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Pathophysiology > Module 9: Nervous System > Flashcards

Module 9: Nervous System Flashcards

1
Q

This restricts the entry of pathogens into the brain and meninges

Hematogenous spread of organisms
requires spread through at least 2
layers to infect the brain

A

Blood Brain Barrier

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2
Q

3 Hematogenous Spread (Bloodborne Invasion) into the CNS?

A

Growing across (Microbes can grow in the endothelial cells)

Passive (Transported across in intracellular vacuoles)

Carried in infected cells (Infected inflammatory cells)

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3
Q

This virus may invade Muscle Cells at the Bite Site > Move up the Nerves to the Dorsal Root Ganglia > Spinal Cord > Brain

A

Rabies and other Lyssaviruses

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4
Q

This virus may migrate up the nerves
using normal retrograde transport
mechanisms

A

Herpes viruses

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5
Q

Inflammation of the Meninges of the brain due to viral etiology.
- (Eg. By Herpes Simplex Virus)

A

Viral Meningitis

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6
Q

Inflammation of the Meninges of the Brain
due to Bacterial Etiology.
- (Typically: Neisseria Meningitidis,
Streptococcus Pneumoniae, Hemophilus
Influenzae

A

Bacterial Meningitis

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7
Q

Inflammation of the Brain
- (Typically due to Viruses – eg. Herpes
Simplex)

A

Encephalitis

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8
Q

Inflammation of the Brain & the Meninges

A

Meningoencephalitis

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9
Q

Inflammation of the Spinal Cord > Disrupts
CNS functions liking the brain & limbs.
- Eg. Poliovirus (Poliomyelitis)

A

Myelitis

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10
Q

Inflammation of the Brain and Spinal Cord
- Typically Immune-mediated following a viral
infection.
- (Eg. Acute Disseminated Encephalomyelitis
– Following Influenza, enterovirus, measles,
mumps, rubella, varicella zoster, etc.)

A

Encephalomyelitis

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11
Q

Encapsulated Pus or Free-Pus in the Brain after an Acute Focal Purulent Infection.
- (Focal Infections include: Otitis Media/Sinusitis)

A

Brain Abscesses

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12
Q

Presentation: Meningism:
- *Neck Stiffness
- *Photophobia
- *Headache
- (Fever/Malaise)

A

MENINGITIS

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13
Q

How many Samples are taken for CSF Examination? And what types?

A

3 (Serology, Biochemistry, Bacteriology)

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14
Q

What type of bacteria can cause Bacterial Meningitis?

Description:
- Gram Negative Diplococci
- Usually in Stressed/Crowded
- Severe toxin sequalae > Tissue damage
- Vaccine only for Serotypes A & C (Not B –
Which is the most common)
- Immune System has to Start Again because of Immunogenicity of its capsule

A

Neisseria Meningitidis

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15
Q

What type of bacteria can cause Bacterial Meningitis?

Description:
- Gram Negative Cocco-bacilli
- Usually in Children / Babies
- Toxin production > Tissue damage
- Vaccine Available (Hib Vaccine)

A

Hemophilus Influenza

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16
Q

What type of bacteria can cause Bacterial Meningitis?

Description:
- Gram Positive Cocci
- Predisposed Adults
- Neonates

A

Streptococcus Pneumoniae

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17
Q

Other Etiologies: Type of Meningitis?
- Escherichia coli
- Group B Streptococci
- High Mortality Rates (35% of cases)

A

Neonatal Meningitis

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18
Q

Other Etiologies: Type of Meningitis?
- Mycobacterium tuberculosis
- Acid fast bacilli (Stains with Ziehl Neelsen
stain)
- Patients Typically have a Focus of Infection
Elsewhere

Most of cases are associated with Miliary
(disseminated) Tuberculosis

A

Tuberculous Meningitis

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19
Q

Features Suggestive of etiology of Meningitis:

erythematous, petechial / purpuric.
Suggests meningococcus (rarely Pneumococcus or Hemophilus influenzae type b)

A

Rash

20
Q

Features Suggestive of etiology of Meningitis:

Basal skull fracture
a. Pneumococcus, H. influenzae, Hemolytic
Strep.
b. (CSF Rhinorrhea refers to the drainage of
Cerebrospinal Fluid through the nose. It is a
sign of Basal Skull Fracture)

A

CSF rhinorrhea or otorrhea

21
Q

Mainly Cryptococcus Neoformans
- Typically in Immunosuppressed
- Can be treated with antifungal drugs

A

Fungal Meningitis

22
Q

Less Severe than Bacterial
- More Common than bacterial.

(HSV, Mumps, Poliovirus, Enterovirus 71, Japanese encephalitis, HIV)

A

Viral Meningitis

23
Q

What virus that causes inflammation to the brain?

