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NUR 406 > Neuro: ALS, GBS, TIA, CVA, infectious disease > Flashcards

Neuro: ALS, GBS, TIA, CVA, infectious disease Flashcards

1
Q

Transient ischemic attack

A

Acute, focal cerebral insufficiency last < 24 hrs
Usually < 60 min.
No residual effects

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2
Q

TIA’s happen more often to males or females?

A

males

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3
Q

patients who have a TIA have an increased risk for stroke how long after?

A

highest risk of stroke within 1 month of TIA

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4
Q

TIA presentation

A

varies patient to patient but recurrent TIA’s usually similar.
symptoms are associated with location of defect.
follow a vascular line
carotid area vs. vertebrobasilar area

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5
Q

onset of TIA’s

A

onset & recovery abrupt

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6
Q

TIA: carotid area presentation

A

Weakness, heaviness in contralateral arm, leg or face
Numbness
Dysphagia
Ipsilateral monocular visual loss

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7
Q

TIA: vertebrobasilar area presentation

A

Dim or blurry vision
Vertigo
Dysphasia
Ataxia
Motor or sensory changes: Ipsilateral face, Contralateral body.

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8
Q

what does ipsilateral mean?

A

stays on the same side

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9
Q

what does contralateral mean?

A

crosses over the midline, opposite side of the body.

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10
Q

dysphagia

A

difficulty swallowing

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11
Q

dysphasia

A

impairment of speech

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12
Q

TIA: diagnostic

A

History and physical: Identify any pattern, history, Any vascular problems.
CT, MRI or MRA: Rule out hemorrhage, lacunar infarcts or aneurysms
Carotid doppler studies: Carotid stenosis
Echocardiogram: Assess for cardiac source

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13
Q

lacunar infarcts

A

tiny infarcts that don’t present with symptoms but can be soon scan

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14
Q

TIA: treatment

A

Depends upon etiology
Anticoagulation: ASA- No benefit of high dose (up to 1500 mg/day) over lower dose (75-325 mg/day); clopidogrel (Plavix)- Antiplatelet drug; Heparin and warfarin if cardiac related.
Carotid endarterectomy with > 70% stenosis

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15
Q

ALS: definition

A

A rare, progressive neuro disorder characterized by the loss of motor neurons; Upper and lower motor neurons

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16
Q

ALS: etiology

A

unknown

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17
Q

ALS: RF

A

Age: 40-70; Gender: Male; Genetics (10%); Smoking

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18
Q

ALS: prognosis

A

Death usually occurs around 3 years after diagnosis

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19
Q

ALS: patho

A

Motor neurons in the brainstem and spinal cord gradually degenerate
Electrical and chemical messages from the brain do not reach the muscles

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20
Q

ALS: CM

A

Weakness of upper extremities (sometimes begins in the legs), Muscle wasting, Spasticity
Dysarthria, dysphagia, drooling
Cognitive and behavioral changes
Constipation
Sleep problems
Breathing

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21
Q

Discuss the excitotoxicity hypothesis of ALS development and the role of glutamate

A

Excessive levels of glutamate initiate a cascade of events that lead to neuron death
Glutamate = excitatory neurotransmitter
Why do we think this plays a role? Elevated glutamate levels in the CSF, Antiglutaminergic drug (Riluzole) improves survival.

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22
Q

Riluzole (Rilutek)

A

Classification: Glutamate inhibitor
MOA: Glutamate antagonist; Reduces damage to motor neurons
Indication: ALS
SE: dizziness, GI upset, hepatotoxicity
Effect on life expectancy? Increases life expectancy & slows down deterioration.

