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Flashcards in Neuro Deck (45):
1

Your patient comes to the ER following a car accident with a GCS of 5.

Your patient is likely to aspirate fluids
Difficult or impaired swallowing
Primary esophageal peristalsis is affected

2

Epidural hematoma may be associated with:

Increased ICP
Fractured skull
Arterial bleed
Brain stem compression

3

Which of the following could predispose to cerebral hemorrhage?

Systemic HTN
Cerebral aneurysm
Congenital malformation of cerebral arteries
Head Trauma

4

Manifestations of increased ICP include increased:

Pulse pressure

5

Cerebral edema is associated with decreased:

Cerebral blood flow

6

Subdural hematoma may be associated with:

Increased ICP
Decreased GCS score
Head injury
Brain stem herniation

7

Complications of a spinal cord injury at the C2 level may include:

DVT
UTI
Pressure ulcer
Respiratory failure

8

Which of the following are true?

Complex partial seizures may impair consciousness

9

Seizures may be associated with:

Head injury
Altered consciousness
Tonic-clonic muscle contractions
Brain tumor

10

Patients with complete spinal cord injuries at C1 will exhibit which of the following after food ingestion?

Absence of GI peristalsis
Impaired GI food absorption
Impaired digestion
NONE OF THESE

11

Clinical manifestations of CVA may include:

Paralysis of one side of the face
Inability to communicate
Lack of spontaneity
Change in visual field

12

Site of exercise helping this Alzheimer's patient:
Mechanism:

neurons in cerebral cortex
Cognitive exercisekeeps synapses in cortex functioningdec loss of neural function from disuseinc synaptic connections to increase higher level thinkingsystains cortex functionAlzheimer’s treated

13

Site for Drug Treatment of Alzheimer's 1: Tau Protein
Mechanism:

Drug acts on Tau proteinprevents hyperphosphorylation of Tauno added negative chargeno improper foldingno neuritic tanglesno neural loss or degeneration of hippocampus/amygdalaAlzheimer’s treated

14

Site for Drug Treatment for Alzheimer's 2: APP
Mechanism:

Drug acts on APPprevents abnormal splicing of APPno BAP createdno toxic BAP acting on neuronsno neural damage of degenerationAlzheimer’s treated

15

Give the site and mechanism for exercise helping prevent a CVA.

Site: Internal carotid artery
Mechanism: Exercisedec LDL, inc HDLopens up vesselsdec likelihood of plaque formation and clot developing in carotid arterydec stasisallows smooth blood flow to brainno CVA

16

Why is M.S. rarely seen in the tropics? Mechanism?

Reason: tropics have a warmer climate and more sunlight (vitamin D)
Mechanism:
Tropic locationinc sunlight and warm climateinc vitamin Ddec auto immunitydec Ab produced against oligodendrocytesdec Ab causing demyelination of CNSno M.S.

17

Give a non-drug treatment and the mechanism for Parkinson’s.

Non-drug treatment: stem cells
Mechanism:
Stem cellsreplaced damaged neurons in substantia nigranew neurons in substantia nigranew neurons can produce dopamineinc dopamineinc smooth fluid muscle movementno Parkinson’s

18

Give three causes for increased ICP.

Cause 1: hemorrhage
Mechanism:
Hemorrhageblood accumulates in braininc ISF in braintakes up spaceinc pressureinc ICP

Cause 2: hydrocephalus
Mechanism:
Hydrocephalusinc production, dec absorption of CSFinc CSF in brainventricles distendinc pressure in braininc ICP

Cause 3: tumor
Mechanism:
Tumor in braintumor compresses brain structureinc pressure on brain in skullinc ICP

19

Three manifestations for increased ICP

Manifestation 1: fixed, dilated pupils
Mechanism:
Inc ICPinc pressure in braininc pressure on cranial nerves 2-7dec papillary light reflexfixed dilated pupils

Manifestation 2: headache and dizziness
Mechanism:
Inc ICPinc brain pressureskull isn’t elasticpressure on cranial nervesdec O2 blood supply to brainstretching and pressure in brainheadache and dizziness

Manifestation 3: projective vomiting
Mechanism:
Inc ICPinc pressure in braininc pressure on emetic centerprojectile vomitting

20

A drug treatment for increased ICP

Drug treatment: Mannitol
Mechanism:
Mannitolacts on braindraws on fluid from braindec brain pressuredec ICP

21

Two non-drug treatments for increased ICP

Non-drug treatment 1: surgery
Mechanism:
Surgery on skullremove portion of skullrelieves pressure in braindec ICPtreatment

Non-drug treatment 2: drain
Mechanism:
Drain placed in braindraws out excess fluiddec fluid in braindec pressuredec ICPtreated

22

Give three causes for cerebral edema and the mechanism.

