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Adv Patho > Exam 4-Neuro > Flashcards

Exam 4-Neuro Flashcards

1
Q

STROKE

A

Etiology: blood supply to part of the brain is suddenly interrupted or when a blood vessel in the brain bursts, spilling blood in the spaces surrounding brain cells.

Manifestations:

  • Sudden onset of weakness or numbness on one side of the body.
  • Sudden speech difficulty or confusion.
  • Sudden difficulty seeing in one or both eyes.
  • Sudden onset of dizziness, trouble walking or loss of balance.
  • Sudden, severe headache with no known cause.

Pathophysiology: brain cells die because they don’t get enough oxygen and nutrients;

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2
Q

HYPERNATERMIA

A

occurs when serum sodium levels exceed 145mEq/L.

Risk Factors: advanced age, AMS, fever, diarrhea, vomiting, uncontrolled DM.

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3
Q

Infants with severe diarrhea are at risk for?

A

hypernatermia

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4
Q

HYPONATREMIA

A

occurs when serum sodium levels are less than 135 mEq/L.
-usually due to inappropriate secretion of ADH leading to SIADH or cerebral salt wasting syndrome ( CSWS).

**most common electrolyte d/o with increased morbidity and mortality

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5
Q

When sodium is too low in blood, extra water goes into body cells and causes swelling which can be dangerous to brain cells because

A

it can results in neurological symptoms such as headache, confusion, irritability, seizures, or coma

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6
Q

PARTIAL (aka focal) SEIZURES

A
  • can impair consciousness or not impair it
  • may or may not include motor activity
  • -aura: ex: lip smacking, chewing, smells, rapid eye blinking
  • clinical finding may be subtle
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7
Q

GENERALIZED SEIZURES

A
  • can be motor or nonmotor (absence seizures; can happen multiple times a day)
  • sudden LOC
  • tonic clonic, clonic (twitching), tonic (stiff), atonic (no muscle tone-just fall to ground), or myoclonic (sudden rapid muscle contractions-very fast; happen in morning and usually d/t no sleep)
  • mental status impairment
  • possible focal neurological deficits
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8
Q

TENSION TYPE HEADACHE (TTP)

A
  • BILATERAL pain distribution (band, pressure); gradual onset; more common in WOMEN
  • genetic disposition; may be episodic or chronic
  • more localized pain and tenderness of pericranial muscles; last 30 min-week
    cause: trigeminal hypersensitivity (central); myofacial afferent sensitivity (peripheral); usually exacerrabated by stress and fatigue
  • most common type of headache

Txt: caffeine and relaxation ; NSAIDs and chronic pain can be treated with amitriptyline and tricyclic antidepressants

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9
Q

CLUSTER HEADACHE

A
  • group of disorders-headache for several days followed by remission
  • usually in MALES 20-50 YR OLD
  • EXCRUCIATING, STABBING PAIN UNILATERALLY BEHIND ONE EYE
  • LAST 8-10 WEEKS PER YEAR; SAME TIME EVERY DAY 15 MIN TO 3 HOURS
  • usually associated with autonomic symptoms on affected side: PTOSIS, MIOSIS, LACRIMATION, NASAL CONGESTION

-nasoactive peptides, neurogenic inflammation, pain activation

TXT: inhaled oxygen and sumatriptans

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10
Q

Ischemic stroke

A

blockage of a blood vessel supplying the brain

-can be caused by thrombus from atherosclerosis or can be embolic

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11
Q

Pathophysiology etiologies of AMS

A
  • arousal (RAS) vs awareness
  • structural changes
  • trauma
  • infection
  • toxic substances
  • metabolic (sodium, glucose, oxygen)
  • dementia vs. delerium
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12
Q

Hemorrhagic stroke

A

bleeding into or around the brain

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13
Q

Which type of stroke is most common in the US?

