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6010 Advanced Patho Test 6 COMPLETE ☑️ > Module 12: Neuro Disorders Adult (b) > Flashcards

Module 12: Neuro Disorders Adult (b) Flashcards

1
Q

Seizures

-Description

A
  1. Sudden, Transient alteration in brain electrical function caused by an abrupt, explosive and excessive discharge of cerebral neurons
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2
Q

Seizures

-Causes

A
  1. Hypoglycemia
  2. Water intoxication — Hyponatremia
  3. Alcohol intoxication
  4. Fever
  5. Stress
  6. Cerebral lesions
  7. Biochemical disorders
  8. Trauma
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3
Q

Seizure Classification

-Types of Seizures

A
  1. Generalized Seizures — Originate in both sides of the brain simultaneously — arises from deeper subcortical region of the brain
  2. Focal (partial Seizures — Originate from ONE area of the brain — Seizure activity is limited to one hemisphere
    —Seizure can manifest as motor or non-motor
  3. Status Epilepticus — Seizure phase lasts longer than 5 minutes — Prolonged or recurrent seizure before fully regaining consciousness
    —Needs Emergency intervention
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4
Q

Seizures

-Phases of Clinical Manifestation

A
  1. Pre-Ictal — Prodrome present — Ex: Some symptom like confusion or anxiety that indicates imminent seizure — Focal Auras
  2. Ictal — Ictus phase is when you have TONIC-CLONIC activity and is the ACTUAL seizure
    - TONIC PHASE - Occurs as result of exitation of the subcortical, THALMUS, and brainstem area
    - CLONIC PHASE - Occurs when seizure d/c is interrupted resulting in alternating contraction and relaxation of muscles
  3. Postictal — manifest in a long deep sleep, headache, confusion, memory loss or aphasia
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5
Q

Seizure Consequences

A
  1. 250% increase in ATP consumption during seizure
  2. 60% increase oxygen consumption
  3. 250% increase in cerebral blood flow
  4. Available glucose and oxygen are depleted
  5. Increase lactate in the brain leading to cellular exhaustion and destruction
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6
Q

Delirium

-Patho

A
  1. ACUTE confused states are transient states of confusion or awareness
  2. Typically acute w/ an abrupt onset but can be gradual or insidious in onset which can be caused by some type of toxin exposure.
  3. Causes
    - Drug intoxication; alcohol or drug withdrawal; electrolyte imbalance; neuro dz or trauma; heart, liver or kidney failure; febrile illness; Post-anesthesia
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7
Q

Delirium

-Clinical Manifestation

A
  1. Difficulty Focusing
  2. Restlessness or irritability
  3. Highly distraught
  4. Incoherent
  5. Delirium usually resolves w/in a few days of onset **
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8
Q

Dementia

-Patho

A
  1. Dementia is the progressive failure of cerebral and cognitive functions not caused by an imported level of consciousness, like a TBI
  2. Results in nerve cell degeneration and brain atrophy
  3. Typically there is a slow reduction in cognitive function and its usually insidious
  4. There are some potentially reversible causes of dementia including
    - Infections caused by meningitis, encephalitis, or neurosyphilis; Vit B deficiencies, ETOH, sedatives.
    - Rule out the above causes when evaluating pt w/ dementia
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9
Q

Dementia

-Permanent Causes

A
  1. Alzheimer’s
  2. Lewy body dementia
  3. Vascular Dementia

CLinical Manifestation
-Loss of recent and remote memory **

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10
Q

Dementia

-Creutzfeldt-Jakob

A
  1. NON-Reversible Neurologic disorder w/ abnormalities of gait, speech, and dementia.
    - Caused by PRIONS, which are infectious particles of nucleic acid
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11
Q

Alzheimer’s

-Info

A
  1. Alzheimer’s is thought to have a genetic component regardless of subtype
    - Familial AD — Autosomal dominant gene mutation that affects amyloid processing and clearance
    - Non-Hereditary AD — Sporadic and generally late onset
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12
Q