Cause 1: hydrocephalus
Mechanism:
Hydrocephalusinc production and dec absorption of CSFinc CSFventricles distendedinc ISFinc ICPcerebral edema

Cause 2: infection
Mechanism:
Infectioninc blood accumulation in braininc ISFinc ICPcerebral edema

Cause 3: Hemorrhage
Mechanism:
Hemorrhageinc blood in braininc ISFinc ICPcerebral edema

23

Give three causes and the mechanism for a CVA developing.

Cause 1: thrombosis
Site: endothelial in internal carotid
Mechanism:
Damaged endo in internal carotidmonocytes and platelet adhesionmacros engulf lipoproteinsform foam cellsrelease GFproliferation of SM cells and ECMstable plaque in carotidruptures and platelet aggregationunstable thrombosisocclusiondec blood flow to brainCVA

Cause 2: Emboli
Site: middle cerebral artery
Mechanism:
Patient with A-fibdec function of pumpstasis and turbulent blood flowclot forms in LHtravels through aortaemboli in middle cerebral arterydisrupts blood flow to brainCVA

Cause 3: hemorrhage
Site: vessels in brain
Mechanism:
Untreated HTN in patientinc vessel pressureballooning out of vesselaneurysmrupturesdisrupts blood flowbleeding in brainCVA

24

Three manifestations of a stroke

1. Dec LOC
2. Aphasia
3. Loss of central vision

25

Drug treatment of a stroke

Drug Treatment: tPA
Mechanism:
tPAacts on clotallows adequate blood flowO2 and blood to brainno CVA

26

Three non-drug treatments of a stroke

Non-drug treatment: angioplasty
Mechanism:
Angioplastyballoon in vesselinflates and opens vesselstent placedholds vessel openallows blood flow to brainno CVA

Non-drug treatment: diet and exercise
Mechanism:
D&Edec LDL, inc HDLopens vesselallows good blood flowdec risk of clot formationno CVA

Non-drug treatment: catheter
Mechanism:
Catheterplaces coil in aneurysmfills in and plugs aneryusmno inc in pressure in aneurysmno ruptureno bleeding or disruption in blood flowno CVA

27

Give three sites for Alzheimer’s developing and the mechanism.

Site 1: Tau protein
Mechanism:
Tau protein becomes hyperphosphorylatedadded negative chargeimproper foldingneuritic tanglesirreversible neural loss and degenerationdec function of hippocampus and amygdalaAlzheimer’s

Site 2: APP
Mechanism:
Abnormal splicing of APPforms BAPBAP toxic to neuronsdamages neurons in hippocampus, amygdala, cortexneural loss and degenerationAlzheimer’s

Site 3: neurons
Mechanism:
Neurons destroyeddec working neuronsdec cortex/hippocampus/amygdala functiondegeneration of neuronsbrain atrophyAlzheimer’s

28

Three manifestations of Alzheimer's

1. Acalculia
2. Personality changes
3. Progressive memory loss

29

Three lab manifestations of Alzheimer's

1. BAP and hyperphosphorylated Tau present in CSF in lumbar puncture
2. Brain atrophy, normal ventricles
3. inc AchE, dec Ach, dec CAT

30

One non-drug treatment

Treatment site: cognitive exercise
Mechanism:
Cognitive exercisekeeps synapses workinginc GFsustains brain functiontreatment

31

Give three different sites and the mechanism that a new possible drug could act on to treat Alzheimer’s.

Treatment site 1: phosphorylation prevention
Mechanism:
Drug acts on Tauprevents hyperphosphorylationno improper foldingno neuritic tanglesno degeneration, no neural loss in structuresno Alzheimer’s

Treatment site 2: kill BAP
Mechanism:
Drug acts on BAPkills BAPdec toxicity to neuronsno neural loss or degenerationno Alzheimer’s

Treatment site 3: Antibodies
Mechanism:
Drug acts on immune systemproduces anti-BAP antibodiesAb attack BAPno BAPno neural loss and degenerationno Alzheimer’s

32

Give three sites for causing Parkinson’s and the mechanism.