A

ischemic

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14
Q

Frontal stroke deficits

A

problem solving, perseveration, expressive aphasia, personality changes

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15
Q

Temporal stroke deficits

A
  1. receptive aphasia
  2. recognizing faces
  3. short term memory loss
  4. aggressive behavior
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16
Q

Parietal stroke deficits

A
  1. object naming
  2. confusion
  3. difficulty with tactile senses
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17
Q

Occipital stroke deficits

A
  1. visual field and color identification

2. word blindness

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18
Q

Cerebellum stroke deficits

A
  1. gross and fine motor movement
  2. posture
  3. tremor
  4. speech
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19
Q

Brainstem stroke deficits

A
  1. temperature
  2. heart rate
  3. respiratory rate
  4. swallaow
  5. balance
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20
Q

Which common artery is the most commonly effected?

A

MCA - middle cerebral artery

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21
Q

Contralateral

A

symptoms occur on opposite side of the stroke

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22
Q

Ipsiliateral

A

symptoms occur on same side as stroke

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23
Q

Symptoms of MCA injury

A
  • contralateral face and arm weakness and sensory loss
  • mild or no leg weakness
  • head and eyes deviated towards side of stroke
  • if left sided may produce aphasia
  • if right sided, may cause deficits of spatial perception, hemineglect, and apraxia (trouble completing movements)
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24
Q

Symptoms of Posterior Cerebral Artery injury (PCA)

A
  • visual problems
  • prosopagnosia (can’t recognize faces)
  • alexia (inability to read)
  • aphasia (can’t comprehend spoken words)
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25
Q

Symptoms of Anterior Cerebral Artery injury (ACA)

A 
-contralateral leg weakness
and sensory loss
-mild or no upper extremity involvement
-balance problems
-may produce aphasia if left sided
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26
Q

Right brain injury symptoms

A
  • paralyzed left side
  • special perceptual deficits
  • quick impulsive behavior
  • memory deficits
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27
Q

Left brain injury symptoms

A
  • paralyzed right side
  • speech language deficits
  • slow, cautious behavioral style
  • memory deficits
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28
Q

How does high repetition help after a stroke?

A

helps create and reinforce new pathways in the brain

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29
Q

What is meningitis

A

inflammation of the meninges surrounding the brain and spinal cord usually due to a bacterial or viral infection

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30
Q

what are the 3 membranes in the brain and spinal cord

A
  1. dura mater
  2. arachnoid
  3. pia mater
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31
Q

Bacterial meningitis

A

can be cause by strep. pneumoniae, H. influenza, neisseria meningitiis, group B strep

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32
Q

Viral meningitis

A
  • most common type of mengiitis
  • less severe than bacterial
  • most get better without txt
  • echovirus most common cause of viral meningitis
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33
Q

BACTERIAL MENINGITIS CSF FLUID

A 
Opening pressure: increased
WBCS: >1000
Glucose: greater than or = 40
Protein: >100
Cells: PMNs
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34
Q

VIRAL MENINGITIS CSF FLUID

A 
Opening pressure: normal
WBCs: <1000
Glucose: normal
Protein: normal or <100
Cells: neutrophils (early
          lymphocytes (late)
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35
Q

Encephalitis

A

inflammation of brain itself that can be caused by virus, bacteria, fungus, parasites
- inflammation of the active tissues of the brain caused by an infection or an autoimmune response. The inflammation causes the brain to swell, which can lead to headache, stiff neck, sensitivity to light, mental confusion and seizures.

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36
Q

Common symptoms of encephalitis

A 
fever
headache
stiff neck
sensitivity to bright light
vomiting
changes in behavior
seizures
LOC
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37
Q

What is a symptom in infants of who have meningitis or encephalitis?

