CNS Flashcards

1
Q

Infection predominantly involving the subarachnoid space (Meninges)

A

Meningitis

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2
Q

Infection diffusely involving the brain tissue

A

Encephalitis

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3
Q

Focal infection of brain tissue with no capsule formation

A

Cerebritis

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4
Q

Focal infection of brain tissue with capsule formation

A

Abscess

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5
Q

General Routes of CNS Infections: (enumerate the 5 routes)

A
  1. Hematogenous
  2. Direct of Local Extension
  3. Implantation
  4. Along nervous system pathways
  5. Bony defects
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6
Q

General Routes of CNS Infections: Hematogenous
__________: From primary infection in the lungs or heart valves

A

Arterial

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7
Q

General Routes of CNS Infections: Hematogenous
__________: From infected scalp veins, orbital infections via the cavernous sinus

A

Venous

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8
Q

From the mastoid, middle ear, sinuses, or infected tooth

A

Direct of Local Extension

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9
Q

As a result of mechanical trauma (gunshot wound, surgical procedures e.g. craniotomy, or lumbar puncture)

A
  • Implantation
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10
Q

Usually occurs in viral infections like Rabies, Herpes Zoster, and
Poliomyelitis

A

Along nervous system pathways

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11
Q

Congenital or acquired (fractures)

A

Bony defects

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12
Q

_______ plus signs of brain parenchymal involvement which can result to altered sensorium, behavioral changes, psychosis.

A

Meningismus

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13
Q

In addition to the acute febrile illness with evidence of meningeal involvement, the patient commonly has an? (Name the 3)

A
  1. altered LOC
  2. depressed LOC
  3. focal or diffuse neurologic signs and symptoms
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14
Q

Common Etiologies of Viral Encephalitis

A
  • Herpes viruses (Herpes Simplex Virus 1)
  • Varicella zoster virus
  • Epstein Barr virus
  • Arthropod-borne viruses
  • La Cross Virus
  • West Nile Virus
  • St. Louis encephalitis virus
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15
Q

Less Common Etiologies of Viral Encephalitis

A
  • Rabies
  • Eastern equine encephalitis
    virus
  • Western equine encephalitis
    virus
  • Powassan virus
  • Cytomegalovirus
  • Enterovirus
  • Colorado tick fever
  • Mumps
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16
Q

Laboratory Diagnosis of the CSF Profile in Viral ENCEPHALITIS

A

*CSF lymphocytic pleocytosis, normal glucose, normal or mildly elevated protein
*20% may be hemorrhagic

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17
Q

Laboratory Diagnosis Of Viral Encephalitis:

A
  1. CSF TEST
  2. MRI
  3. EEG
  4. PCR STUDIES
  5. VIRAL CULTURE
  6. SEROLOGIC STUDIES
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18
Q

Clinical Presentation Of V. E

A
  • Meningismus MINUS profound alteration in consciousness, seizures and
    focal deficits
  • Headache (frontal or retroorbital)
  • Photophobia
  • Pain in moving the eyes
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19
Q

Constitutional signs Of V.E

A
  • Malaise
  • Myalgia
  • Anorexia
  • Nausea and vomiting
  • Abdominal pain and/or diarrhea
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20
Q

Treatment (V. ENCEPHALITIS)

A

*May be empiric or symptomatic
*May be treated as an outpatient basis
*Hospitalize if immunocompromised or with signs of encephalitis
*Acyclovir 10 mg/kg/day for 14 to 21 days
*Seizure control with anticonvulsants

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21
Q

Nursing Management For V.E

A

*Assess for neurologic function
*Initiate seizure precaution
Maintain a quiet environment
*Administer fluids as ordered
*Measure input and output

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22
Q

Prevention and Control Measures For V.E

A

*Secretion precautions
*Wearing of long-sleeved shirts and long pants *Use of mosquito repellant and netting *Mosquito and tick control

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23
Q

is a zoonotic, vector-borne virus, spread
primarily by Culex mosquitoes.

A

Japanese encephalitis virus (JEV)

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24
Q

_____ is one of the most
important causes of human viral encephalitis in Asia .

A

Japanese encephalitis virus (JEV)

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25
Q

Various species of birds are the

A

natural reservoir

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26
Q

are considered the main maintenance or amplifying host.

A

pigs

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27
Q

Virus that belongs to Flavi Virus common in Southeast Asia.

