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

Infectious Pathologies of the CNS Flashcards

(85 cards)

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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
describe mortality rate and recovery of encephalitis
high mortality rate 10-50% recovery (depends on pathogen)
26
what is meningitis
inflammation of meninges of brain and spinal cord; some forms can be contagious
27
etiology meningitis
bacteria, virus, fungus, toxins
28
meningitis pathogens attack what areas
inner ear, sinus or URI
29
sudden onset of s/s of meningitis
high fever, HA, photophobia, nucal rigidity (neck stiffness), drowsiness, stupor, seizures
30
dx meningitis
lumbar puncture, Kernig's sign, brudsinski's sign
31
test that stretches the meninges and will cause severe pain
kernig's sign
32
tx meningitis
vaccines for bacterial, meds, quiet dark environment
33
prognosis meningitis
- bacterial: MEDICAL EMERGENCY - can be fatal in infants and elderly - viral - has to run its course
34
what is the hallmark sign of meningitis
nucal rigidity (neck stiffness)
35
describe kernig's test
- 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
describe brudzinksi's test
flexion of neck causes of hips and knees while pt is supine - this occurs bc the pain has pain with neck flexion
37
what is poliomyelitis
viral infection affecting LMN's in brainstem and spinal cord
38
how does poliomyelitis enter the body
through mouth and nose (PNS disorder)
39
list the 3 infection mechanisms for poliomyelitis
- asymptomatic (carrier) - symptomatic - flu-like - symptomatic with paralysis (due to virus entering anterior horn cells)
40
s/s poliomyelitis
mm weakness of UE/LE, neck stiffness, mm atrophy, N&V, respiratory system due to paralysis
41
dx poliomyelitis
by culture
42
tx poliomyelitis
braces, respiratory support (ie. iron lung)
43
describe post-polio syndrome
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
describe zika virus and how is it transmitted
- single strand of RNA virus - transmitted: mosquito bite, also spread mother to baby, sex, blood transfussion
45
what % of people infected with zika virus are asymptomatic
80%
46
s/s zika virus if symptomatic
fever, HA, joint pain, mild rash
47
what does zika virus cause in fetus/unborn child and why
microcephaly - causes apoptosis and inhibition of neural cell differentiation leading to cortical thinning and microcephaly
48
tx zika virus
no cure tx is mosquito eradication recommended safe sex (M 6mo, W 2mo) post traveling to area of high zika transmission
49
describe botulism
neuromuscular poisoning resulting from bacteria invasion by clostridium botulinum - neurotoxin (neuromuscular poison) interferes with releease of acetylcholine at peripheral N endings
50
etiology botulism
- 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
s/s botulism
double vision, blurred vision, droopy eyelids, slurred speech, difficulty swallowing, dry mouth, respiratory decline, progressive muscle weakness starting at shoulders
52
mortality rate botulism
60-70% if not treated immediately
53
tx botulism
- 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
describe tetanus
acute infectious disease characterized by convlusions and intermittent spasms of voluntary muscles - bacterial infection - clostridium tetani found in soil and animal feces
55
what does tetanus produce that effects skeletal muscles and blocks release of inhibitory neurotransmitters
toxin - tetanospasmin
56
transmission tetanus
acquired from open wound infection (rusty nail, tin can lid, barbed wire)
57
s/s tetanus
contractions of muscles of mastication (lock-jaw), general muscle spasms
58
tx tetanus
life supporting procedures, wound debridement, penicillin and tetracycline
59
outcomes of tetanus
fatal due to paralysis of respiratory muscles if not treated
60
preventative tx tetanus
keep up with shots, need booster every 10 years at minimum
61
describe rabies
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
what does rabies cause
encephalomyelitis - neuro and muscular system inflammation
63
s/s rabies
fever, pain, paralysis, convulsions, rage, mm spasms especially of swallowing (foaming at mouth), hydrophobia
64
what is the incubation period of rabies
3-10 days
65
tx rabies
immediately washing wound, anti-rabies injections before virus spreads to brain, confine and tx or destroy the biting animal
66
prognosis rabies
can be fatal if untreated ASAP
67
describe shingles (herpes zoster)
actue CNS infection involving DRG resulting in vesicular eruptions and severe pain along the cutaneous areas supplied by the nerve root
68
etiology shingles (herpes zoster)
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
prevalence shingles (herpes zoster)
1/3 persons who had chickenpox, increased with age over 60
70
s/s shingles (herpes zoster)
itching, sharp stabbing pain, red rash with pustules along the path of sensory N (dermatome) running toward midline (often trunk)
71
tx shingles (herpes zoster)
anti-virals (acyclovir), analgesics, meds for itching, isolation precautions must be observed during active infection, vaccine for persons 50+
72
describe ramsey-hunt
shingles virus affecting facial N (paralysis) possible hearing loss (CN 8 - 7 and 8 pass through same foramen)
73
prognosis shingles (herpes zoster)
may recur anytime immune system is depressed or stressed, may develop post-herpetic neuralgia
74
describe brain abscess
space-occupying lesion of local infection with effects similar to a brain tumor
75
what population does brain abscess affect
individuals with compromised immune system, persons with systemic illness (HIV)
76
etiology brain abscess
bacteria, fungi, parasites, sinusitis, mastoiditis, infections from heart/lungs, cranial osteomyelitis (bone infections)
77
presentation brain abscess
evolves over 1-14 days where capsule of necrotic tissue develops as a result of inflammatory process
78
S/S brain abscess
may not have fever or increased WBC, HA, disturbed consciousness, nuchal rigidity, N/V, seizures, visual disturbances, dysarthria, hemiparesis, sepsis
79
tx brain abscess
identification of mass via MRI, antibiotics, surgical drainage, or excisions of capsule, tx of other areas of infection
80
outcomes brain abscess
50% will be left with some neurologic sequelae, mortality increases if there is hemorrhage
81
describe prion disease
included a family of encephalopathies to include Creutzfeldt-jakob disease, kuru, and mad cow disease
82
a protin that can replicate in the nervous system and results in neuronal cell death
prion
83
etiology of prion disease
ingested from infected beed or protein products containing infected material (hormone therapy)
84
tx prion disease
no known tx, sx management focus on
85
clinical presentation/prognosis prion disease
abnormal movement, ataxia, progressive usually fatal

PT 680 Clinical Medicine (18 decks)

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