A

bulging fontanel

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38
Q

Common viruses that cause encephalitis

A

herpes, varicella zoster, measles, mumps, and rubella viruses

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39
Q

Encephalitis autoimmune evaluation

A

rapid onset of on or more cognitive symptoms, seizures, psychiatric disturbances, particularly in patients who have background of autoimmunity, cancer, or smoking hx

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40
Q

Which has more neurological deficits

A

encephalitis

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41
Q

Seizures

A
  • transient disruption in electrical function with excessive discharges of cortical neurons
  • balance between excitation and inhibition of impulses disrupted
  • uncontrolled shaking that is rapid, rhythmic, with muscles contracting an relaxing repeatedly
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42
Q

What are seizures normally associated with

A

cerebral lesions (tumor), biochemical alterations, trauma, epilepsy

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43
Q

S/S of seizures

A
  • blackout with period of confusion
  • changes in behavior
  • drooling
  • loss bladder or bowel
  • mood changes
  • shaking of entire body
  • sudden falling
  • teeth clenching
  • uncontrolled muscle spasms
  • temporary stop in breathing
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44
Q

Path of seizure

A

can be conceptualized as occurring when there is distortion of the normal balance between excitation and inhibition in the brain which can alter brain function. Can be genetic or acquired

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45
Q

How to control seizures

A

control abnormal neuronal activity by elevated threshold of neuron responsible to electrical or chemical stimuli. Stabilize neuron membrane, reducing neuron conduction.

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46
Q

Cause of seizures:

A
  • drugs
  • epilepsy
  • fever
  • head injury
  • stroke
  • heart disease
  • brain tumor
  • brain infections
  • congenital brain defects
  • brain injury to baby during delivery
  • abnormal levels of sodium or glucose in blood
  • poisoning
  • phenylketonuria (PKU)
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47
Q

Four phases of a seizure

A
  1. prodromal-symptoms start to appear; depression/angry/anxiety,..etc.; starts days before a seizure
  2. early ictal (aura): happens within seconds to minutes
  3. ictal: 1-3 minutes; MAKE SURE TO TIME BC IF GREATER THAN 5 MIN IT BECOMES STATUS ELIPITICUS
  4. post ictal: brain takes time to recover; hours to days; sleepy, confused, headache, injury (tongue, cheek, body)
48
Q

Status elipticus

A

Etiology: 50% acute, symptomatic

  • 5 or more minutes of continuous clinical and/or EMG seizure activity or recurrent seizure activity without recovery between seizures
  • glucose and glycogen stores depleted rapidly
  • huge increase in cerebral metabolic rate
  • life threatening emergency
  • tachycardic
  • bp increases
  • cerebral blood flow, brain glucose, and parenchymal oxygenation decrases
  • ICP incrases
49
Q

Status elipticus: strigger stimulus evokes activity

A

stage 1-generalized tonic clonic seizures; increase in autonomic activity with increased cerebral blood flow
stage 2-failure of cerebral autoregulation; decreased cerebral blood flow, increase intracranial pressure, decreased bp; electromechanical dissociation (twitching)

50
Q

2 types of TBI

A
  1. close (dura mater intact): MVCs, sport injuries, baby shaking
  2. penetrating or open (dura mater interrupted): GSW, blunt trauma, skull fx
51
Q

Subdural hematoma

A

bleeding between the dura mater and the brain

52
Q

Epidural hematoma

A

bleeding between dura mater and skull

53
Q

Intracerebral hematoma

A

within the brain

54
Q

secondary TBI

A

cause by hypotension, cerebral ischemia, impaired autoregulation, cerebral edema, inflammation

55
Q

Dementia

A

chronic onset; slow decline in cognitive function with no impairment of awareness; impairs daily functioning

56
Q

Delerium

A

acute onset; fluctuating cognitive impairment with varying states of awareness

57
Q

What common electrolyte imabalance is found in neurological disorders

A

hyponateremia d/t inappropriate secretion of ADH or cerebral salt wasting syndrome

58
Q

Negative short term and long term effects of a concussion

A

Short: headaches, dizzy, lightheaded, n/v, LOC, difficulty with coordination

Long: increased risk for Alzheimer’s, trouble with verbal communication, trouble reasoning, depression, personality changes, memory loss, aggression

59
Q

Negative short term and long term effects of a TBI

A

Short: headache, fatigue, irritability, memory problems, dizziness

Long: loss of balance, nausea, neck pain, ringing ears, confusion, sensitivity to light, shot term memory problems, sleep disturbance, personality changes

