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Small Animal Final Year > Inflammatory Disease > Flashcards

Inflammatory Disease Flashcards

1
Q

Name 4 infectious inflammatory CNS diseases (5)

A

–Viral

–Bacterial

–Protozoal

–Algae

–Parasitic

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2
Q

Name 5 non infectious CNS inflammatory diseases (7)

A

–GME

–NME

–NE

–SRMA

–Cauda equina neuritis

–Pachimeningitis

–Eosinophilic

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3
Q

Label

A

A) Grey matter

B) White matter

C) Meninges

D) Ventricles

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4
Q

How do you diagnose:

  • GME granulomatous meningoencephalomyelitis
  • NME necrotising meningoencephalitis
  • NLE necrotising leukoencephalitis
A

Histopathology

If no histopathology = MUA

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5
Q

What are the clinical signsof inflammatory CNS disease?

A

–Acute/sub-acute in onset

–Progressive in nature

–Associated with multifocal/diffuse neuroanatomical localisation

–Systemic signs rarely reported

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6
Q

A) What is GME?

B) What is characteristic?

A

A) Inflammatory (immune-mediated) disease of unknown aetiology

B)

•Characteristic granulomatose, angiocentric encephalitis

–Macrophages

–Lymphocytes

–Plasma cells

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7
Q

With GME is there more:

White matter and meninges OR

Grey matter?

A

Grey

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8
Q

What 3 things are seen with angeiocentric encephalitis with GME?

A

–Macrophages

–Lymphocytes

–Plasma cells

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9
Q

What is this?

A

Angiocentric encephalitis

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10
Q

What are the 2 classifications of GME?

A
  • Clinical
  • Histopathological
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11
Q

What are the 3 clinical forms of GME?

A

•Disseminated

–Most common, acute rapidly progressive multifocal signs

–Cerebrum, caudal brainstem, cerebellum, or cervical spinal cord

•Focal

–Acute or slowly progressive signs reflecting single space-occupying mass lesion

•Ocular

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12
Q

What are the 3 major pattern of lesion distribution with GME?

A

•Common disseminated form

–Spinal cord, brainstem and mid-brain (<

  • Disseminated form with angiocentric expansion (multiple coalescing lesions)
  • Focal form, single discrete mass lesion

–Spinal cord, brainstem and mid-brain, thalamus, optic nerves, cerebrum

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13
Q

What are the clinical features of GME?

A

•Young adult dogs (average age 4.5yrs range from 6 months to 12 years)

  • Any gender
  • Female, toy and terrier breeds over- represented
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14
Q

What do the clinical signs of GME reflect?

A

Lesion distribution

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15
Q

What are the clinical signs of GME?

A

–Vestibulo-cerebellar

–Cranial nerves deficits

–Visual impairment

–Paresis (tetra)

–Cervical pain

–Body turn

–Altered mentation

–Seizures

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16
Q

How do you diagnose GME?

A

–Rule out systemic dx

–Advanced imaging (MRI)

  • Multiple hyperintensities on T2-weighted or (FLAIR) throughout the CNS white matter.
  • Variable intensity in T1-weighted
  • Variable contrast uptake on T1 post gadolinium
  • Variable meningeal enhancement

–CSF

•Mononuclear mixed pleocytosis, increased TP

–Histopathology

  • Angiocentric
  • Mixed-lymphoid
  • With matter encephalitis
  • Lymphocytic meningitis
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17
Q

How do you treat GME?

A

–Supportive

•Mannitol?

–Immunomodulatory

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18
Q

A) What is NME?

B) Where is there pan-encephalitis?

C) Where is mainly affected?

A

A) Inflammatory (immune-mediated) disease of unknown aetiology

B)

–Meninges

–Grey matter

–White matter

C) Cerebral hemispheres mainly

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19
Q

What is this?

A

•Non-suppurative, necrotising ME

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20
Q

What are the clinical features of NME?

A
  • Young adult dogs mean age 2Yr (6mo to 7Yr)
  • No gender predisposition
  • Breeds? Pug, Maltese, Pekingese…
  • Rapidly progressive signs

–Seizures

–Depression

–Circling

–Visual deficits

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21
Q

How do you diagnose NME?