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23
Q

GBS: definition

A

Autoimmune disorder, Myelin sheath is damaged by autoantibodies

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24
Q

GBS: etiology

A

Viral infection
Bacterial infection: Campylobacter jejuni
Post Surgery (5-10%)

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25
Q

GBS: onset

A

days to weeks following a viral infection

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26
Q

GBS: CM

A

Initially: Weakness/tingling in lower extremities
Ascend to descend pattern
Severity of symptoms increases over hours or weeks
Potentially life-threatening if respiratory muscles are involved
Uncoordinated movements
Numbness and decreased sensation
Loss of bowel/bladder control
Blurred vision- can be an early sign.
Difficulty, breathing, swallowing, chewing

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27
Q

GBS: prognosis

A

95% survive
75% completely recover
25-30% have residual weakness after 3 years
About 3% may suffer relapse of muscle weakness & tingling many years post initial attack

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28
Q

is there a cure for GBS?

A

no

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29
Q

Describe the basic drug therapies of GBS

A

Steroid therapy
High-dose immunoglobulin therapy (IV): Shortens severity & duration, Shortens length of stay

30
Q

GBS: goal of treatment

A

Reduce severity and accelerate recovery

31
Q

meningitis: definition

A

Acute inflammation of the meningeal tissues of the brain and spinal cord

32
Q

meningitis: Etiology

A

Infection (lungs or bloodstream) or penetrating wounds

33
Q

meningitis: main culprits

A

Streptococcus pneumoniae and Neisseria meningitidis (bacterial), Enteroviruses (viral)

34
Q

meningitis: where does it occur?

A

Pia mater, subarachnoid space, ventricular system, CSF

35
Q

meningitis: when does it occur?

A

Fall or winter

36
Q

meningitis: What does it usually follow?

A

Otitis or sinusitis or those with an immunocompromised state or PNA

37
Q

meningitis: age

A

Older adults (>40yrs)
College students
Prisoners

38
Q

meningitis: patho

A

Infection of arachnoid mater and CSF
Inflammatory response and pus secretion
Increase in CSF production
Increase in ICP

39
Q

meningitis: classic triad

A

fever, headache, stiff neck

40
Q

meningitis: other CM

A

Nausea/vomiting
Photophobia
Altered mental status: Drowsiness → Coma, Seizures (30%)
Meningococcus: Skin rash, Petechiae
Positive Kernig sign: Resistance to leg extension
Positive Brudzinski sign: Neck flexion causes hip/knee flexion

41
Q

Acute Bacterial Meningitis

A

Most common form
Fatality rate? High, can kill within hours
Long term effects? Hearing loss, seizures, damage to brain

42
Q

Acute Viral Meningitis

A

Milder form, often do not see elevated WBS with lumbar puncture when looking at CSF.
Long term effects? None

43
Q

Bacterial Meningitis: Treatment

A

Aggressive Antibiotic Therapy: IV, often multiple drugs used, ceftriaxone (Rocephin); Vancomycin, Acyclovir.
Steroid Therapy
Prophylaxis: Vaccines- Available for Meningococcus, pneumococcus, H. influenzae

44
Q

encephalitis: definiton

A

acute inflammation of the brain

45
Q

encephalitis: etiology

A

viral
West Nile encephalitis (mosquitoes)
Measles, chicken pox, mumps
Herpes simplex virus-1 (HSV)

46
Q

encephalitis: CM

A

Signs appear on day 2 or 3 of infection
Range from mild changes in mental status to coma
Other symptoms: Fever, Headache, N/V, Other CNS changes (such as seizures)

47
Q

encephalitis: pharmocology

A

Viral infection: Acyclovir (Zovira) is used for HSV infection, Reduces mortality, Does not reduce neurological complications
Seizure disorders: Antiseizure medications.