60
Q

3 childhood neuropathologies

A
  1. febrile seizure
  2. spina bifida
  3. cerebral palsy
61
Q

Patho of Alzheimer’s Dementia

A

Results in neuritic plaque formation, insoluble filaments»disrupted neuron impulse transmission»neuron death

Loss of neurons and synapses in cerebral cortex and subcortex lead (memory function)

End result is atrophy , decreased brain weight and volume: loss of neurotransmitters

  • late onset:(sporadic) : genetic (APOE GENE) and environmental; older age; amyloid plaques outside of the cells and tangles inside cells
  • familial: aka early onset Alz; dominant gene that speeds progression; increased risk with down syndrome

Dx: brain biopsy after autopsy

62
Q

2 pathologic hallmarks of Alzheimers are:

A

Extracellular beta-amyloid deposits (in senile plaques) and Intracellular neurofibrillary tangles (paired helical filaments)

The beta-amyloid deposition and neurofibrillary tangles lead to loss of synapses and neurons, which results in gross atrophy of the affected areas of the brain, typically starting at the mesial temporal lobe

63
Q

PATHO OF PARKINSON’S DISEASE

A

Basal ganglia degeneration&raquo_space; decreased dopamine generating cells in substantia nigra (midbrain)

  • presence of lewy bodies
  • lack of dopamine&raquo_space; resting tremor, rigidity, bradykinesia, postural instabilitt
  • degeneration of locus cerulesu&raquo_space; lack of norepinepherine and worsening behavrioal symptoms (depression, cognitive slowing)

**degeneration and death of dopamine neurons in the substantia nigra

*tremors worse when at rest; can have cognitive impairment or psychiatric symptoms.

Txt: restore depleted dopamine levels; dopamine does not cross blood brain-barrier so a precursor of dopamine (L-dopa) is given

64
Q

PATHO OF NEUROMUSCULAR SHEATH D/O

A

localized demyelination (plaques) occur with destruction of oligonendroglia, perivascular inflammation, and chemical changes in lipid and protein constituents of myelin in and around plaques

EX: multiple sclerosis

65
Q

What are lewy bodies

A

abnormal aggreates of protein that develop inside nerve cells in Parkinson’s Disease (PD), Lewy body dementia, and some other disorders.

66
Q

Effects of Aging

A
  • decrease body, size
  • increase atherosclerosis
  • increase permeability of blood brain barrier
  • decrease in myelin, dendrititc processes, synapse connections
  • neurotransmitters, decrease in sensory function
  • decrease in tendon reflexes, vibaratory sense
67
Q

Causes of TBI

A
  • mvc
  • sports
  • assualts
  • falls
  • blast concussion
  • shaken babies
68
Q

2 types of TBI

A
  1. closed: MVC and sports

2. open: GSW, skull fx

69
Q

Primary brain injury

A

Closed (dura mater intact) and opened (dura mater interrupted) head injuries

Closed head injury: intracranial pressure ICP increase,,,, peak 18‐36 hours after severe head injury. MVC, sports, baby shaking

Open head injury:GSW, skull fx, blunt trauma

70
Q

Subdural hematomas

A

(bleeding between the dura mater and the brain). 1‐2%

71
Q

Epidural hematomas

A

(between dura mater and the skull) 10‐20%

72
Q

Intracerbral hematomas

A

(within the brain) 2‐3%

73
Q

Secondary Brain Injury

A

hypotension, hypoxia, cerebral ischemia, impaired autoregulation of blood flow; cerebral edema, inflammation…

74
Q

Concussion

A

A concussion is actually an injury to the brain caused by a direct blow to the
head. Concussions are graded in various methods according to the signs and symptoms presented. Symptoms following a concussion can vary from person to person. Loss of consciousness, blurry vision, dizziness, confusion, nausea, vomiting, headache, change in emotion, trouble concentrating, memory loss, ringing in the ears, and a loss of balance can
occur.