A

–Rule out systemic dx

–Advanced imaging (MRI)

  • hyperintense on T2-weighted and FLAIR
  • Isointense to slightly hypointense on T1-weighted
  • Variable contrast enhancement on T1-weighted
  • Loss of grey/white matter demarcation

–CSF (lymphocytic), increased TP

–Histopathology

  • Lymphocytic meningitis
  • Polioencephalitis
  • Necrotising leukoencephalitis
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22
Q

How do you treat NME?

A

–Supportive

  • Antiepileptic
  • Mannitol?

–Immunomodulatory

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23
Q

NLE:

A) What is it?

B) What does it cause?

C) What is seen?

A

A) Inflammatory (immune-mediated) disease of unknown aetiology

B) Non-suppurative, necrotising encephalitis

C)Hemispheric white matter, and brainstem

•Cortex and meninges not involved

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24
Q

What is this?

A

•Non-suppurative, necrotising encephalitis

25
Q

What is this?

A

•Hemispheric white matter, and brainstem

26
Q

What are the clinical features of NLE?

A
  • Young adult dogs mean age 4.5Yr (4mo to 10Yr)
  • No gender predisposition
  • Breeds? Yorkshire terrier, Pomeranian, French bulldog
27
Q

What are the signs of NLE?

A

Rapidly progressive signs

  • Depression
  • Circling
  • Vestibulocerebellar signs
  • Visual deficits
  • Seizures
28
Q

How do you diagnose NLE?

A

–Rule out systemic dx

–Advanced imaging (MRI)

  • Hyperintense on T2-weighted and FLAIR images
  • Multiple cystic areas of necrosis
  • Hypointense or isointense on T1-weighted images,
  • Contrast enhancement is variable

–CSF monocytic, increased TP

–Histopathology

  • Asymmetric, bilateral necrotising encephalitis
  • Hemispheric white matter and brainstem
  • Overlying cortex and meninges not involved
  • Histiocyte, microglia and macrophages cell infiltrates and lymphocytic perivascular cuffing
29
Q

How do you treat NLE?

A

–Supportive

•Mannitol?

–Immunomodulatory

30
Q

How can you treat MUA?

A

Immunosuppression

  • Corticosteroids
  • Cytosine arabinoside
  • Ciclosporines
  • Azathioprine
31
Q

How can we treat MUA with corticosteroids?

A
  • Prednisolone, 1.5mg/kg BID then progressively reduced over 6 months to a maintenance dose of 0.5mg/kg EOD
  • Dexamethasone, 0.2mg/kg SID then progressively reduced over about 6 months to a maintenance dose of 0.05mg/ kg EOD
32
Q

How can you treat MUA with Cytosine Arabinoside?

A
  • Synthetic nucleoside analog, competes for incorporation into nucleic acidsà inhibits DNA polymerase in mitotically active cells
  • 50gm/m2 SC every 12 hours for two consecutive days, this protocol is repeated every 3 to 6 weeks (or longer intervals according to clinical signs)
  • Monitor haematology
33
Q

How can you treat MUA with ciclosporin?

A
  • Suppressing T-lymphocyte activation and proliferation
  • 6mg/kg PO every 12 hours
  • Can be combined with ketoconazole
  • Adverse effects:
    • GI upset
    • Gingival hyperplasia
    • Change in coat (shedding or hirsutism)
34
Q

How can you treat MUA with azathioprine?

Include the side effects

A
  • Thiopurine, interferes with the productions of purine nucleotides = increased lymphocytes proliferation
  • =Hepatic metabolism
  • 2mg/kg SID
  • Tapered to 0.5-1mg/kg EOD long term

Side effects:

Bone marrow suppression and GI upset

35
Q

What is SRMA?

What is seen?

A

SRMA steroid responsive meningitis arteritis

  • Inflammatory (immune-mediated) disease
  • Suppurative inflammation (neutrophilc)
  • Leptomeninges spinal cord
  • Necrotising fibrinoid arteritis
36
Q

What is the predisposition of SRMA?

