Malformations Flashcards

1
Q

What is hydromyelia?

A

Spinal cord abormality. Cavity, connected to 4th ventricle

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2
Q

What is syringomyelia?

A

(Syrinx). MC. Cyst within cord. adults. Developmental or traumatic, Arnold-chiari malf (type 1).

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3
Q

What is Intraparenchymal hemorrhage:

A

Prematurity, near ventricles, may cause hydrocephalus

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4
Q

What are some features of an infarct (malformation)?

A

Prematurity, supratentorial white matter, chalky plaques, possible cysts.

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5
Q

What is cerebral palsy?

A

Non-progressive defects in motor neurons (movement disorder)

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6
Q

What are some features of cerebral palsy?

A

Damage during cerebral development
Prematurity, hypoxia, infection, etc
1/3 have decreased congnition or seizures

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7
Q

How may bacteria, viruses, and fungi travel within the nervous system?

A

Hematogenous (MC), direct implant (trauma), local extension (mastoiditis, teeth), PNS (rabies, VZV)

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8
Q

What is an epidural abscess?

A

Adjacent infection (sinusitis, osteomyelitis) -> epidural space. Cord compression, neurosurgical emergency

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9
Q

What is a subdural empyema?

A

Infection of skull or sinus -> subdural space: emergency. Accumulation of pus.

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10
Q

What are some features of a subdural empyema?

A

SOL (accumulation of pus), thrombosis, infarct. Pyrexia, HA, cervicalgia, neuro dysfxn. Lethargy, coma.

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11
Q

How do you distinguish meningitis of the leptominiges (arachnoid from pia)?

A

CSF examination

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12
Q

What are some features of acute pyogenic meningitis?

A

Bacterial. Very rapid onset. HA, nuchal rigidity, photophobia (3 features known as meningism).

Also, iirritability, pyrexia, decreased congnition, neuro dysfxn. Fatal if untreated. Favorable with tx.

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13
Q

What are some features of the CSF in acute pyogenic meningitis?

A

Bacterial culture, increased pressure, increased neutrophils, increased proteins (exudate), decreased glucose.

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14
Q

What is found in the subarachnoid space in acute pyogenic meningitis?

A

Pus, exudate, neutrophils

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15
Q

What condition can a cerebral abscess possibly found in?

A

Acute pyogenic meningitis?

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16
Q

What is aseptic (viral) meningitis?

A

Relatively acute onset, pyrexia, consciousness, nuchal rigitidy, edema.

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17
Q

T/F

Aseptic meningitis must be stopped via medical intervention

A

False,

Self-limiting. CSF: increased lymphocytes

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18
Q

How does chronic meningitis onset?

A

Insidious onset.

19
Q

What is spirochetal meningitis?

A
Third degree syphilis or lyme disease.
Neuronal loss (tabes dorsalis), progressive loss of cognition and physical function (ataxia, anesthesia), polyneuropathies, encephalopathy.
20
Q

What is tuberculous (chronic) meningitis?

A

HA, malaise, confusion, vomiting. Tuberculoma in brain. CSF: moderate increased WBC’s and proteins

21
Q

What is a bacterial abscess?

A

Parenchymal infection. Localized, liqufactive necrosis. Bacerial: spesis, endocarditis, pulmonary infxn. Progressive neuro destruction, increased ICP.

22
Q

What is viral encephalitis?

A

Diffuse, from meningitis, mononuclear WBCs, neuronophagia. Rabies virus, poliovirus, rubella, west nile, HSV-1, HSV-2, VZV, CMV, HIV

23
Q

What is a fungal parenchymal infection?

A

Localized or diffuse (mixed) granulomas, meningitis, MC in immunosuppressed. Candida albicans, aspergillus fumigatus

24
Q

What are some features of poliovirus (poliomyelitis)?

A

Gastritis. Grey matter: cord/brainstem. Motor neuron damage. Wasting, flaccidity.

25
Q

What is MS?

A

Idiopathic/autoimmune, white matter demyelination. MC disorder of myelin

26
Q

What are some features of MS?

A

Episodes of neurologic deficits. “Relapsing-remitting” neurological dysn (acute attacks that come and go). Incomplete recovery.

27
Q

What happens to myelin with MS?

A

Chronic inflammation: lymphocytes, macrophages. White matter lesions (plaques).

28
Q

Who is at risk for MS?

A

Young adults, females (2x), family HX. (15x) 25% monozygotic twins, decrease for dizygotic. HLA-DR2

29
Q

What are some primary features of MS?

A

Episodes of neurologic deficits. “Relapsing-remitting” neurological dysn (acute attacks that come and go). Incomplete recovery.

30
Q

Who is at risk for MS?

A

Young adults, females (2x), family HX. (15x) 25% monozygotic twins, decrease for dizygotic. HLA-DR2

31
Q

Where do plaques of MS occur?

A

Anywhere in the CNS. MC cerebrum, near ventricles, optic nerve/optic chiasm, brainstem, spinal cord, cerebellum

32
Q

What are the two types of MS plaques?

A

Active: Ongoing myelin breakdown
Inactive: Little myelin and minimal inflammation

33
Q

What are some other features of MS?

A

Highly variable, progressive

34
Q

What are some characteristics of early stage MS

A

Unilateral vision impariments/diplopia. CN dysfxn, ataxia, motor/sensory impairments. Bowel/bladder dysfxn, sexual dysfxn. Seizures, decreased cognition, depression, etc.

35
Q

What is the management plan for MS?

A

No cure: I.V. corticosteroids. Immunosuppression: decrease relapses. Many patients report use of CAM

36
Q

What are some features of Thaimine deficiency?

A

Wernike-Korsakoff syndrome, confusion, memory, ataxia, chronic alcoholics, chronic gastritis; necrosis, macrophages in thalamus

37
Q

What is beriberi?

A

LE paresthesia, paralysis, nystagmus.

38
Q

What are some features of Thaimine deficiency?

A

Wernike-Korsakoff syndrome (encephalopathy, memory dysfunction), confusion, memory, ataxia, chronic alcoholics, chronic gastritis; necrosis, macrophages in thalamus

39
Q

What is beriberi?

A

Systemic effects of thiamine deficiency. LE paresthesia, paralysis, nystagmus.

40
Q

What CNS affects are found with Cobalamin deficiency?

A

Demyelination, “subacute combined degeneration of the spinal cord” (destroys ascending and descending tracks in the cord), ataxia, paraplegia.

41
Q

What are some affects of hypoglycemia?

A

Mimics global hypoxia (edema), hippocampus is susceptible to injury

42
Q

What are some affects of hyperglycemia?

A

Uncontrolled DM, hyperosmal state (glycosuria, decreased H20), confusion, stupor, coma.

43
Q

What are some affects of hyperglycemia?

A

Uncontrolled type II diabetes, hyperosmal state (glycosuria, decreased H20), confusion, stupor, diabetic coma.