75
Q

Diffuse axonal injury

A

is the result of traumatic shearing forces that occur when the head is rapidly accelerated or decelerated.
-It causes scattered lesions over a widespread area
in white matter tracts as well as gray matter.
-primary cause of concussion
-outcome usually coma

76
Q

coup injury

A

occurs under the site of impact with an object, and a countrecoup injury occurs on the side opposite the area that was hit. Associated with cerebral contussions

77
Q

Adult AMS, neuromuscular, myelin sheath disorders

A

Dementia, Alzheimer’s Diseases, Parkinson’s Disease,

Nueuromuscular‐‐‐Myasthenia Gravis, Amyotrophic lateral sclerosis,

Myelin Sheath disorders ‐‐‐GuillainBarre Syndrome, Multiple Sclerosis,

78
Q

FEBRILE SEIZURES

A

Febrile seizures are convulsions that occur in a child who is between six months and five years of age and has a temperature greater than 100.4ºF (38ºC). It is the most common seizure disorder of childhood. While scary to parents, febrile seizures usually do not last long and do not cause brain damage, learning disabilities
or epilepsy.
-can be generalized or focal
-highly associated with herpes virus; (fever first and rash later)

79
Q

SPINA BIFIDA

A

Causes: genetic, nutritional, and environmental; deficiency in folic acid is key factor for mom’s diet along with obesity and diabetes

ETIOLOGY: vertebra fail to close; *meningocele-meninges protrude through vertebral arch
*myelomeningocele (most common an severe)- meninges dilated, part of the cord protrude through vertebral defect

  • associated with hydrocephalus
  • motor, sensory alterations depend on location and severity of defect
80
Q

CEREBRAL PALSY

A
  • usually occurs before 3 yrs
  • injury or abnormal development of brain; numerous prenatal, perinatal, postnatal etiologies
  • results in d/o of movement, muscle tone, posture,
  • cognitive disability
  • effects are permanent but not progressive
81
Q

PRIMARY SCI

A

arise from mechanical disruption, transection, or distraction of neural elements

82
Q

SECONDARY SCI

A

process involves swelling and hemorrhage, which leads to increased free radicals and decreased blood flow, causing even greater cell membrane dysfunction and cell death.

83
Q

MANIFESTATIONS OF SPINAL SHOCK

A 
Loss of reflexes
Loss of motor control
Low blood pressure (if the SCI occurs at the T6 level or higher)
Decreased heart rate (if the SCI occurs at the T6 level or higher)
Flaccid paralysis
Urinary retention
Fecal incontinence
Spasms/ increased muscle tone
Loss of sensation
84
Q

MANIFESTATIONS OF AUTONOMIC HYPER-REFLEXIA

A

-is a condition in which your involuntary nervous system overreacts to external or bodily stimuli.

  • a dangerous spike in blood pressure
  • slow heartbeat
  • constriction of your peripheral blood vessels
  • other changes in your body’s autonomic functions

-can result in stroke, retinal hemorrhagic, cardiac arrest, pulmonary edema

85
Q

Amyotrophic Lateral Sclerosis (ALS)

A

degeneration of upper and lower motor neurons

Etiology: mutation in Superoxide Dismutase (SOD-1 gene). Fewer neurons; axons degenerate, demyelinate, sclerose

86
Q

Myasthenia Gravis

A
  • a chronic autoimmune disorder in which antibodies destroy the communication between nerves and muscle, resulting in weakness of the skeletal muscles.
  • autoimmune (common women 20-40); type II hypersensitivity that produce antibodies to acetylcholine receptors
  • decreased receptors for acteylcholine due to autoimmune attack on postsynaptic acetylcholine receptors, which disrupts neuromuscular transmission.
  • wake up fine but progressively get weaker during the day; can effect extraoccular muscle, diplopia, muscle weakness; often involves thymus

Txt: anitcholiestrase drugs and immunomodulating treatment, plasmapheresis

87
Q

Amyotrophic Lateral Sclerosis (ALS)

A

degeneration of upper and lower motor neurons

*characterized by stiff muscles, muscle twitching, and gradually worsening weakness due to muscles decreasing in size. It may begin with weakness in the arms or legs, or with difficulty speaking or swallowing. About half of the people affected develop at least mild difficulties with thinking and behavior and most people experience pain.[11][12] Most eventually lose the ability to walk, use their hands, speak, swallow, and breathe.