A
  • Young dogs 6-18months
  • No gender predisposition
  • Any breed but over represented

–Beagle

–Boxer

–Bernese mountain dog

–Weimaraner

–etc

37
Q

What are the clinical features of SRMA?

A
  • Profound cervical hyperaesthesia
  • Pyrexia
  • Depression
  • Neutrophilia
38
Q

What are the 2 forms of SRMA?

A
  • Acute “typical”
  • Chronic, due to inadequate treatment or relapses of acute disease
39
Q

How do you diagnose SRMA?

A

–Neutrophilia

–(MRI) longus colli myositis, altered CSF signal

–CSF

  • Acute: marked neutrophilic pleocytosis and raised TP
  • Chronic: mixed or mononuclear pleocytosis and raised TP
  • Measure IgA in serum and CSF
40
Q

What is this?

A

SRMA steroid responsive meningitis arteritis

41
Q

What does this show?

A

SRMA steroid responsive meningitis arteritis

42
Q

How can you treat SRMA?

A

Immunosuppression

  • Corticosteroids
  • Cytosine arabinoside
  • Ciclosporines
  • Azathioprine
43
Q

What is the prognosis of SRMA?

A

Fair to good

44
Q

A) What is Cauda equina neuritis?

B) What is occassionally affected?

C) What is the likely origin?

D) Who is most affected?

A

A) Rare and sporadic disease in horses and Involves the nerves on the cauda equina

B) Occasionally affects CN, VII, VIII and rarely V

C) Likely autoimmune or post infectious origin (herpes, adenovirus)

D) Adult female mostly affected

45
Q

What does cauda equina neuritis lead to?

A

To tail paralysis and sphincters incompetence

46
Q

What makes Cauda equina neuritis lymphoplasmacytic?

A

•The inflammation starts in the intradural portion of the nerve root

47
Q

What makes Cauda equina neuritis granulomatous?

A

The inflammation continues in the extradural portion forming large “mass- like” lesions

48
Q

How do you diagnose Cauda equina neuritis?

A

•Compatible clinical signs

–Tail paralysis, incontinence, gait deficits, CN

•CSF (lumbar)

–Non-suppurative pleocytosis

–Elevated TP

•Post mortem

49
Q

What is the prognosis of Cauda equina neuritis?

A

Poor

50
Q

A) What is Eosinophilic meningoencephalitis (EME)?

B) Who is at risk?

C) What is seen?

A

A) Inflammatory likely immune-mediated, allergic mechanism?!?

B) Young, male Golden Retrievers and Rottweilers may be over-represented, any breed and gender can be affected

C) Severe meningitis and periventriculitis with infiltration of underlying parenchyma

51
Q

How do you diagnose Eosinophilic meningoencephalitis (EME)?

A
  • MRI multifocal changes
  • CSF = eosinophilic pleocytosis
52
Q

What is this?

A

Eosinophilic meningoencephalitis (EME)

•eosinophilic pleocytosis

53
Q

What is the prognosis of Eosinophilic meningoencephalitis (EME)?

A

–Immunosuppressive doses of corticosteroids

–Occasionally needs additional immunosuppressive drugs such as cytosine

54
Q

Pachimeningitis (hypertrophic chronic):

A) What is this?

B) Which breeds are at risk?

C) What is it chracterised by?

A

A) Inflammatory likely immune mediated origin

B) Greyhounds and crossed-sight hounds are over-represented

C) Charaterised by diffuse thickening of the dura mater by fibrosing inflammatory process

55
Q

What do the clinical signs of Pachimeningitis (hypertrophic chronic) reflect?

A

Multiple CN deficits

56
Q

What is the most common sign of Pachimeningitis (hypertrophic chronic)?

A

Dropped jaw

57
Q

How do you diagnose Pachimeningitis (hypertrophic chronic)?

A
  • MRI
  • CSF may be inflammatory
58
Q

How do you treat Pachimeningitis (hypertrophic chronic)?

A

–Immunosuppressive doses of corticosteroids

–Occasionally needs additional immunosuppressive drugs such as cytosine

59
Q

What is the prognosis of Pachimeningitis (hypertrophic chronic)?

A

–Fair, most dogs achieve clinical remission however a cure is difficult to obtain

Small Animal Final Year (317 decks)

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