Site 1: substantia nigra
Mechanism:
Acts on substantia nigraprevents dopamine productiondec dopamine effectsdec SM movementParkinson’s

Site 2: striatum
Mechanism:
Acts on striatumdec dopamine effects on striatumdec SM movementParkinson’s

Site 3: substantia nigra
Mechanism:
Acts on substantia nigradestroys axons and cell bodies in SNdec functiondec dopamine produceddec smooth muscle movementParkinson’s

33

Three manifestations for Parkinson's

1. Tremor at rest
2. Bradykinesia
3. Mast face, lead pipe, cogwheel

34

Three lab manifestations for Parkinson's

1. dec dopamine, inc dopamine inhibitors
2. inc AchE

35

Three treatments for Parksinon's

Treatment 1: stem cells
Mechanism:
Stem cellsreplace neuronsnew functioning neurons in SNinc movementParkinson’s treated

Treatment 2: DA-agonists/L-Dopa
Mechanism:
L-Dopacrosses BBBinc metabolizing of dopamine in SNinc dopamineinc movementno Parkinson’s

Treatment 3: exercise and music
Mechanism:
Exercise and musickeeps neurons activedec neurons lost to disuseinc plasticity in braindec rigidityno Parkinson’s

36

Give three different sites and the mechanism for MG.

Site 1: Ach receptor
Mechanism:
Damaged Ach receptordec Ach binding on muscledec neuromuscular transmissionMG

Site 2: Ab
Mechanism:
Ab producedAb attach to Ach receptordec Ach receptorsdec Ach bindingdec neuromuscular transmissionMG

Site 3: end-plate
Mechanism:
Damaged end-platede-differentiation of end plate and dec Ach receptorsreplaced with connective tissuemuscles aren’t activateddec neuromuscular transmissionMG

37

Three manifestations for MG

1. Weakness of extremities, progressive fatigue
2. Ocular muscle weakness and diplopia
3. Difficulty swallowing and chewing

38

Two lab manifestations for MG

1. Inc Ab
2. dec Ach receptors

39

Three treatment types for MG

Treatment 1: prednisose
Mechanism:
Prednisoneturns off autoimmuneno Abno destruction of Ach receptorAch binds normally to receptorinc neuromuscular transmissionno MG

Treatment 2: plasmaphoresis
Mechanism:
Plasmaphoresisfilters plasmarid plasma of Abdec Ab circulatingdec destruction of Ach receptorsinc neuromuscular transmissionno MG

Treatment 3: AchE inhibitor
Mechanism:
AchE inhibiteddec AchE effectsdec Ach breakdown by AchE inc Achinc activation of muscles by Ach bindingdelay de-differentiationno MG

40

Give three sites and the mechanism for developing MS. List three manifestations and three LAB manifestations. Give three possible treatments and the mechanisms for treating MS.

Site 1: Ab
Mechanism:
Ab activationAb acts on myelindemyelinationdec insulationdec signal transmission through bodyMS

Site 2: White matter lesions
Mechanism:
White matter lesionsdamage myelin nerve axonsdec signal transmissionMS

Site 3: oligodendrocytes
Mechanism:
Acts on oligodendrocytescauses inflammation of oligodendrocytesscarringdec myelin functiondec signal transmissionMS

41

Three manifestations of MS

1. Cerebellar ataxia
2. Proprioceptive disorder
3. Diplopia

42

Three lab manifestations of MS

1. inc Ab, inc WBC
2. dec vitamin D
3. scarring on myelin

43

Three treatments for MS

Treatment 1: vitamin D
Mechanism:
Vitamin dturns off auto-immunityno Abno demyelinationno MS

Treatment 2: decoy
Mechanism:
Decoymimics oligodendrocytes on myelinAb attack decoyhost cells unaffectedno MS

Treatment 3: prednisone
Mechanism:
Prednisoneimmune suppression anti-inflammatoryno Ab produced, no inflammation of oligodendrocytesno demyelination or scarringno MS

44

Why is increased ICP an emergency?

Inc ICPdec blood supply and O2 supply to braincell necrosisprominent irreversible brain damage

45

Give the goal and the mechanism for Cushing’s reflex.

Goal: restore CPP and maintain perfusion
Mechanism:
Inc ICPdec HRinc diastolic filldec systolicwidens pulse pressureinc contraction forceinc CPP