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Flashcards in Pathology II Deck (25)
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1
Q

What is the clinical presentation of inflammatory demyelinating polyradiculopathy?

A

Symmetric ascending muscle weakness/ paralysis beginning in the lower extremities with facial paralysis in 50% of the cases. Autonomic function may be severely affected (cardiac irregularities, hypertension, hypotension, etc) (p.444)

2
Q

What is the prognosis for inflammatory demyelinating polyradiculopathy?

A

Almost all patients survive and the majority recover completely after weeks to months (p.444)

3
Q

What lab findings are characteristic of acute inflammatory demyelinating polyradiculopathy?

A

Increased CSF protein with normal cell count (albuminocytologic dissociation); increased protein may cause papilledema (p.444)

4
Q

What conditions are associated with acute inflammatory demyelinating polyradiculoopathy?

A

Infections

5
Q

What organisms/ viruses are the most common causes of acute inflammatory demyelinating polyradiculopathy?

A

Campylobacter jejuni, CMV (p.444)

6
Q

What causes the autoimmune response in acute inflammatory demyelinating polyradiculopathy?

A

Autoimmune attack of peripheral myelin due to molecular mimicry, inoculations, and stress but no definitive link to pathogens (p.444)

7
Q

How is acute inflammatory demyelinating polyradiculopathy treated?

A

Respiratory support is critical until recovery. Additional treatment includes plasmapheresis, IV immune globulins (p.444)

8
Q

Name five less common demyelinating/ dysmyelinating diseases.

A

Progressive multifocal leukoencephalopathy (PML); Acute disseminated (postinfectious) encephalomyelitis; metachromatic leukodystrophy; Charcot-Marie-Tooth disease; Krabbe’s disease (p.445)

9
Q

What is Progressive multifocal leukoencephalopathy (PML)?

A

Rapidly progressive and usually fatal condition of demyelination of the CNS due to oligodendrocyte destruction (p.445)

10
Q

What conditions are associated with Progressive multifocal leukoencephalopathy (PML)

A

JC Virus; seen in 2-4% of AIDS patients due to reactivation of latent viral infection (p.445)

11
Q

What is Acute disseminated (postinfectious) encephalomyelitis?

A

Multifocal perivenular inflammation and demyelination after infection or certain vaccinations (p.445)

12
Q

What vaccinations can contribute to Acute disseminated (postinfectious) encephalomyelitis?

A

Measles, VZV (p.445)

13
Q

What infections can contribute to Acute disseminated (postinfectious) encephalomyelitis?

A

Rabies, Smallpox (p.445)

14
Q

What is metachromatic leukodystrophy?

A

An autosomal recessive lysosomal storage disease (p. 445)

15
Q

What deficiency causes metachromatic leukodystrophy?

A

Arylsulfatase A deficiency (p. 445)

16
Q

What is the pathophysiology associated with metachromatic leukodystrophy?

A

Buildup of sulfatides leads to impaired production of myelin sheath (p. 445)

17
Q

What is Charcot Marie Tooth disease?

A

A hereditary sensory and motor neuropathy related to the defective production of proteins involved in the structure and function of peripheral nerves or the myelin sheath (p. 445)

18
Q

What is Krabbe’s disease?

A

An autosomal recessive lysosomal storage disease (p. 445)

19
Q

What deficiency causes Krabbe’s disease?

A

Galactocerebrosidase (p. 445)

20
Q

What is the pathophysiology associated with Krabbe’s disease?

A

Buildup of galactocerebrosidase destroys myelin sheath (p. 445)

21
Q

What characterizes a seizure?

A

Synchronized, high frequency neuronal firing (p. 445)

22
Q

What is a partial (focal) seizure?

A

A seizure affecting one area of the brain. It is often proceeded by an aura and can spread to a generalized seizure (p. 445)

23
Q

Where do focal (partial) seizures most commonly originate?

A

The medial temporal lobe (p. 445)

24
Q

Name the two types of partial (focal) seizure.

A

Simple partial, complex partial (p. 445)

25
Q

What distinguishes a simple partial seizure from a complex partial seizure?

A

In simple partial seizures, consciousness is intact; in complex partial seizures, consciousness is impaired (p. 445)