Etiology: mutation in Superoxide Dismutase (SOD-1 gene). Fewer neurons; axons degenerate, demyelinate, sclerose

88
Q

Headaches:

A
  • primary have no structural or metabolic abnormality (90% of headaches)
  • secondary is caused by structural or metabolic abnormality )sinusitis, otitis media, meningitis

Patho:result from traction to or irritation of the meninges and blood vessels which cause norcioreceptors to send message up the length of the nerve fiber to the nerve cells in the brain signaling the body to hurt

89
Q

Phase of migraine

A
  1. premonitory
  2. aura
  3. headache
  4. recovery

Patho:Brainstem neuronal hyperexcitability; abnormalities in
neurotransmitters, including 5‐HT, GABA, glutamate, CGRP (calcitonin gene‐related
peptide), Norepinephrine (NE), Dopamine, NO and endorphins. Genetic abnormality in the
genes affecting these molecules can cause headache, Migraine. Trigeminal activation can
also cause migraine.

90
Q

Chronic traumatic encephalopathy (CTE):

**football

A

progressive degenerative disease of the brain found in people with a history of repetitive brain trauma (often athletes), including symptomatic concussions as well as asymptomatic subconcussive hits to the head that do not cause symptoms. There is relatively little known regarding the pathobiological mechanisms underlying CTE.

91
Q

Biomarkers for TBI

A
  1. (Brain derived neurotrophic factor) BDNF, a ubiquitously expressed neurotrophinin
    the brain, is an intriguing target for TBI intervention research due to its role in neuronal survival, neurogenesis, and plasticity.
  2. GFAP (Glial fibrillary Acidic Protein) is an intermediate filament protein found in the
    cytoskeleton of astroglia. Recent work has indicated that GFAP may serve as a serum marker of traumatic brain injury(TBI) that is released after central nervous system cell damage.
92
Q

Increased Intracranial Pressure

A

increased ICP&raquo_space; decrease in cerebral perfusion pressure (CPP), decrease in cerebral blood flow (CBF)&raquo_space; cerebral ischemia

93
Q

Brain circulation regulation is regulated by?

A
  1. vasogenic autoregulation- Cerebral pressure autoregulation, which maintains a constant flow in the face of changing cerebral perfusion pressure.
  2. metabolic regulation- Flow‐metabolism coupling refers to the brains ability to vary blood flow to match metabolic activity.
  3. regulation of respiratory gases-An extensive arborization of perivascular nerves also serves to modulate cerebral blood flow, so‐called neurogenic regulation.
94
Q

Pathologies of AMS

A
  1. arousal (RAS-reticular activating system) vs awareness (all cognitive functions)
  2. structural change (tumor, stroke, bleed)
  3. trauma
  4. infection
  5. toxic substances (alcohol, heavy metals, venom, sedatives/hypnotics)
  6. metabolic (sodium, glucose, oxygen)
  7. dementia vs. delerium
95
Q

What does hyperkalemia and hypokalemia do?

A

depress PNS with muscle weakness as the major clinical manifestation

96
Q

What does hyper calcemia and hypermagnesemia do?

A

produce CNS and PNS depression with encephalopathy and muscle weakness

97
Q

What does hypocalcemia and hypomagnesemia do?

A

produce CNS and PNS irritability with seizures and tetany, respectively, being the major clinical manifestations

98
Q

Which neurodegenerative disease d/ is the most expensive disease?

A

Alzheimer’s

99
Q

What are the strongest genetic risk factor influencing susceptibility to late onset Alzheimer’s disease?

A

apolipoprotein E (APOE) genotype

100
Q

Parkinsonisms

A

a general term that refers to a group of neurological disorders that cause
movement problems similar to those seen in Parkinson’s diseasesuch as tremors, slow
movement and stiffness.

