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Flashcards in Pathology II Deck (25)
1

What is the clinical presentation of inflammatory demyelinating polyradiculopathy?

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

What is the prognosis for inflammatory demyelinating polyradiculopathy?

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

3

What lab findings are characteristic of acute inflammatory demyelinating polyradiculopathy?

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

4

What conditions are associated with acute inflammatory demyelinating polyradiculoopathy?

Infections

5

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

Campylobacter jejuni, CMV (p.444)

6

What causes the autoimmune response in acute inflammatory demyelinating polyradiculopathy?

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

7

How is acute inflammatory demyelinating polyradiculopathy treated?

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

8

Name five less common demyelinating/ dysmyelinating diseases.

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

9

What is Progressive multifocal leukoencephalopathy (PML)?

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

10

What conditions are associated with Progressive multifocal leukoencephalopathy (PML)

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

11

What is Acute disseminated (postinfectious) encephalomyelitis?

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

12

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

Measles, VZV (p.445)

13

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

Rabies, Smallpox (p.445)

14

What is metachromatic leukodystrophy?

An autosomal recessive lysosomal storage disease (p. 445)

15

What deficiency causes metachromatic leukodystrophy?

Arylsulfatase A deficiency (p. 445)

16

What is the pathophysiology associated with metachromatic leukodystrophy?

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

17

What is Charcot Marie Tooth disease?

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

What is Krabbe's disease?

An autosomal recessive lysosomal storage disease (p. 445)

19

What deficiency causes Krabbe's disease?

Galactocerebrosidase (p. 445)

20

What is the pathophysiology associated with Krabbe's disease?

Buildup of galactocerebrosidase destroys myelin sheath (p. 445)

21

What characterizes a seizure?

Synchronized, high frequency neuronal firing (p. 445)

22

What is a partial (focal) seizure?

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

Where do focal (partial) seizures most commonly originate?

The medial temporal lobe (p. 445)

24

Name the two types of partial (focal) seizure.

Simple partial, complex partial (p. 445)

25

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

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