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patho II > Neuro II (a) > Flashcards

Neuro II (a) Flashcards

1
Q

cause of Epidural Abscess

A

Direct local spread from an adjacent focus of infection (e.g. sinusitis, osteomyelitis, etc.)

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2
Q

CF of Epidural Abcesses

A

Fever, headache and neck stiffness,
but also a variety of neurologic signs, lethargy and
coma if left untreated

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3
Q

Progression and Complications of Epidural Abscess: Extension to the ———– -> ————- –> Mass effect –> ————- of the bridging veins –> Venous occlusion –> Brain Infarction

A

Extension to the subdural space -> Subdural Empyema –> Mass effect –> Thrombophlebitis of the bridging veins –> Venous occlusion –> Brain Infarction

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4
Q

Epidural Absces –> ————

A

Subdural Empyema

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5
Q

The 3 forms of Infectious Meningitis

A

1) Acute pyogenic (bacterial)
2) Aseptic (viral)
3) Chronic (Tbc)

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6
Q

cause of Acute Pyogenic Meningitis in neonants

A

E. coli, group B Streptococci

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7
Q

Cause of Acute Meningitis in adolescents and young adults

A

Neisseria meningitidis

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8
Q

Cause of Acute Meningitis in older individuals

A

Streptococcus pneumoniae and Listeria monocytogenes

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9
Q

CF of Acute Pyogenic Meningitis

A

1) Positive Kernig’s and Brudzinki signs
2) Neck stiffness
3) Vomiting
4) headache
5) Photophobia
6) Clouding of Consciousness
7) Irritablity

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10
Q

Lab findings of Acute Pyogenic Meningitis

A

CSF examination:
* Abundant neutrophils
* Elevated protein
* Reduced glucose

Lumbar puncture: Increased pressure

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11
Q

Macroscopic Features:
* Leptomeningeal exudate, over the surface
of the brain
* Engorged and prominent meningeal vessels

Microscopic Findings:
* Neutrophil cell infiltrates within subarachnoid
space
* Phlebitis and a thrombus
* Gram stain –> Pneumococcus meningitis- purulent exudate

featurse of?

A

Acute Pyogenic Meningitis

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12
Q

Complications of Acute Pyogenic Mengitis

A

1) Formation of intracerebral Abscess
2) Development of Phlebitis –> Venous occlusion and haemorrhagic Infarction of the underlying brain
3) Scarring at the site of foramina of Luschka and Magendie –> CSF flow obstruction –> Obstructive non-communicating Hydrocephalus
4) Scarring at the arachnoidal granulations –> Reduction in CSF reabsorption –> Communicating Hydrocephalus

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13
Q

cause of Aseptic Meningitis

A

Viral infection

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14
Q

CM of Aseptic Meningitis

A

1) Meningeal irritation
2) Fever
3) Alterations in consciousness

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15
Q

lab findings in Aseptic Meningitis

A

CSF:
* Lymphocytosis
* Moderate protein elevation
* Normal glucose level

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16
Q

Macroscopic Features:
* Brain swelling
* subtle Hyperaemia

Microscopic Findings:
* Mild to moderate leptomeningeal lymphocytic infiltrate

features of?

A

Aseptic Meningitis

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17
Q

cause of Tuberculous Meningitis

A

Mycobacterium tuberculosis

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18
Q

CM of Tuberculous Meningitis

A
  • Headache
  • Malaise
  • Mental confusion
  • Vomiting
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19
Q

lab fidings in Tuberculous Meningitis

A
  • Moderate increased cellularity; Mononuclear cells or
    a mixture of polymorphonuclear and mononuclear cells
  • Elevated protein level
  • Moderately reduced or normal glucose content
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20
Q

progression and complications of Tbc Meningitis

A

Arachnoid fibrosis –> Hydrocephalus

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21
Q

Macroscopic Features:
* Gelatinous or fibrinous exudate at the base of the brain –> Obliteration of the cisterns and wrapping of cranial nerves
* Obliterative Endarteritis of the arteries in the
subarachnoid space

Microscopic Findings:
* Mixtures of lymphocytes, plasma cells and macrophages
* Well formed granulomas with caseous necrosis (florid cases)

features of?

