the pathogenesis for a brain abscess?

A

Collection of infection in the parenchyma (liquefactive necrosis with PMNs and cellular debris)

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16
Q

What is the presentation of a brain abscess?

A

Spiking Fevers
Confusion
Projectile vomiting (increased ICP)
Focal neurological deficits

17
Q

What do you see on biopsy and lumbar puncture in a patient with a brain abscess?

A

Biopsy best investigation: Mixed flora or Polymicrobal flora (combination of anaerobes and aerobes)
Lumbar Puncture: Elevated WBC, elevated protein and normal glucose (b.c the problem is in the brain not the CSF)

18
Q

What is seen on CT scan in patient with brain abscess?

A

CT scan with contrast:

Ring Enhancing lesion

19
Q

What are the 5 conditions that give you a ring enhancing lesion on CT?

A 
Glioblastoma Multiform
Mets 
Abscess 
Lymphoma
Toxoplasmosis
20
Q

What are the complications of a brain abscess?

A

Rupture into ventricles —– ventriculitis —- obstruction of ventricles —- hydrocephalus (non communicating)
Also from broad spectrum abx = CDIFF or toxic megacolon

21
Q

A quick review on Meningitis, what are the bacterial causes for the various age groups?

A

Bacterial:

  • Neonate: E.coli or strep
  • –Children: H.influenza or N.meningitides
  • Adolescents: N. meningitides
  • Adults: S. pneumoniae or L. monocytogenes
22
Q

What is seen on histology and CSF for meningitis?

A

Histology: Exudates covering the leptomeninges and engorgement of the meningeal vessels
CSF: increased WBCs, increased protein and decreased glucose

23
Q

Fungal Meningitis usually occurs in the immunocompromised, what are the various bugs?

A 
Meningeal: 
-cryptococcosis: soap bubble appearance 
-candida: microabscesses 
Vasoinvasive --- thrombotic occlusion--infarction and hemorrhage 
--aspergillus
-mucomycosis
24
Q

The last meningitis to be discussed is Tuberculous meningitis. What are some features?

A
  • -TB granulomas in the parenchyma (TB)
  • -May complicate primary hematogenous dissemination
  • -Cell mediate immunity – formation of Rich’s/Gohn’s Focus – depression of CMI — reactivation and rupture of focus into subarachnoid space
25
Q

Moving on to viral encephalitis, what is this?

A

Perivascular lymphocytic infiltrate
Individual neuronal necrosis with phagocytosis
Focal collection of microglia

26
Q

Now there are various viral infections that cause encephalitis, each card will go through the various causes, what is the most common viral cause?

A

HIV-E = most common world wide

27
Q

The next viral encephalitis is Herpes virus, explain the various herpes viruses that cause encephalitis

A

Agressive encephalitis in immunocompromised hosts

  • Herpes Simplex (HSV 1 &2)- acute necrotizing encephalitis
  • edema, focal hemorrhagic necrosis, asymmetric involvement of temporal lobe
  • Burn Out HSV: extensive cavitation & gliosis
  • Neonatal HSV: 1=postnatally and 2=delivery
  • VZV infection: cerebellitis, meningoencephalitis, encephalitis, and myeloradiculitis (also caused by CMV & HSV2)
  • EBV: aspetic meningitis
28
Q

The next viral encephalitis is Rabies (Rhabdovirus-RNA), explain the complications of rabies encephalitis?

A

Transmitted by bite of rapid animal

  • -replicates in muscle – retrograde axonal transport to CNS
  • -anterograde axonal transport to salivary and lacrimal glands
  • -Incubation period shorter in children and with bites closer to CNS
  • Lymphocytic meningoencephalitis, neuronophagia, extensive neuronal invasion (Negri Bodies =cytoplasmic inclusions)
29
Q

The next viral encephalitis is HIV, what are some complications of this?

A

HIV: infects microglial cells and macrophages – patchy loss of myelin
–widespread mild inflammation: perivascular lymphocytosis, microglial nodules and multinucleated cells

30
Q

The final viral cause of viral encephalitis is JC virus, w hat are some complications?

A

JC virus: reactivation of polyomavirus– progressive multifocal leukoencephalopathy in immunosuppressed patients

  • -enlarged virus laden oligodendrocytic nuclei and multiple foci of demyelination
  • -bizarre astrocytes
31
Q

Briefly, lets touch on parasite infections of the brain. The first is Toxoplasmosis Gondii, what are some features?

A

Definitive Host= Cats
Acquired by consumption of undercooked meat or ingestion of contaminated cat feces
Usually immunocompromised patients
Ill-defined multiloculated and necrotizing abscess in deep grey matter (MULTIPLE RING ENHANCING LESIONS)

32
Q

Finally the other parasitic infection of the brain is Cysticercus Cellulose, what are some features?

A

Larval form of pork tapeworm = Taenia Solium
Definitive host = humans
Cysticercosis occurs when humans become the intermediate host
Involvement of subarachnoid space – racemose cysticercosis

33
Q

Finally the last topic for this card deck is prion disease, what is the cause?

A

CJD: sporadic – rapidly progressive dementia and myoclonus

Variant CJD: associated with BSE meat consumption (slower onset and more personality changes)

34
Q

What is the pathogenesis for prion disease?

A

Accumulation of altered form of prion protein — neuronal death, gliosis, accumulation of extracellular amyloid (Kuru plaques) and vacuolization of grey matter
(natural prion protein converted to neurotoxic prion protein)

35
Q

What does gross image of prion disease look like?

A

Spongiform degeneration of grey matter

Pathology Post Midterm (50 decks)

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