Alzheimer’s

-Patho

A
  1. Patho is altered beta amyloid processing and the development of neurotoxic fragments in plaques and tangles
  2. Results in loss of neurons causing BRAIN ATROPHY
  3. As deep groves for in cerebral cortex, there is a loss in synapses and acetylcholine — Resulting in memory loss
    - LONG prodromal dz before manifestations of AD are obvious
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13
Q

Parkinson’s

-Info

A

Primary and secondary Causes

  1. Primary Causes — Mostly idiopathic; 10% has familial association
  2. Secondary Causes
    - Repeated head trauma
    - Huntington’s disease
    - Fragile X syndrome
    - Neurosyphilis
    - Toxin exposure
    - MS
    - Huge variety of other neurodegenerativa diseases
    - Drug induced causes are usually reversible
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14
Q

Parkinson’s Disease

-Patho

A
  1. Results from degeneration of the pigmented dopaminergic neurons that are found in the SUBSTANTIA NIGRA
  2. Loss of pigmented neurons in the substantia nigra which secrete dopamine, results in dopamine deficiency
  3. Lewy bodies and amyloid plaques have been found in the brain of Parkinson’s sufferers so there is clearly some type of patho similarity to Alzheimer’s
  4. There is also general loss of basal ganglia, which are a group of structures near the thalamus that coordinate movement
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15
Q

Parkinson’s

-Clinical Manifestations

A
  1. Can start on one side of the body and progress
  2. Tremor is often the first symptom
  3. Symptoms include
    - Rigidity of movement
    - Loss of facial expression
    - Propulsive gait
    - Absent arm swing
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16
Q

Amyotrophic Lateral Sclerosis

-Info

A
  1. Results in progressive muscle weakness — Motor neuron degenerative disorder of upper and lower motor neurons
    - Causes progressive weakness, Respiratory failure and death
    - Normal intellectual and cognitive function
  2. 3-5 year life expectancy
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17
Q

Brain Trauma

-Risk factors

A
  1. 6 months to 2 years
  2. School-age children
  3. Adolescents and young adults 15-35 yrs
  4. Increase in people over 70 yrs
  5. Men are 1.5 x as likely to sustain TBI
  6. Falls are the #1 cause of brain injury
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18
Q

Brain Trauma

-Primary and Secondary

A
  1. Primary head trauma is result of direct focal hit to the skull causing injury
  2. Secondary brain injury is an indirect injury often a result of a CVA, ischemia, hemorrhage, oxidative stress or inflammation
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19
Q

Brain Trauma

-Classification of Severity

A
  1. Mild — Momentary LOC — No MRI findings — N/V, HAs, confusion/disorientation
  2. Moderate — LOC for 30 minutes or more — Retrograde amnesia for 24 hrs — may have skull fracture — memory and attention deficits
  3. Severe — HALLMARK of severe brain injury is LOC for 6 hrs or more. — associated with Brainstem signs
20
Q

Types of Head Trauma

A
  1. Blunt — Focal injury and Diffuse injury to the axon
  2. Penetrating
  3. Focal — Localized to site of impact; scalp lac; skull fracture; contusions; hemorrhage
  4. Polar —Coup Counrecoup — Brain bounces off skull — Ex: Car accident
  5. Chronic Traumatic Encephalopathy CTE — Football players, military, trauma survivors
21
Q

Epidural Hematoma

-Info

A
  1. Bleeding between dura and skull
  2. Always ARTERIAL BLEEDS — DANGEROUS
  3. Process is — period of unconscious followed be a period of lucidity then return to unconscious
  4. S/Sx’s
    - Drowsiness, seizure, confusion, headache, vomiting
22
Q

Subdural Hematoma

A
  1. Bleeding between dura mater and brain
  2. Can be acute and develops w/in hours of injury or subacute and develop over 48 hrs to 2 weeks
  3. About 50% associated with skull fractures
  4. Can occur with falls in older adults
  5. In acute and subacute, the tearing of bridging veins that extend from the dura to the brain surface is the major cause of hematoma**
  6. Clinical manifestations
    - Unconscious
    - Respiratory depression
    - Focal motor dysfunction
    - Pupillary dilation
23
Q