48
Q

Brain abscess: definition

A

accumulation of pus within the brain tissue

49
Q

Brain abscess: etiology

A

Local or systemic infection
Most common = from ear, tooth, mastoid, or sinus infection

50
Q

Brain abscess: major culprits

A

Streptococci or staphylococcus aureus

51
Q

Brain abscess: CM

A

Similar to those of meningitis and encephalitis: Headache, Fever, N/V
Signs of ICP: Drowsiness, confusion, seizures
Focal symptoms may reflect area of abscess: Example: temporal lobe = visual field defects

52
Q

CVA: major risk factors

A

Hypertension
Hyperlipidemia: High cholesterol
Tobacco abuse
Diabetes
Race- African Americans
Oral contraceptives
Age*- advances age
Gender- men
Sickle cell anemia
History of TIA
Atrial fibrillation

53
Q

CVA: CM

A

Numbness or weakness on one side of body (face, arm, or leg)
Sudden confusion
Trouble speaking
Slurred speech (dysarthria)
Trouble seeing
Ataxia
Severe headache

54
Q

Which type of ICH would be evident when doing a lumbar puncture?

A

Subarachnoid hemorrhage
Most sensitive for detecting a subarachnoid hemorrhage 12 hours after onset of symptoms.

55
Q

Why would a CT scan be a better option for an initial test than an MRI?

A

A CT scan can show if there is a hemorrhage and drives treatment.
MRI’s take longer than a CT, remember time is tissue.

56
Q

Alteplase (tPA)

A

Class: thrombolytic
MOA: Promotes conversion of plasminogen to plasmin.
SE: Increased risk of intracranial bleeding.
Indication: Acute MI, PE, ischemic stroke
Antidote: aminocaproic acid (amicar)- anti-thrombolytic

57
Q

causes of thrombotic ischemic stroke?

A

atherosclerosis
hypercoagulable state

58
Q

causes of embolic ischemic stroke?

A

Cardiac source
*Mural thrombus
*Atrial fibrillation: Left atrial thrombus, Inability of atria to contract effectively, Blood can become stagnant
*Venous clot if atrial septal defect or patent foramen ovale
*Thrombus of vegetation of valves: Mitral valve vegetation, frequently infectious in nature
Carotid plaque: Carotid bruit

59
Q

Hemorrhagic stroke

A

Bleeding within the brain parenchyma
Associated with long standing, severe hypertension
38% mortality: Minutes to hours
Aneurysm: Bulging of blood vessel

60
Q

Hemorrhagic stroke: presentation

A

*Age 30 – 60 years
*High morbidity and mortality rates
*Serious disabilities
*“Worst headache of my life”- Hemorrhagic stroke
*Rapid change in level of consciousness (LOC)
*Irritation of the meninges: Nuchal rigidity: Similar to meningitis, Photophobia

61
Q

Hemorrhagic stroke: prognosis

A

Based on Age, Location and size, & How rapid the bleed causes brain distortion and shift on scan

62
Q

Epidural intracranial hemorrhage (ICH).

A

between skull and dura
Skull fractures
Arterial
Injury is usually less severe

63
Q

subdural intracranial hemorrhage (ICH).

A

below the dura
Bridging veins
Brain moves within skull, vessels don’t
Rapid decline – severe injury
Can be slow: 2-10 days later

64
Q

subarachnoid intracranial hemorrhage (ICH).

A

Space between outer arachnoid membrane and pia mater
Area filled with cerebral spinal fluid (CSF)
Rupture of: Cerebral aneurysm, Arterio-venous malformation (AVM)

65
Q

what is the most common aneurysm that can rupture in the brain?

A

berry aneurysms.

66
Q

Arterio-venous malformation (AVM)

A

blood flow is flowing directly from an artery to a vein without slowing down through the capillaries.
the high pressures weaken the vessel walls that may lead to rupture.

67
Q

penumbra procedure

A

go in and try to remove the clots

68
Q

what are the visuals disturbances that can happen as a consequence of a CVA?

A

contralateral field blindness
homonymous hemianopia

69
Q

aphasia

A

some degree of inability to speak or to comprehend

70
Q

Expressive aphasia

A

comprehension intact but cannot express

71
Q

Receptive aphasia

A

can communicate but cannot comprehend what is being said ”can’t receive”

72
Q

Dysarthria

A

imperfect speech sounds

NUR 406 (7 decks)

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