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PT 680 Clinical Medicine > Infectious Pathologies of the CNS > Flashcards

Infectious Pathologies of the CNS Flashcards

1
Q

what is the significance of infectious CNS disorders

A

rare
major cause of morbidity and mortality

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2
Q

how do infectious CNS disorders occur

A

when pathogens invade the CNS/PNS via various modes of transmission and get past protective barriers

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3
Q

what type of germs present a challenge in prevention and treatment

A

drug-resistant germs

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4
Q

how are bacteria and viruses removed in the CNS

A

via reticuloendothelial system in the blood brain and blood cerebrospinal fluid barriers

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5
Q

glial cells go to work once an infectious pathogen in identified

A

immune system

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6
Q

what type of cells are the main cells in the immune system of nervous system

A

microglial cells

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7
Q

A network of blood vessels and tissue that is made up of closely spaced cells and helps keep harmful substances from reaching the brain

A

blood brain barrier

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8
Q

what substances can easily pass through BBB and which can pass via active transport

A

easy: water and O2
active transport: glucose and amino acids

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9
Q

why is there a reduction in immune protection if a pathogen invades CSF

A
  • CSF has 1/200 the amount of antibody and WBC’s are very low
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10
Q

is there a lymphatic system to protect the brain

A

no

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11
Q

what are the families of infectious CNS/PNS pathologies

A

encephalitis
meningitis
poliomyelitis
botulism
tetanus
rabies
shingles

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12
Q

what populations are most commonly effected

A

can effect children, but more often in adults or immuno-compromised individuals

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13
Q

describe the outcomes of CNS pathologies

A

varies on pathogen
can be very serious is not dx early and when not appropriately managed

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14
Q

list some differential diagnosis s/s that could indicate CNS infection

A
  • seizure activity
  • profound alteration in consciousness (GCS, MMSE, seizure monitoring)
  • cognitive and perceptual assessment
  • sensory integrity
  • cardiopulmonary sequelae
  • movement disorders reflect the insult of brain structures (decorticate/decerebrate)
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15
Q

what may be the first sign of CNS infection

A

seizures

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16
Q

describe encephalitis

A

an acute inflammation to brain tissue

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17
Q

another name for brain tissue

A

parenchyma

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18
Q

what matter does encephalitis primarily effect

A

gray matter

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19
Q

etiology of encephalitis

A

viruses (mosquitos/ticks), complications from chicken pox, measles or mumps, herpes simples

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20
Q

what can encephalitis lead to

A

neuronal death, cerebral edema, vascular damage to cerebral vessels

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21
Q

S/S of encephalitis

A

HA, N/V, elevated temp, lethargy, stiff neck, agitation, confusion and coma, focal signs and paralysis depending on areas of brain most involved, seizure activity

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22
Q

how to dx encephalitis

A

lumbar puncture, MRI and EEG changes

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23
Q

Tx encephalitis

A

antivirals, antibodies (IV(, possibly corticosteroids, surgical decompression
- depends on cause

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24
Q

why are corticosteroids not great for treating encephalitis

A

high dose can decreased immune system function

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25
Q

describe mortality rate and recovery of encephalitis

A

high mortality rate
10-50% recovery (depends on pathogen)

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26
Q

what is meningitis

A

inflammation of meninges of brain and spinal cord; some forms can be contagious

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27
Q

etiology meningitis

A

bacteria, virus, fungus, toxins

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28
Q

meningitis pathogens attack what areas

A

inner ear, sinus or URI

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29
Q

sudden onset of s/s of meningitis

A

high fever, HA, photophobia, nucal rigidity (neck stiffness), drowsiness, stupor, seizures

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30
Q

dx meningitis

A

lumbar puncture, Kernig’s sign, brudsinski’s sign

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31
Q

test that stretches the meninges and will cause severe pain

A

kernig’s sign

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32
Q

tx meningitis

A

vaccines for bacterial, meds, quiet dark environment

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33
Q

prognosis meningitis

A
  • bacterial: MEDICAL EMERGENCY - can be fatal in infants and elderly
  • viral - has to run its course
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34
Q

what is the hallmark sign of meningitis

A

nucal rigidity (neck stiffness)

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35
Q

describe kernig’s test

A
  • performed with pt supine or in chair
  • hip and knee flexed to 90deg and attempt made to extend knee
  • (+) pain in neck or back
36
Q

describe brudzinksi’s test

A

flexion of neck causes of hips and knees while pt is supine
- this occurs bc the pain has pain with neck flexion

37
Q

what is poliomyelitis

A

viral infection affecting LMN’s in brainstem and spinal cord

38
Q

how does poliomyelitis enter the body

A

through mouth and nose (PNS disorder)

39
Q

list the 3 infection mechanisms for poliomyelitis

A
  • asymptomatic (carrier)
  • symptomatic - flu-like
  • symptomatic with paralysis (due to virus entering anterior horn cells)
40
Q

s/s poliomyelitis

A

mm weakness of UE/LE, neck stiffness, mm atrophy, N&V, respiratory system due to paralysis

41
Q

dx poliomyelitis

A

by culture

42
Q

tx poliomyelitis

A

braces, respiratory support (ie. iron lung)

43
Q

describe post-polio syndrome

A

occurs 20-30 ears after initial infection with new mm weakness and fatigue due to pruning and lack of metabolic support for enlarged motor units

44
Q

describe zika virus and how is it transmitted

A
  • single strand of RNA virus
  • transmitted: mosquito bite, also spread mother to baby, sex, blood transfussion
45
Q

what % of people infected with zika virus are asymptomatic

A

80%

46
Q

s/s zika virus if symptomatic

A

fever, HA, joint pain, mild rash

47
Q

what does zika virus cause in fetus/unborn child and why

A

microcephaly - causes apoptosis and inhibition of neural cell differentiation leading to cortical thinning and microcephaly