Intracerebral Hematoma

A
  1. Bleeding that most often takes place in the frontal and temporal lobes
  2. Caused by penetrating force or a shearing force that injures small blood vessels — also caused by hemorrhagic strokes
  3. Clinical manifestations include
    - Increased ICP
    - Decreased LOC or coma
    - Positive babinski reflexes
    - Changes in breathing
    - Temporal lobe Herniation
24
Q

Spinal Cord Injury

-Info

A
  1. Can be result of shearing, compression or penetrating trauma
  2. Secondary spinal cord injury occurs after the initial trauma
    - Combination of vascular, cellular, and biochemical events that result in edema, ischemia, excessive stimulation by neurotransmitters, inflammation, oxidative damage, and cell death
25
Q

Spinal Cord Injury

-Transient Vs. Permanent Loss of function & Sensation

A
  1. Depends on level and extent of injury
  2. After an acute injury you might have sudden loss of voluntary movements, sensation and spinal/autonomic reflexes below injury
  3. Reflexes usually return in a few weeks
26
Q

Spinal Cord Injury

-Spinal Shock

A
  1. Occurs IMMEDIATELY s/p injury d/t continuous loss of impulses to the brain below area of spine injury
  2. S/Sx’s:
    - All motor and sensory functions below the area of injury may cease, temporarily
    - Bladder function, thermal control and circulation are impacted
    - May last days to weeks and when it passes, reflex activity may return
27
Q

Spinal Cord Injury

-Neurogenic Shock

A
  1. Occurs w/ Cervical or thoracic injury
  2. Loss of sympathetic outflow that results in unopposed parasympathetic input mediated by vagus nerve

S/Sx’s include:

  • Vasodilation
  • Hypotension
  • Hypothermia
  • Bradycardia
28
Q

Spinal Cord Injury

-Autonomic Hyperreflexia

A
  1. This may follow after spinal shock — Injury above T5-T6
  2. Reflex sympathetic discharge w/ uncompensated cardiac response
    - The unopposed sympathetic response causes diffuse vasoconstriction
    - Raises BP
    - Diaphoresis, blurred vision, severe HA
  3. Essentially there is vasoconstriction below level of injury and vasodilation above the level of injury

S/Sx’s

  • Paroxysmal HTN
  • Pounding headache
  • Blurred vision
  • Bradycardia
29
Q

Spondylosis

A
  1. The pars auricular is of the vertebral arch has degeneration and over time can have micro fractures
30
Q

Spondylolisthesis

A
  1. Spondylolisthesis occurs when there is a shift forward of vertebrae (stress Fx and sliding of vertebra)
31
Q

Spinal Stenosis

A
  1. Spinal stenosis is a narrowing of the spinal canal and is something that should always be in your differential list when considering someone who has leg pain w/ movement
32
Q

Disk Degeneration & Herniation

A
  1. DDD is common in people over 30 yrs — 1/2 of adults have some compression — normal part of aging
  2. As nucleus palposus loses water and buoyancy, disk spaces narrow
    - Result can be shrinkage of the nucleus palposus, disk protrusion, tear of the annulus and Herniation of the disk contents outside the disk space
33
Q

Radiculopathy

A
  1. Herniation or pressure on the spinal cord from the disk
  2. This can result in nerve pain or Radiculopathy
  3. Pain is exacerbated by coughing sneezing or raising the leg
34
Q

Radiculopathy

-Complications

A
  1. Most emergency consequence of nerve compression is CAUDA EQUINA or SADDLE ANESTHESIA.
  2. Can result in neurogenic bladder, absent reflexes and numbness
35
Q

Ischemic Stroke

A
  1. Ischemic Strokes — inadequate blood supply that results in inadequate cell oxygen and death of tissue
  2. Thrombotic Strokes — atrial occlusion by a thrombus that is formed in the brain or intracranial vessels
    —Can be from Atherosclerosis or stenosis
  3. Embolic stroke — fragments break from a thrombus formed outside the brain —Ex: A fib, fat or air emboli
36
Q

Hemorrhagic Stroke

A
  1. Result of spontaneous bleeding in the brain — Less common
  2. Risk factor - Long-standing HTN; ruptured aneurysm
37
Q

Intracranial Aneurysm

A
  1. Can result from:
    - arteriosclerosis; congenital; trauma; vascular wall stress
  2. Can cause remodeling, thickening and angiogenesis
38
Q