The infection progresses back to the
temporal lobe of the brain. 70% mortality rate in untreated patients

  • Treatment with Acyclovir > ↓Mortality rate
A

Herpes Simplex Virus

24
Q

Clinical Feature: Paralysis may extend from a single muscle to virtually every skeletal muscle
- There may be involvement of respiratory
muscles > Lifelong Assisted Ventilation

A

Poliovirus (Encephalitis)

25
Q

Advantages:
- Easy Administration - Given Orally
- Cheap
- Induces intestinal local immunity
- More Robust Immune Response

Disadvantage:
- Rarely causes paralysis (1 in 2.5million)

A

Live Attenuated (Oral Polio Vaccine)

26
Q

Advantages:
- Carries NO risk of Vaccine-Associated Polio
Paralysis
- Very Robust Immune Response

Disadvantage:
- Difficult Administration - Has to be injected
- Confers little Mucosal Immunity in the
Intestinal Tract.
- 5 Times more expensive than OPV

A

Inactivated Polio Vaccine (IPV)

27
Q

Organism:
- Rhabdovirus (A Bat Virus)

Transmission:
- by the bite of an infected animal
- The virus is present in the saliva of the
infected animal (Dogs, foxes and other wild
species)

A

Rabies Encephalitis

28
Q

Sites of Focal Infection that could lead to
this infection?
o Otitis Media
o Sinusitis
o Penetrating trauma
o Hematogenous dissemination

A

BRAIN ABSCESS

29
Q

Etiology:
- Alcohol Abuse > Vit B1[Thiamine] Deficiency

Clinical Features:
- Cortical Atrophy > Impaired Memory
(Anterograde & Retrograde) + Confabulation
- Mamillary Body Damage > Vision Changes,
Nystagmus, Unequal Pupils Cerebellar
Atrophy > Ataxia

A

WERNICKES-KORSAKOFF SYNDROME
(Alcoholic Encephalopathy)

30
Q

Global Degeneration Dementias
- (Age-Related (Senile) Dementia
- Alzheimer’s
- Lewy-Body Dementia
- Fronto-Temporal Dementia/Pick’s Disease

A

DEGENERATIVE DISEASES

31
Q

Acquired Global Impairment of Intellect, but with no ALOC.

Epidemiology:
o 5% of >55yrs are demented
o 20% of >80yrs are demented
o Prevalence Doubles every 5yrs beyond Age:60.
o 50% of dementia pts have clinically significant
behavioral/psychological symptoms

A

Dementia

32
Q

Etiology: Old Age

Macro:
- Cortical atrophy
- Enlarging ventricles (Compensatory
hydrocephalus)
- Thickening of Leptomeninges (Pia Mater &
Arachnoid Mater) (The “Thin” Meninges)

Clinical Features:
- Dementia: All Spheres of Intellect affected

A

AGE-RELATED (SENILE) DEMENTIA

33
Q

Most common cause of dementia

Etiology:
- Exact etiology Unknown
- Genetic & Environmental Components
- (Inevitable in Down-Syndromes)

Pathogenesis:
- Excess β-Amyloid Protein Formation (A
Degradation product of Amyloid Precursors)

Early Signs: (Neuronal Atrophy Starts in the
Hippocampus)
Memory Loss is : the First Sign

Progressive Signs: (Neuronal Atrophy Progresses to the Cortex)

A

ALZHEIMERS DISEASE

34
Q

β-Amyloid Protein Deposition around Neurons

A

Neuritic Plaques

35
Q

β-Amyloid Protein Deposition in Blood Vessels

A

Amyloid Angiopathy

36
Q

What clinical feature of Alzheimer’s?
§ Increased Memory Loss
§ Confusion, Apathy, Anxiety
§ Difficulty Handling Money

A

Mild Cortical Atrophy

37
Q

What clinical feature of Alzheimer’s?
§ Difficulty Recognizing People
§ Difficulty with Language
§ Wandering & Disorientation

A

Moderate Cortical Atrophy

38
Q

What clinical feature of Alzheimer’s?
§ Seizures, Incontinence
§ Groaning/Moaning/Grunting

A

Late Signs: (Extreme Global Cortical
Atrophy)

39
Q

Treatment of Alzheimer’s Disease?
CLUE: AEI

A

Acetylcholine-Esterase Inhibitors

40
Q

A clinical syndrome characterized by sudden
onset of a focal neurological deficit
presumed to be on a vascular basis; avoid
‘CVA’ (‘confused vascular assessment’)

A

STROKE

41
Q

(80%) Results from focal ischemia leading to cerebral infarction. Mechanisms include embolism from heart or proximal arteries, small vessel thrombosis, or hemodynamic from a drop in
the local perfusion pressure. Global ischemia (e.g. from cardiac arrest or hypotension) causes a diffuse encephalopathy.

A

Ischemic Stroke

42
Q

(20%) Abrupt onset with focal neurological deficits, due to spontaneous (non-traumatic) bleeding into the brain. When blood vessels in the brain ruptures causing bleeding and damage to surrounding tissues.

A

Hemorrhagic Stroke

43
Q

STROKE TERMINOLOGY: Amaurosis Fugax, Transient Monocular Blindness (TMB). Due to episodic retinal ischemia, usually associated with ipsilateral carotid artery stenosis or embolism of the retinal arteries resulting in a
sudden, and frequently complete, transient loss of vision in one eye

A

Transient Ischemic Attack (TIA)

44
Q

STROKE TERMINOLOGY: Stroke syndrome with a persisting neurological deficit suggesting cerebral infarction; the ensuing neurological defect can last days, weeks, or permanently; even after maximal recovery, at least minimal neurological difficulties often remain.

A

Completed Stroke (CS)

45
Q

STROKE TERMINOLOGY: Neurological deficits begin in a focal or restricted distribution but over the ensuing hours spread gradually in a pattern reflecting involvement of more and more of the particular vascular territory.

A

Progressing Stroke (Stroke In Evolution)

46
Q

inadequate perfusion of brain due to
* an embolus from an atherosclerotic plaque in a large vessel (artery to artery embolus) (most
common)
* a large vessel thrombosis with low distal flow

A

Atherosclerotic Plaque

Pathophysiology (7 decks)

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