A

Japanese Encephalitis Virus

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28
Q

Causative agent for JEV

A

Japanese Encephalitis Virus

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29
Q

Mode of transmission For JEV

A

bite of infect mosquito “Culex Species” and may become infected and also biting pigs, horse and birds

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30
Q

Signs and Symptoms For JEV ( increased ICP)

A

✔ Flexor Posturing: flexion of the elbows with external rotation (specific damage to
✔ cortex) Also known as Decorticate Posturing (one E for both: flExor = decorticatE).
✔ Extensor Posturing: rigid extension of the neck, arms and legs (extensive cortex injury)
✔ also known as Decerebrate Posturing (count the letter “E”. multiple E for both: 4 in
✔ DEcErEbratE 2 E in ExtEnsor).

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31
Q

Signs and Symptoms For JEV

A
  • fever
  • ⬆️ ICP DAMAGES INDICATES:
    1. Cerebral cortex damage
    2. Headache not relieved by pain meds
    3. stroke respiration
    4. Apnea
    5. Hemianopia
    6. Hemiparesis or paralysis
    7. Doll’s Eye Reflex
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32
Q

Signs and Symptoms For JEV ( increased ICP)

A

✔ Flexor Posturing: flexion of the elbows with external rotation (specific damage to
✔ cortex) Also known as Decorticate Posturing (one E for both: flExor = decorticatE).
✔ Extensor Posturing: rigid extension of the neck, arms and legs (extensive cortex injury)
✔ also known as Decerebrate Posturing

33
Q

Signs and Symptoms For JEV ( increased ICP)

A

✔ Persistent Vegetative State: no perception of cognitive function but sleep and wake
✔ cycle, eye opening and brainstem function remains.
✔ Brain Dead: there is no electrical reading in the electroencephalogram.

34
Q

Signs and Symptoms For JEV where damage to the hypothalamus =

A

Rising Temperature, Vomiting.

35
Q

Signs and Symptoms For JEV Damage to Reticular Activating System Diencephalon=

A

Altered LOC: Confusion dullness, lethargy and stupor

36
Q

Damage in ______=Light Coma

A

MIDBRAIN

37
Q

Damage in ________= Deep Coma

A

Medulla Oblongata and Pons

38
Q

Damage to ______: Pupillary Dilation, Eye Fixation in one Position, Nystagmus (rolling of the eyeball), Projectile vomiting, Loss of GABA, Seizure

A

Brainstem

39
Q

Persistent loss of GABA and rising levels of glutamic acid=

A

Status Epilepticus

40
Q

reveals elevated WBC, RBC, Protein and in severe conditions, hazy color due to pus.

A

CSF exam by lumbar puncture in JEV

41
Q

is used if CSF and Lumbar puncture is not feasible to reveal the infectious organism and adjust antibiotic therapy as appropriate.

A
  • Blood Culture
42
Q

What is the purpose of oxygen therapy in preventing an increase in intracranial pressure (ICP)?

A

Oxygen therapy (6-10 liters per minute by nasal cannula) or intubation, depending on oxygen saturation and ABG results, helps prevent cerebral hypoxia.

43
Q

What is the dosage and administration route for Mannitol used to manage increased ICP?

A

Mannitol 15-25% solution is administered at a dosage of 1.5 to 2 grams/kg IV infusion for not less than 30 minutes.

44
Q

How is Furosemide used to manage increased ICP?

A

Furosemide is given at a dosage of 20 to 40 mg slow IV push for not less than 1 minute.

45
Q

What is the initial dose of Dexamethasone for managing increased ICP, and what is the subsequent dosing regimen?

A

The initial dose is 10 mg IV, followed by 4 mg IM every 6 hours until edema is resolved.

46
Q

Why are stool softeners like Lactulose or mineral oil used in patients with increased ICP?

A

Stool softeners prevent straining and the Valsalva reflex during defecation, which can increase ICP.

47
Q

Nursing management to Prevent increase of ICP, (JEV)

A

-Oxygen therapy
-Osmotic Diuretic
-Loop Diuretic
-Corticosteroids
-Stool Softeners

48
Q

Prevent and manage seizure (JEV)

A

Anti-Convulsants Hydantoin: Phenytoin 10-15 mg / kg slow IV push (not less than 1 minute)

49
Q

Raise LOC and provide adequate neural stimulation (JEV)

A

Piracetam 1.6 to 9.6 grams tablet pre orem per day

50
Q

Manage Headache due to Increase in ICP

A

NSAID: Acetaminophen 500 mg tablet per orem every 6 hours
* Put the patient in semi fowler’s position to promote venous
return.
* Provide oxygen to prevent rebound vasodilation due to
hypoxia.
* Promote normal bowel elevation to prevent straining during
defecation.