A

Tbc Meningitis

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22
Q

causes of Brain Abscess

A

Bacterial infections

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23
Q

CF of Brain Abscess

A
  • Progressive focal deficits
  • General signs related to increased intracranial
    pressure
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24
Q

lab findings of Brain Abscess

A
  • Increased numbers of white blood cells
  • high protein levels
  • Normal glucose content
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25
Q

Macroscopic Features:
* Discrete lesion
* Central liquefactive necrosis
* Surrounding fibrous capsule

Microscopic Findings:
* Granulation tissue and oedema around the necrotic core
* Zone of reactive gliosis, outside the fibrous capsule

features of?

A

Brain Abscess

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26
Q

complications of Brain Abcesse
1) Increased intracranial pressure –> ——-
2) Abscess rupture –> ————, —————–, and ———

A

1) Increased intracranial pressure –> Herniation
2) Abscess rupture –> Ventriculitis, Meningitis, and Venous sinus Thrombosis

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27
Q

Venous sinus Thrombosis –> ——-

A

Haemorrhagic Venous infarction

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28
Q

Characteristic Histologic Features:
* Perivascular and parenchymal mononuclear cell infiltrates
* Microglial nodules
* Neuronophagia
* Presence of inclusion bodies

features of?

A

Viral Encephalitis

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29
Q

Important cause of Epidemic Encephalitis?

A

ARBO (ARthropod-BOrne) virus

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30
Q

CM of ARBO (Arthropod-borne) disease

A
  • Seizures
  • Confusion
  • Delirium
  • Stupor or Coma
  • Reflex asymmetry
  • Ocular Palsies
  • yellow fever
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31
Q

Types of ARBO (ARthropod- Borne) viruses

A

1) Eastern and Western Equine Encephalitis
2) West Nile virus infection

32
Q

Lab findings of ARBO (Arthropod-borne) viruses

A

CSF:
* Colourless
* Early neutrophilic pleocytosis –>Conversion
to lymphocytosis
* Elevated protein level
* Normal glucose

33
Q

Microscopic Findings:
* Perivascular lymphocytic Meningoencephalitis
* Micro-Abscess in the white matter
* Multifocal gray and white matter necrosis
* Neuronophagia
* Microglial nodules
* Necrotising Vasculitis with focal haemorrhages
(severe cases)

features of?

A

Eastern Eqine Encephalitis
(ARBO Viruses)

34
Q

Epi of HSV-1

* Herpes virus

A

Most common in children and young adults

35
Q

CM of HSV-1

A

Alterations in mood, memory and behaviour

36
Q

**

Macroscopic Features:
* Inferior and medial regions of the temporal lobes
and the orbital gyri of the frontal lobes
* Heamorrhagic Necrosis in the Temporal and frontal lobe

Microscopic Findings:
* Necrotising and haemorrhagic infection
* Perivascular inflammatory infiltrates
* Large eosinophilic intranuclear viral inclusions
(Cowdry type A bodies)

features of?

A

HSV Encephalitis (caused by HSV-1)

37
Q

HSV Encephalitis (caused by HSV-1)

Macroscopic Features:
* Inferior and medial regions of the temporal lobes
and the orbital gyri of the frontal lobes
* Heamorrhagic Necrosis in the ———- and ———

Microscopic Findings:
* Necrotising and haemorrhagic infection
* Perivascular inflammatory infiltrates
* Large eosinophilic intranuclear viral inclusions
(——————-)

A

Macroscopic Features:
* Inferior and medial regions of the temporal lobes
and the orbital gyri of the frontal lobes
* Heamorrhagic Necrosis in the Temporal and frontal lobe

Microscopic Findings:
* Necrotising and haemorrhagic infection
* Perivascular inflammatory infiltrates
* Large eosinophilic intranuclear viral inclusions
(Cowdry type A bodies)

38
Q

HSV-2 occures as:
* ——— in adults
* ——————- in neonates, born by mothers with active primary HSV genital infections

A
  • Meningitis in adults
  • Disseminated severe Encephalitis in neonates, born by mothers with active primary HSV genital infections
39
Q