48
Q

tx zika virus

A

no cure
tx is mosquito eradication
recommended safe sex (M 6mo, W 2mo) post traveling to area of high zika transmission

49
Q

describe botulism

A

neuromuscular poisoning resulting from bacteria invasion by clostridium botulinum
- neurotoxin (neuromuscular poison) interferes with releease of acetylcholine at peripheral N endings

50
Q

etiology botulism

A
  • food borne: improper canning procedures, raw honey
  • wound borne: bacteria invades wound and secretes neurotoxin
  • infant botulism: bacteria grows in intestnes of children; also associated with ingestion of honey in infants < 1 year
51
Q

s/s botulism

A

double vision, blurred vision, droopy eyelids, slurred speech, difficulty swallowing, dry mouth, respiratory decline, progressive muscle weakness starting at shoulders

52
Q

mortality rate botulism

A

60-70% if not treated immediately

53
Q

tx botulism

A
  • food borne: toxins are readily destroyed by exposure to heat - cooking foods at temperatures at 176deg for 30 minutes
  • induce vomiting to expel toxins
  • close monitoring of respiratory status - may require intubation and respiratory support
  • antibiotics and vaccines are useless - effect is from toxins
  • trivalent antitoxin from CDC in pandemics to slow progression
54
Q

describe tetanus

A

acute infectious disease characterized by convlusions and intermittent spasms of voluntary muscles
- bacterial infection - clostridium tetani found in soil and animal feces

55
Q

what does tetanus produce that effects skeletal muscles and blocks release of inhibitory neurotransmitters

A

toxin - tetanospasmin

56
Q

transmission tetanus

A

acquired from open wound infection (rusty nail, tin can lid, barbed wire)

57
Q

s/s tetanus

A

contractions of muscles of mastication (lock-jaw), general muscle spasms

58
Q

tx tetanus

A

life supporting procedures, wound debridement, penicillin and tetracycline

59
Q

outcomes of tetanus

A

fatal due to paralysis of respiratory muscles if not treated

60
Q

preventative tx tetanus

A

keep up with shots, need booster every 10 years at minimum

61
Q

describe rabies

A

acute infectious disease of mammals characterized by CNS irritation followed by paralysis and death
- virus carried in saliva of infected animals (dogs, raccoons, squirrels, cats, skunks)

62
Q

what does rabies cause

A

encephalomyelitis - neuro and muscular system inflammation

63
Q

s/s rabies

A

fever, pain, paralysis, convulsions, rage, mm spasms especially of swallowing (foaming at mouth), hydrophobia

64
Q

what is the incubation period of rabies

A

3-10 days

65
Q

tx rabies

A

immediately washing wound, anti-rabies injections before virus spreads to brain, confine and tx or destroy the biting animal

66
Q

prognosis rabies

A

can be fatal if untreated ASAP

67
Q

describe shingles (herpes zoster)

A

actue CNS infection involving DRG resulting in vesicular eruptions and severe pain along the cutaneous areas supplied by the nerve root

68
Q

etiology shingles (herpes zoster)

A

caused by varicella zoster - same as chickenpox may be dormant for years; may be activated by systemic diease or in persons receiving immunosuppressive therapy

69
Q

prevalence shingles (herpes zoster)

A

1/3 persons who had chickenpox, increased with age over 60

70
Q

s/s shingles (herpes zoster)

A

itching, sharp stabbing pain, red rash with pustules along the path of sensory N (dermatome) running toward midline (often trunk)

71
Q

tx shingles (herpes zoster)

A

anti-virals (acyclovir), analgesics, meds for itching, isolation precautions must be observed during active infection, vaccine for persons 50+

72
Q

describe ramsey-hunt

A

shingles virus affecting facial N (paralysis)
possible hearing loss (CN 8 - 7 and 8 pass through same foramen)

73
Q

prognosis shingles (herpes zoster)

A

may recur anytime immune system is depressed or stressed, may develop post-herpetic neuralgia

74
Q

describe brain abscess

A

space-occupying lesion of local infection with effects similar to a brain tumor

75
Q

what population does brain abscess affect

A

individuals with compromised immune system, persons with systemic illness (HIV)

76
Q

etiology brain abscess

A

bacteria, fungi, parasites, sinusitis, mastoiditis, infections from heart/lungs, cranial osteomyelitis (bone infections)

77
Q

presentation brain abscess

A

evolves over 1-14 days where capsule of necrotic tissue develops as a result of inflammatory process

78
Q

S/S brain abscess

A

may not have fever or increased WBC, HA, disturbed consciousness, nuchal rigidity, N/V, seizures, visual disturbances, dysarthria, hemiparesis, sepsis

79
Q

tx brain abscess

A

identification of mass via MRI, antibiotics, surgical drainage, or excisions of capsule, tx of other areas of infection

80
Q

outcomes brain abscess

A

50% will be left with some neurologic sequelae, mortality increases if there is hemorrhage

81
Q

describe prion disease

A

included a family of encephalopathies to include Creutzfeldt-jakob disease, kuru, and mad cow disease

82
Q

a protin that can replicate in the nervous system and results in neuronal cell death

A

prion

83
Q

etiology of prion disease

A

ingested from infected beed or protein products containing infected material (hormone therapy)

84
Q

tx prion disease

A

no known tx, sx management focus on

85
Q

clinical presentation/prognosis prion disease

A

abnormal movement, ataxia, progressive
usually fatal

PT 680 Clinical Medicine (18 decks)

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