Intracranial aneurysms

-Subtypes

A
  1. Saccular (berry) — small sacs that expand over time — caused by congenital malformation or vessel wall stress and inflammation
    - Highest risk of rupturing between 20-50 yrs old
  2. Fusiform — GIANT aneurysms in basilar artery or terminal carotid arteries — D/t arteriosclerotic changes
  3. Mycotic aneurysms — rare and the result of bacterial infection
  4. Traumatic dissecting aneurysms — weakening of arterial wall d/t trauma — might occur during embolization
39
Q

Meningitis

A
  1. Inflammation of the brain or spinal cord
  2. Microbial invasion of the CNS
  3. It is more common to be caused by bacterial invasion — Can also be caused by viruses, fungi or parasites

Bacterial Meningitis — Pyogenic (pus forming) infection that invades the pia mater and arachnoid

40
Q

Encephalitis

A
  1. Acute febrile illness that is an infection of the brain itself — Usually viral origin w/ nervous system involvement
  2. Most common forms caused by — Mosquito borne illness; HSV
    - As viruses enter the CNS, edema and necrosis develop — Can progress to increased ICP and Herniation

S/Sx’s

  • Altered mental status
  • Delirium
  • Unconsciousness
  • Seizure
  • Cranial nerve palsies
  • abnormal reflexes
41
Q

Multiple Sclerosis

A
  1. Progressive, inflammatory, demyelination, autoimmune disorder of the CNS — Results in scaring and loss of axons
  2. Myelin auto antigens trigger production of antibodies that cause demyelination
  3. S/Sx’s
    - People may have optic neuritis or cerebelar syndromes that show gait instability, lack of coordination, tremor or ataxia
  4. Causes are vitamin D deficiency — ages between 20-40 and females are 2x more likely to get MS
42
Q

Guillain Barre

A
  1. Acquired inflammatory disease that causes demyelination of the PERIPHERAL NERVES w/ relative sparing of axons
  2. Acute onset w/ a characteristic ascending motor paralysis
  3. Demyelination is progressive from distal to próxima
  4. Caused by Zika, URI, GI infection, Flu vaccine
  5. Manifestation — Most significant consequence can lead to RESPIRATORY MUSCLE involvement w/ mechanical ventilation
  6. Recovery is slow but does occur
43
Q

MS Vs Guillain Barre

A
  1. MS is a CNS disorder & Guillain Barre is PNS

2. MS causes scaring and loss of axons — Guillain Barre is axon sparing

44
Q

Myasthenia Gravis

A
  1. Chronic inflammatory disorder where acetylcholine receptor antibodies attack the neuromuscular junction
    - Main defect is T-cell dependent autoantibodies
  2. Treatment for Myasthenia Gravis is REMOVAL of the THYMUS
  3. Clinical Manifestations
    - Generalized weakness — starting at the head, face and neck
    - Weakness and fatigue of the muscles of the eyes and throat — Diplopia & difficulty chewing, talking, swallowing
  4. Treatment
    - Anticholinesterase drugs, steroids, immunosuppressive, potential surgery
45
Q

Schizophrenia

A

Term used to describe thought disorders

  1. Advanced imaging has found:
    -Distinct, structural neuroanatomista altercation in this disorder including
    —Enlargement of lateral and third ventricles
    —Widening of the frontal cortical fissures and sul I
    —Progressive loss of cortical gray matter in the frontal and temporal lobes
  2. Causes
    - Prenatal infection; perinatal complications; upbringing; Neurotransmitter hypothesis — alteration in brain dopamine pathways
46
Q

Schizophrenia

-Hallmark S/Sxs

A
  1. Hallmark of schizophrenia is disorganized thought w/ positive and negative Sx’s
47
Q

Mood disorders

A
  1. Mood refers to a sustained emotional state
  2. Biological factors that are theorized to contribute to depression
    - Abnormal sleep
    - Neurotransmission dysregulation — Reduced serotonin
  3. Increased stress can cause chronic activation of the hypothalamic-pituitary adrenal system

6010 Advanced Patho Test 6 COMPLETE ☑️ (6 decks)

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