CM of Polio Virus

A

1) Muscle wasting
2) Hporefelxia
3) Death from respiratory muscles paralysis (Acute)
4) Mild Gastroenterits
5) Paralytic Poliomeylitis

40
Q

Pathogensis and CM of Polio virus
* Subclinical or ————-
* Invasion of the CNS and destruction of the motor
neurons in spinal cord and brain stem (————–)
* Loss of motor neurons –> ———— and
————–, in the affected body region
* Paralysis of the respiratory muscles, in acute disease –> ———-

A
  • Subclinical or mild Gastroenteritis
  • Invasion of the CNS and destruction of the motor
    neurons in spinal cord and brain stem (Paralytic Poliomyelitis)
  • Loss of motor neurons –> Muscle wasting and
    hyporefelxia, in the affected body region
  • Paralysis of the respiratory muscles, in acute disease –> death
41
Q

* Polio virus

patho and CM of Post-Polio syndrome:
* manifests ——- yrs after the initial illness
* CM: —————– associated with decreased
muscle bulk and pain

A
  • manifests 25-35yrs after the initial illness
  • CM: Progressive weakness associated with decreased muscle bulk and pain
42
Q

cause of Rabis Virus

A

Bite from diseased animals (fox)

43
Q

Pathogenesis of Rabies Virus

A

Ascent of the virus along the
peripheral nerves from the wound site

44
Q

CM of Rabies Virus

A
  • Malaise
  • Headache
  • Fever
  • Extra-ordinary CNS excitability (the slightest touch
    is painful)
  • Contracture of the pharyngeal musculature –>
    Hydrophobia
  • Periods of mania and stupor progress to coma and death
45
Q

Microscopic Findings:
* Discrete, intra-cytoplasmic, deeply eosinophilic
inclusions within neurons (Negri bodies)

features of?

A

Rabies virus

46
Q

Rabies virus

Microscopic Findings:
* Discrete, intra-cytoplasmic, deeply eosinophilic
inclusions within neurons (————–)

A

Negri bodies

47
Q

Varicella-Zoster Virus causes?

A

Chickenpox (primary infection)

48
Q

Varicella-Zoster Virus can reactivate in adults and mainfest as?

A

Shingles
(painful vesicular skin eruption in deramtomes distribution)

49
Q

CM of HIV

A
  • Cognitive dysfunction (ranging from mild to marked
    dementia)
  • Aseptic [Viral] Meningitis (1-2 weeks after onset of primary infection; 10% of patients)
50
Q

Lab findings in HIV

A
  • Antibodies to HIV
  • Isolation of the virus from the CSF
51
Q

Microscopic Findings:
* Predominantly, in subcortical white matter, diencephalon and brain stem
* Presence of microglial nodules, with multinucleate giant cells
* Abnormally prominent endothelial cells
* Perivascular foamy or pigment-laden macrophages
* Foci of tissue necrosis and reactive gliosis
* Multifocal or diffuse areas of myelin pallor, with axonal swellings and gliosis
* Identification of virus in CD4+ lymphocytes and multinucleate macrophages and microglia

features of?

A

HIV

52
Q

Myelin in the White matter can be identified using which histochemical stain ?

A

LFB- Luxol Fast Blue

53
Q

cause of Polymoa-Virus & Progressive multifocal leukoencenphalopathy

A

JC virus

54
Q

pathogensis of Polymoa-Virus & Progressive multifocal leukoencenphalopathy

A

Infection (preferentially) of the oligodendrocytes –> Oligodendrocytes’ injury and death with resultant demyelination

55
Q

Imaging studies of?
imaging: Extensive, often multifocal, ring-enhancing lesions in the hemispheric or cerebellar white matter

A

Polymoa-Virus & Progressive multifocal leukoencenphalopathy

56
Q

CF of Polymoa-Virus & Progressive multifocal leukoencenphalopathy

A

Focal and progressive neurologic symptoms and signs

57
Q

Macroscopic Features:
* Patchy, irregular, ill-defined areas of white matter destruction

Microscopic Findings:
* Centrally localised lipid-laden macrophages and reduced number of axons
* In the periphery of the lesion, enlarged oligodendrocyte nuclei (Plum-coloured) with glassy-appearing amphophilic viral inclusions
* Bizarre giant forms of astrocytes (irregular, hyperchromatic, sometimes multiple nuclei)

features of?