101
Q

Carbidopa‐Levodopa

A

Carbidopa prevents the breakdown of levodopa in the bloodstream so more levodopa (L‐DOPA) can enter the brain. Carbidopa can also reduce some of
levodopa’s side effects such as nausea and vomiting primarily used to manage the symptoms of Parkinson’s disease but does not change the course of the disease.

102
Q

4 neuro pathologies

A
  1. ALS-A nervous system disease that weakens muscles and impacts physical function.
  2. Myasthenia gravis- is a chronic autoimmune disorder in which antibodies destroy the communication between nerves and muscle, resulting in weakness of the skeletal muscles.
  3. Multiple sclerosis- nerve damage disrupts communication between the brain and the body.Multiple sclerosis causes many different symptoms, including vision loss, pain, fatigue, and impaired coordination.
  4. Guillain-Barre Syndrome-a rare, autoimmune disorder in which a person’s own immune system damages the nerves, causing muscle weakness and sometimes paralysis.
103
Q

Spinal cord injury

A

sudden traumatic blow to spine that fractures or dislocates vertebrae. The damage begins at the moment of injury when displaced bone fragments, disc material, or ligaments bruise or tear into the spinal cord tissue

-classified as complete or incomplete

104
Q

Question: What level of spinal cord injury causes paraplegia?

A

Paraplegia occurs in spinal cord injuries below the first thoracic spinal levels (T1‐L5).
Paraplegics are able to fully use their arms and hands, but the degree to which their legs are disabled depends on the injury.

105
Q

Primary Headaches examples

A

tension
migraine
cluster

106
Q

Secondary headaches examples

A

-acute
infection, brain tumor, serious brain injury
-subarachnoid hemorrhage: sudden, 10/10 pain, “worst headache” of my life
-carotid artery dissection: sudden

107
Q

Migraine Headaches

A

-more common in females
-family hx
-triggers: specific foods, weather, bright lights, loud noises, physical exertion, lack of sleep
-4-72 hours long
-SEVERE, UNILATERAL, PULSATING, THROBBING, AGGRAVATED BY MOVEMENT
-can have n/v
-photobia and phonobia (lights and noises) so go to dark room
-aura: tinnitus, aphasia, confusion, temporary paralysis
TXT: NSAIDs, sumatripatan

108
Q

Clinical Manifestations of Parkinsons

A
  1. tremor
  2. rigidity
  3. bradykinesia or hypokenia
  4. postural instability
    * *no weakness
  5. depression
  6. dementia
  7. difficulty smelling
  8. sleep disturbances
109
Q

Post concussion syndrome

A

Symptoms occur within the first 10 days and go away within three month; can sometimes persist for a year or more

Dizziness, vertigo, fatigue, memory problems, trouble concentrating, sleeping problems, insomnia

110
Q

How do you dx meningitis and encephalitis?

A

lumbar puncture to analyze CSF

111
Q

Toxoplasmosis

A
  • parasite
  • can cause encephalitis
  • effects pregnant women and immunocompromised
  • abscess in the brain appear as a ring-enhancing lesion with CT scan
112
Q

Cryptococcosis

A
  • can cause encephalitis
  • fungal
  • from bird dropping
  • can affect any organ of the body
  • headache, fever, changes in mental status
113
Q

Toxin

A

-can cause encephalitis
-solvents such as toluene, following exposure to heavy metals such as manganese; or exposure to extreme concentrations of any natural toxin such as
cyano-toxins found in shellfish or freshwater cyanobacteria crusts.

114
Q

Causes for a seizure

A 
CAUSES: 
Vascular (ischemic or hemorrhagic stroke)
Infection
Toxins and trauma
Autoimmune
Metabolic imbalance
Idiopathic (aka epilepsy)
Neoplasms
S (pyschogenic seizures syncope)
115
Q

Guillian Barre Syndreom

A
  • weakness from legs and moves up
  • is a rare, autoimmune disorder in which a person’s own immune system damages the nerves, causing muscle weakness and sometimes paralysis. GBS can cause symptoms that last for a few weeks to several years. Most people recover fully, but some have permanent nerve damage.

Adv Patho (23 decks)

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