51
Q

JEV Infection Control: Limit the Spread of Infection

A
  • Assess for Infection Risk
  • Assess for possible Infectious case
  • Practice Standard Precaution at all times for nurses and visitors
  • No VISITOR on the first 72 hours upon antibiotic treatment
  • After 72 hours of antibiotic therapy, patient is no longer
    infectious. Visit may be allowed as
  • appropriate observing standard precaution.
  • Practice Hand washing
  • Observe Principles of Asepsis
  • Observed Disinfection and Antiseptic Procedures
52
Q

Prevention, Treatment and Nursing Management
(Vector Control: Mosquitoes)

A
  • Clean Surroundings: Remove vegetation.
    -Bioremediation: Use natural species (plants, fish, bacteria) to control mosquitoes.
    -Repelling Plants: Grow neem, citronella, eucalyptus, and others.
    -Larvivorous Fish: Use tilapia in water bodies; avoid chemicals.
    -Protect Dragonflies: Avoid chemicals in their habitats.
    -Drain Water: Remove stagnant water near homes.
53
Q

A type of viral encephalitis caused by Rhabdo Virus with unique manifestations of violent and impulsive behavior associated to viral damaging effects to the brain.

A

Rabies

54
Q

Rabies Mode of Transmission?

A

is by the bite of Bats and hunting of bats by domestic animals like cats which may infect dogs and other pets.

55
Q

RABIES INCUBATION PD

A

10 days

56
Q

True or False:
All infected animal except bats die of rabies virus

A

True

57
Q

As Rabies V. it travels to the brain, it damages the neuron it passes through leading to:

A

numbness and tingling sensation on the site of injury.

58
Q
  • The inflammatory reaction releases inflammatory chemicals and pyrogenic hormones that produces the classical manifestations of
A

fever, myalgia, body malaise and anorexia.

59
Q

Encephalitis results in increasing ICP Causing:

A

head ache, nausea and vomiting.

60
Q

Damage to CN number 9 (glossopharyngeal nerve) results in

A

painful throat muscles spasm.

61
Q

Rabies Pathognomonic sign

A

Hydrophobia and aerophobia

62
Q

Rabies Histopathology by Brain Biopsy:

A

Presence of Negri Bodies (viral organisms in neurons) is a pathognomonic sign of rabies, used for autopsy in suspected rabies cases.

63
Q

Serology (Antibody Tests):

A

Identifies elevated immunoglobulin levels when symptoms appear.

64
Q

Rabies Pet Observation:

A

Confine and observe the biting animal for 10 days. If it dies, perform a brain tissue biopsy.

65
Q

Keypoints in Prevention, Treatment and
Nursing Management

A

=Fatality: Rabies is almost always fatal once symptoms appear.
=Rare Recoveries: Possible with timely vaccination and immunoglobulin.
=Patient Dignity: Preserve dignity and comfort until the end.
=Nursing Care: Prevent infection, minimize suffering.
=Family Support: Comfort and support the family.
=Health Education: Provide moral and emotional support.

66
Q

Botulism Causative agent

A

Clostridium botulinum

67
Q

Found in soil and occasionally in animal feces Soil and water samples

A

Clostridium botulinum

68
Q

Associated with consumption of home-canned/vacuum-packed foods and preserved spiced, smoked fish

A

Clostridium botulinum

69
Q

Clostridium botulinum Diseases

A

Infant botulism (honey – flaccid paralysis), wound botulism, food-borne botulism

70
Q

Clostridium botulinum
Morphology

A

*Gram-positive bacilli *Spore-forming
*Strict anaerobic

71
Q

Clostridium botulinum
Antigenic Structures/Virulence Factors

A

*Spore formation
*Binary toxin (Disrupts vascular permeability)

72
Q

Botulinum toxin Has how many types?

A

Seven types: A, B, C, D, E, F, G
*A, B, E, and F – cause human illness with a lethal dose of 1 to 2 microgram
* A, B – associated with a variety of food/canned food
* E – fish products
* E, F – infant botulism

73
Q

Consists of neurotoxin and non-toxic subunits

A

Botulinum toxin

74
Q

Block neurotransmission of peripheral cholinergic synapses by preventing release of neurotransmitter acetylcholine

A

Botulinum toxin

75
Q

Results to lack of muscle contraction and paralysis

A

Botulinum toxic

76
Q

Botulinum Toxin Activities

A

*Blocks the release of acetylcholine
*Prevents the production of signal produced when acetylcholine binds to the post-synaptic receptor

77
Q

Infant ingests spores of C. botulinum

A

Infant Botulism

78
Q

floppy baby =

A

Flaccid paralysis

79
Q

Botulsim Lab Diagnosis

A

//Specimen
* Contaminated food
* Blood (Serum)
* Feces (for infant botulism)
//Cultural/Growth Characteristics * Blood-enriched anaerobic media
* (+) lipase production
* (+) hydrolyze gelatin
* (+) ferment glucose
* (+) digest milk proteins