A

Polymoa-Virus & Progressive multifocal leukoencenphalopathy

58
Q

CF of Fungal Encephalitis caused by Cryptococcus Neoformans

A
  • Fulminant and fatal (2 weeks)
  • Indolent behaviour, with development over months or years
59
Q

CSF examination of Fungal Encephalitis caused by Cryptococcus neoformans show?

A

1) Elevated protein;
2) Mucoid encapsulated yeasts (India ink);
3) Positive test for cryptococcal Ag

60
Q

Morphology:
Proliferation of the organisms in the Virchow-Robin spaces –> Characteristic “soap bubble” like appearance

Features of?

A

Fungal Encepahlitis caused by Cyrptococcus Neofromans

61
Q

Fungal encephalitis caused by cryptococcus neoformans

Morphology:
Proliferation of the organisms in the Virchow-Robin spaces –> Characteristic ”————–” like appearance

A

“soap bubble”

62
Q

cause of Cerebral Toxoplasmosis

A

Toxoplasma gondii

63
Q

Epi of Cerebral Toxoplasmosis

A
  • Immunosuppressed adults
  • Newborns; trans-placentally from an infected mother
64
Q

CM of Cerberal Toxoplasmosis in Adults

A

Subacute symptomatology, evolving within 1-2 weeks

65
Q

CM of Cerebral Toxoplasmosis in Newbrons

A

Triad of:
* Chorioretinitis (causes blurred vision)
* Hydrocephalus
* Intracranial calcifications

66
Q

Macroscopic Features:
* Multiple Abscesses in the gray-white junction and the deep gray nuclei (immunosuppressed individuals)
* Oedema

Microscopic Findings:
* Central foci of necrosis with small haemorrhages
and mixed inflammatory cell infiltrates and vascular
proliferation
* Free Tachyzoites and encysted Bradyzoites at the periphery of the necrotic foci

features of?

A

Cerebral Toxoplasmosis

67
Q

cause of Cysticercosis

A

Taenia solium

68
Q

CM of cysticercosis

A

Mass lesion –> Seizures

69
Q

Macroscopic Features:
* Cysts with a smooth lining, within the brain and subarachnoid space

Microscopic Findings:
* Body wall and hooklets from mouth parts
* Intense inflammatory infiltrate (with eosinophils) - incase of dead encysted organism
* Marked gliosis

features of?

A

Cysticercosis

70
Q

cause of Prion disease :
Abnormal form of a cellular protein;
Conformational change from its normal shape (α-Helical ——) to an abnormal conformation (β-sheet ——-)

A

Abnormal form of a cellular protein; Conformational change from its normal shape (α-Helical
PrPc) to an abnormal conformation (β-sheet PrPsc)

71
Q

Prion disease

patho:
Spontaneous change of PrPc to PrPsc conformation–> ———–

A

Sporadic form of CJD (Creutzfeldt-Jakob disease)

72
Q

Prion disease

patho:
Mutations in the PRNP gene (encoding PrPc) –> ———

A

Familial form of CJD (Creutzfeldt-Jakob disease)

73
Q

Most common form of Creutzfeldt-Jakob disease

A

Sporadic form –> 85% of cases

74
Q

Epi of Sporadic Creutzfeldt-Jakob disease

A

> 70 years

75
Q

Epi of Familial Creutzfelt-Jakob disease

A

Younger people

76
Q

Macroscopic Features:
* Little or no brain atrophy

Microscopic Findings:
* Spongiform changes in the cerebral cortex and deep gray matter structures (e.g. Nucleus caudatus, Putamen)
* Neurons w/ Microscopic vacuoles of variable size within the neuropil and neuronal perikaryon
* Severe cases:
* Severe neuronal loss
* Reactive (astro)gliosis
* Development of “status spongiosus”

features of?

A

Sporadic and Familial Creutzfeldt-Jakob disease

77
Q

Vareint Cretzfeldet-Jakob disease specific microscopic diffrence from other CJD forms

A

Amyloid plaques

patho II (29 decks)

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